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Objective:To figure out the timing of zeroing and the location of the zero line in the central venous pressure (CVP) monitoring and invasive arterial blood pressure (IBP) monitoring, and to provide scientific and accurate data for patients management.Methods:The liquid vessel models were used to simulate the pressure measurement process of the continuous pressure monitoring system. Based on the theory of fluid mechanics and the knowledge of blood pressure physiology and cardiovascular anatomy, the composition and influencing factors of the pressure in the fluid-filled catheter system during the zeroing and placing the transducer in the zero line of CVP and IBP, were analyzed.Results:The pressure in the liquid-filled catheter system was composed of atmospheric pressure, the pressure of pumping bag, the gravity of the water column (the vertical distance between the liquid level of Murphy's dropper and pressure transducer, ΔH), and the resistance of tube wall. This pressure value is set as a pressure of 0 mmHg (1 mmHg ≈ 0.133 kPa). In the process of pressure measurement, when the pressure transducer was placed at a horizontal position of 10 cm below the highest liquid level of the vessel, the pressure measured at different catheter tip positions was all 10 cmH 2O (1 cmH 2O ≈ 0.098 kPa); When the pressure transducer was placed at the horizontal position of the highest liquid level of the vessel, the measured pressure is 0 mmHg. Conclusion:Zeroing should repeatedly be performed only when one or more conditions (atmospheric pressure, pressure of pumping bag, gravity of ΔH water column and resistance of tube wall) are changed. In the measurement process, the pressure transducer should be placed at the zero line position at any time to eliminate the influence of hydrostatic pressure and to ensure the objective and accurate value.
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Objective:To investigate whether myocardial inflammation and apoptosis are involved in right ventricular dysfunction (RVD) induced by injurious mechanical ventilation with high tidal volume (VT) in rats.Methods:Total 30 adult male SD rats were randomly divided into the control group (CON group), the low VT ventilation group (LVT group) and the injurious mechanical ventilation group (HVT group), with 10 rats in each group. The CON group was maintained spontaneous breathing, the LVT group and HVT group were ventilated with different VT 6 mL/kg and 20 mL/kg for 4 hours, respectively. The right jugular vein and the left carotid artery were catheterized and connected with the PowerLab biological signal acquisition and analysis system to record heart rate (HR), mean arterial pressure (MAP), right ventricular systolic pressure (RVSP), the maximum rate of rising of right ventricular pressure (+dp/dt max). Echocardiography was performed to measure left ventricular end-diastolic diameter (LVEDd), right ventricular end-diastolic diameter (RVEDd), tricuspid annulus plane systolic migration (TAPSE) and myocardial performance index (MPI). The rats were sacrified by cervical dislocation. Specimens of right ventricle tissues were taken for hematoxylin-eosin (HE) staining, and morphological changes of right ventricle tissues were observed under light microscope. Real time reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting were used to detect the mRNA and protein expressions of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), caspase-3, apoptosis-related proteins Bax and Bcl-2.Results:HR, MAP, +dp/dt max gradually decreased, while RVSP gradually increased in different group with the increase of VT ventilation. There was no significant difference between the CON group and LVT group. However, there was a statistically significant difference with respect to these index in HVT group as compared to CON group and LVT group [HR (bpm): 397.6±5.7 vs. 433.0±4.8, 441.6±7.8; MAP (mmHg, 1 mmHg≈0.133 kPa): 102.0±2.4 vs. 108.5±2.2, 110.6±2.1; +dp/dt max (mmHg/s): 2 357.65±62.80 vs. 2 661.27±55.62, 2 679.43±75.13; RVSP (mmHg): 28.8±1.0 vs. 22.6±10.8, 21.9±0.4; all P < 0.05]. Echocardiography findings showed that RVEDd/LVEDd and MPI gradually increased, TAPSE gradually decreased in different group with the increase of VT ventilation. There was no significant difference between the LVT group and CON group. However, there was a statistically significant difference with respect to these indexes in HVT group as compared to the CON group and LVT group [RVEDd/LVEDd: 0.36±0.02 vs. 0.26±0.01, 0.23±0.02; MPI: 1.23±0.03 vs. 0.84±0.04, 0.86±0.03; TAPSE (mm): 1.65±0.03 vs. 1.88±0.02, 1.91±0.04; all P < 0.05]. Histopathological observation of the right ventricle tissue showed that myocardial cells of the rats in the CON group were orderly arranged and uniformed in size. In the LVT group, there was a small amount of inflammatory cell infiltration in the myocardial interstitium, while in the HVT group, the myocardial cell arrangement was obviously disordered, the structure was obviously damaged, and more inflammatory cell infiltration was found. RT-PCR and Western blotting analysis showed that the mRNA and protein expressions of IL-6, TNF-α, caspase-3 and Bax in HVT group were significantly higher than those in the LVT group and CON group [mRNA expression (2 -ΔΔCt): IL-6 were 1.97±0.07 vs. 1.09±0.02, 1.02±0.03, TNF-α were 1.69±0.10 vs. 1.10±0.03, 1.05±0.04, caspase-3 were 1.82±0.09 vs. 1.08±0.02, 1.06±0.03, Bax were 2.19±0.14 vs. 1.07±0.03, 1.04±0.03; protein expression (gray value): IL-6 were 0.64±0.02 vs. 0.38±0.03, 0.31±0.04, TNF-α were 0.50±0.04 vs. 0.16±0.01, 0.15±0.01, caspase-3 were 0.58±0.02 vs. 0.29±0.01, 0.25±0.02, Bax were 0.50±0.03 vs. 0.21±0.01, 0.26±0.02; all P < 0.05], and the mRNA and protein expressions of Bcl-2 in the HVT group were lower than those in the LVT group and CON group [mRNA expression (2 -ΔΔCt): 1.23±0.05 vs. 1.43±0.05, 1.50±0.08; protein expression (gray value): 0.42±0.02 vs. 0.62±0.03, 0.65±0.03, all P < 0.05]. Conclusion:Myocardial inflammation and apoptosis may be involved in RVD induced by injurious mechanical ventilation.
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Objective:To explore the effect of different tidal volumes (VT) on the hemodynamics of right heart in acute respiratory distress syndrome (ARDS) rats induced by oleic acid (OA).Methods:Sixty adult male Sprague-Dawley (SD) rats were divided into control group ( n = 20), ARDS model group ( n = 20), low VT (LVT) group ( n = 10) and high VT (HVT) group ( n = 10) by random number table. ARDS model was reproduced by injecting OA 0.15 mL/kg through a jugular vein. The control group was given the same amount of normal saline. The success of modeling was judged by the oxygenation index (PaO 2/FiO 2) 2 hours after modeling, at the same time, the lung tissues were collected, the wet/dry weight (W/D) ratio was determined, and the lung histopathological changes were measured by lung injury score. The rats in the LVT group and HVT group were given mechanical ventilation with VT of 6 mL/kg or 20 mL/kg for 4 hours, respectively at 2 hours after modeling. The rats in the control group and the ARDS model group maintained spontaneous breathing. After mechanical ventilation for 4 hours, the heart rate (HR), right ventricular systolic pressure (RVSP), the maximum rate of rising of right ventricular pressure (dp/dt max), and the blood pressure (BP) were measured. Meanwhile, arterial blood samples were collected for blood gas analysis, including pH value, arterial partial pressure of oxygen (PaO 2), arterial partial pressure of carbon dioxide (PaCO 2) and PaO 2/FiO 2. Results:The rats in the ARDS model group showed symptoms of respiratory distress 1 hour after modeling, and the lung tissue samples showed obvious patchy bleeding 2 hours after modeling, while the control group showed no such changes. The PaO 2/FiO 2 in the ARDS model group was significantly lower than that in the control group [mmHg (1 mmHg = 0.133 kPa): 294.3±5.9 vs. 459.0±4.4, P < 0.01], and the lung W/D ratio and lung injury score were significantly higher (lung W/D ratio: 8.24±0.25 vs. 4.48±0.13, lung injury score: 0.60±0.03 vs. 0.12±0.02, both P < 0.01). It indicated that ARDS model was successfully reproduced. The arterial blood gas analysis and hemodynamic parameters of the ARDS model group were significantly worse than those of the control group. After 4-hour mechanical ventilation, the blood gas parameters of the LVT group were better than those of the ARDS model group and the HVT group [pH value: 7.36±0.02 vs. 7.24±0.02, 7.13±0.01; PaO 2 (mmHg): 92.4±2.1 vs. 61.8±2.3, 76.6±2.2; PaCO 2 (mmHg): 49.6±1.7 vs. 61.8±1.8, 33.6±1.3; PaO 2/FiO 2 (mmHg): 440.0±10.2 vs. 274.3±21.4, 364.7±10.5; all P < 0.05]. HR, BP and dp/dt max in the LVT group were significantly higher than those in the ARDS model group and the HVT group [HR (bpm): 346.9±5.4 vs. 302.3±10.1, 265.5±12.2; BP (mmHg): 125.4±2.2 vs. 110.0±2.5, 89.2±2.8; dp/dt max (mmHg/s): 1 393.3±30.3 vs. 1 236.4±20.5, 896.1±19.5; all P < 0.05], and RVSP was significantly lower than that in the ARDS model group and the HVT group (mmHg: 31.3±0.4 vs. 34.0±1.0, 38.8±0.9, both P < 0.05). Conclusion:Mechanical ventilation with low VT can improve the hemodynamic parameters of the right ventricle and protect the function of the right heart in ARDS rats.
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Objective:To investigate the correlation of monocyte/lymphocyte ratio (MLR) with the prognosis and adverse event in critically ill patients.Methods:Basic information of patients were extracted from Medical Information Mart for Intensive Care-Ⅲ (MIMIC-Ⅲ), including demographics, blood routine, biochemical indexes, systemic inflammatory response syndrome score (SIRS), sequential organ failure assessment (SOFA) score, and outcome, etc. MLR on the first day of intensive care unit (ICU) admission was calculated. The receiver operating characteristic curve (ROC curve) was applied to evaluate the prognostic value of MLR on the 30-day mortality and its cut-off value. According to the cut-off value, the patients were divided into two groups, and the differences between the groups were compared. Logistic regression model was used to analyze the relationship of MLR with 30-day mortality, continuous renal replacement therapy (CRRT), mechanical ventilation, the length of ICU stay, and total hospitalization time.Results:① A total of 43 174 critically ill patients were included. ROC curve showed that area under ROC curve (AUC) of MLR in predicting 30-day mortality was 0.655 [95% confidence interval (95% CI) was 0.632-0.687]. The cut-off value of MLR calculated according to the maximum Yoden index was 0.5. There were 16 948 patients with MLR ≥ 0.5 (high MLR group) and 26 226 patients with MLR < 0.5 (low MLR group). ② Compared with the low MLR group, the high MLR group had higher age, proportion of male, body mass index (BMI) [age (years old): 66.0 (51.7, 78.4) vs. 57.6 (27.1, 74.6), proportion of male: 57.2% vs. 52.5%, BMI (kg/m 2): 26.5 (22.5, 31.1) vs. 24.7 (14.3, 29.7)]. The high MLR group also had higher incidence of complications (hypertension: 49.2% vs. 44.6%, chronic heart failure: 32.6% vs. 21.7%, diabetes mellitus: 27.0% vs. 23.4%, chronic obstructive pulmonary disease: 21.5% vs. 16.1%, renal insufficiency: 19.3% vs. 13.1%), and higher white blood cell count (WBC), blood glucose, lactate (Lac), serum creatinine (SCr), SIRS score and SOFA score [WBC (×10 9/L): 13.8 (9.6, 19.2) vs. 11.5 (8.4, 15.6), blood glucose (mmol/L): 8.66 (6.88, 11.49) vs. 8.27 (6.55, 10.88), Lac (mmol/L): 2.2 (1.5, 3.7) vs. 2.1 (1.4, 3.3), SCr (μmol/L): 106.1 (70.7, 176.8) vs. 88.4 (70.7, 132.6), SIRS score: 3 (2, 4) vs. 2 (2, 3), SOFA score: 4 (2, 7) vs. 3 (1, 5)]. The 30-day mortality, and the proportion of patients with length of ICU stay > 5 days, total hospitalization time > 14 days, CRRT and mechanical ventilation > 5 days were significantly higher in high MLR group (30-day mortality: 20.0% vs. 8.3%, length of ICU stay > 5 days: 33.2% vs. 20.4%, total hospitalization time > 14 days: 33.7% vs. 16.2%, CRRT: 3.6% vs. 0.7%, mechanical ventilation > 5 days: 18.4% vs. 5.7%), with statistically significant differences (all P < 0.05). ③ After adjusted with the related factors, multivariate Logistic regression analysis showed that elevated MLR was an independent risk factor for increased 30-day mortality [odd ratio ( OR) = 1.54, 95% CI was 1.37-1.72, P < 0.001]. Moreover, the increased MLR was independently associated with the increased risk of usage of CRRT ( OR = 2.77, 95% CI was 2.18-3.51), mechanical ventilation > 5 days ( OR = 2.45, 95% CI was 2.21-2.72), the length of ICU stay > 5 days ( OR = 2.29, 95% CI was 2.10-2.49), and total hospitalization time > 14 days ( OR = 2.28, 95% CI was 2.08-2.49), all P < 0.001. Conclusions:Retrospective analysis of large sample shows that MLR elevation is an independent risk factor for 30-day mortality, usage of CRRT, prolonged mechanical ventilation time, prolonged hospitalization, prolonged length of ICU stay. MLR can be used for risk stratification of severe patients.
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Despite the great improvements in the techniques and perioperative management of liver transplantation in recent years, there are still several perioperative complications that may lead to the poor prognosis of recipients. Prolonged mechanical ventilation (PMV) is a common complication in the early stage after surgery and may result in a high incidence rate of postoperative complications, prolonged length of stay in the intensive care unit and hospital stay, and an increase in mortality rate. In recent years, many studies have reported PMV after liver transplantation, but no summarization and statistical analysis have been performed and there are still no effective measures to prevent PMV after liver transplantation. This article summarizes the influencing factors and interventions for PMV after liver transplantation, in order to provide valuable information for reducing the duration of mechanical ventilation after liver transplantation and improving the prognosis of liver transplantation recipients.
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Objective@#To investigate the role of endoplasmic reticulum stress (ERS) in rats with acute respiratory distress syndrome (ARDS) related right ventricular dysfunction and the protective effect of sodium 4-phenylbutyrate (4-PBA) on right ventricle.@*Methods@#Sixty male Spragne-Dawley (SD) rats were randomly divided into control group (CON group), lipopolysaccharide (LPS) model group, 4-PBA prevention group and 4-PBA treatment group, with 15 rats in each group. ARDS rat model was established by intratracheal instillation of LPS 10 mg/kg after tracheotomy; CON group was given the same amount of saline. 4-PBA prevention group and 4-PBA treatment group were given 4-PBA 500 mg/kg intragastric administration 2 hours before and after LPS respectively. Echocardiography was performed 12 hours after treatment to evaluate the right ventricular function. Then, the rats were sacrificed by bloodletting, and the serum and right ventricular tissue were harvested. The histopathological changes of myocardial were observed by hematoxylin-eosin (HE) staining, the levels of tumor necrosis factor-α(TNF-α), interleukins (IL-1β and IL-6) in serum and myocardial were detected by enzyme linked immunosorbent assay (ELISA), and Western Blot was used to detect the expression of the marker proteins of ERS in myocardial, including glucose regulatory protein 78 (GRP78), C/EBP cyclic adenosine phosphate reaction primitive binding transcription factor homologous protein (CHOP), caspase-12 and caspase-3.@*Results@#Compared with the CON group, the echocardiography showed pulmonary artery maximum pressure gradient (PAmaxPG), pulmonary artery acceleration time (PAAT), tricuspid annular plane systolic excursion (TAPSE) in LPS model group were significantly decreased, and right ventricular end-diastolic excursion (RVDd) was significantly increased, and the levels of TNF-α, IL-1β and IL-6 in serum and myocardial, as well as the expressions of GRP78, CHOP, caspase-12 and caspase-3 in myocardial were significantly increased. Compared with LPS model group, TAPSE of 4-PBA preventive and treatment groups were significantly increased (mm: 3.08±0.65, 2.96±0.61 vs. 2.48±0.45), RVDd were significantly decreased (mm: 3.67±0.58, 3.60±0.61 vs. 4.18±0.71), the levels of TNF-α, IL-1β and IL-6 in serum and myocardial were significantly decreased [TNF-α (ng/L): 187.98±18.98, 176.08±17.98 vs. 332.00±19.90 in serum, 135.06±19.00, 132.78±17.00 vs. 155.00±20.00 in myocardial; IL-1β(ng/L): 12.07±2.98, 11.05±2.41 vs. 24.06±4.01 in serum, 19.89±2.80, 21.06±2.80 vs. 26.00±2.60 in myocardial; IL-6 (ng/L): 42.98±7.90, 34.05±6.09 vs. 89.80±10.07 in serum, 129.45±25.00, 127.08±26.06 vs. 145.77±23.00 in myocardial]; the expressions of GRP78, CHOP, caspase-12 and caspase-3 in myocardial were significantly decreased (GRP78/GAPDH: 0.090±0.070, 0.103±0.060 vs. 0.167±0.090, CHOP/GAPDH: 0.109±0.090, 0.090±0.080 vs. 0.186±0.090, caspase-12/GAPDH: 0.769±0.230, 0.799±0.210 vs. 1.040±0.350, caspase-3/GAPDH: 0.391±0.060, 0.401±0.054 vs. 0.603±0.340), with statistically significant differences (all P < 0.05). There were no significant differences in each indexes between 4-PBA prevention group and 4-PBA treatment group (all P > 0.05).@*Conclusions@#ERS is involved in ARDS-related right ventricular dysfunction. 4-PBA can protect the right ventricular function of ARDS rats by inhibiting ERS and alleviating inflammation, and the preventive and therapeutic effects of 4-PBA are similar.
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Objective To investigate the role of endoplasmic reticulum stress (ERS) in rats with acute respiratory distress syndrome (ARDS) related right ventricular dysfunction and the protective effect of sodium 4-phenylbutyrate (4-PBA) on right ventricle. Methods Sixty male Spragne-Dawley (SD) rats were randomly divided into control group (CON group), lipopolysaccharide (LPS) model group, 4-PBA prevention group and 4-PBA treatment group, with 15 rats in each group. ARDS rat model was established by intratracheal instillation of LPS 10 mg/kg after tracheotomy; CON group was given the same amount of saline. 4-PBA prevention group and 4-PBA treatment group were given 4-PBA 500 mg/kg intragastric administration 2 hours before and after LPS respectively. Echocardiography was performed 12 hours after treatment to evaluate the right ventricular function. Then, the rats were sacrificed by bloodletting, and the serum and right ventricular tissue were harvested. The histopathological changes of myocardial were observed by hematoxylin-eosin (HE) staining, the levels of tumor necrosis factor-α (TNF-α), interleukins (IL-1β and IL-6) in serum and myocardial were detected by enzyme linked immunosorbent assay (ELISA), and Western Blot was used to detect the expression of the marker proteins of ERS in myocardial, including glucose regulatory protein 78 (GRP78), C/EBP cyclic adenosine phosphate reaction primitive binding transcription factor homologous protein (CHOP), caspase-12 and caspase-3. Results Compared with the CON group, the echocardiography showed pulmonary artery maximum pressure gradient (PAmaxPG), pulmonary artery acceleration time (PAAT), tricuspid annular plane systolic excursion (TAPSE) in LPS model group were significantly decreased, and right ventricular end-diastolic excursion (RVDd) was significantly increased, and the levels of TNF-α, IL-1β and IL-6 in serum and myocardial, as well as the expressions of GRP78, CHOP, caspase-12 and caspase-3 in myocardial were significantly increased. Compared with LPS model group, TAPSE of 4-PBA preventive and treatment groups were significantly increased (mm: 3.08±0.65, 2.96±0.61 vs. 2.48±0.45), RVDd were significantly decreased (mm: 3.67±0.58, 3.60±0.61 vs. 4.18±0.71), the levels of TNF-α, IL-1β and IL-6 in serum and myocardial were significantly decreased [TNF-α (ng/L): 187.98±18.98, 176.08±17.98 vs. 332.00±19.90 in serum, 135.06±19.00, 132.78±17.00 vs. 155.00±20.00 in myocardial; IL-1β(ng/L): 12.07±2.98, 11.05±2.41 vs. 24.06±4.01 in serum, 19.89±2.80, 21.06±2.80 vs. 26.00±2.60 in myocardial; IL-6 (ng/L): 42.98±7.90, 34.05±6.09 vs. 89.80±10.07 in serum, 129.45±25.00, 127.08±26.06 vs. 145.77±23.00 in myocardial]; the expressions of GRP78, CHOP, caspase-12 and caspase-3 in myocardial were significantly decreased (GRP78/GAPDH: 0.090±0.070, 0.103±0.060 vs. 0.167±0.090, CHOP/GAPDH: 0.109±0.090, 0.090±0.080 vs. 0.186±0.090, caspase-12/GAPDH: 0.769±0.230, 0.799±0.210 vs. 1.040±0.350, caspase-3/GAPDH: 0.391±0.060, 0.401±0.054 vs. 0.603±0.340), with statistically significant differences (all P < 0.05). There were no significant differences in each indexes between 4-PBA prevention group and 4-PBA treatment group (all P > 0.05). Conclusions ERS is involved in ARDS-related right ventricular dysfunction. 4-PBA can protect the right ventricular function of ARDS rats by inhibiting ERS and alleviating inflammation, and the preventive and therapeutic effects of 4-PBA are similar.
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Objective To investigate the role of endoplasmic reticulum stress (ERS) in rats with acute respiratory distress syndrome (ARDS) related right ventricular dysfunction and the protective effect of sodium 4-phenylbutyrate (4-PBA) on right ventricle. Methods Sixty male Spragne-Dawley (SD) rats were randomly divided into control group (CON group), lipopolysaccharide (LPS) model group, 4-PBA prevention group and 4-PBA treatment group, with 15 rats in each group. ARDS rat model was established by intratracheal instillation of LPS 10 mg/kg after tracheotomy; CON group was given the same amount of saline. 4-PBA prevention group and 4-PBA treatment group were given 4-PBA 500 mg/kg intragastric administration 2 hours before and after LPS respectively. Echocardiography was performed 12 hours after treatment to evaluate the right ventricular function. Then, the rats were sacrificed by bloodletting, and the serum and right ventricular tissue were harvested. The histopathological changes of myocardial were observed by hematoxylin-eosin (HE) staining, the levels of tumor necrosis factor-α (TNF-α), interleukins (IL-1β and IL-6) in serum and myocardial were detected by enzyme linked immunosorbent assay (ELISA), and Western Blot was used to detect the expression of the marker proteins of ERS in myocardial, including glucose regulatory protein 78 (GRP78), C/EBP cyclic adenosine phosphate reaction primitive binding transcription factor homologous protein (CHOP), caspase-12 and caspase-3. Results Compared with the CON group, the echocardiography showed pulmonary artery maximum pressure gradient (PAmaxPG), pulmonary artery acceleration time (PAAT), tricuspid annular plane systolic excursion (TAPSE) in LPS model group were significantly decreased, and right ventricular end-diastolic excursion (RVDd) was significantly increased, and the levels of TNF-α, IL-1β and IL-6 in serum and myocardial, as well as the expressions of GRP78, CHOP, caspase-12 and caspase-3 in myocardial were significantly increased. Compared with LPS model group, TAPSE of 4-PBA preventive and treatment groups were significantly increased (mm: 3.08±0.65, 2.96±0.61 vs. 2.48±0.45), RVDd were significantly decreased (mm: 3.67±0.58, 3.60±0.61 vs. 4.18±0.71), the levels of TNF-α, IL-1β and IL-6 in serum and myocardial were significantly decreased [TNF-α (ng/L): 187.98±18.98, 176.08±17.98 vs. 332.00±19.90 in serum, 135.06±19.00, 132.78±17.00 vs. 155.00±20.00 in myocardial; IL-1β(ng/L): 12.07±2.98, 11.05±2.41 vs. 24.06±4.01 in serum, 19.89±2.80, 21.06±2.80 vs. 26.00±2.60 in myocardial; IL-6 (ng/L): 42.98±7.90, 34.05±6.09 vs. 89.80±10.07 in serum, 129.45±25.00, 127.08±26.06 vs. 145.77±23.00 in myocardial]; the expressions of GRP78, CHOP, caspase-12 and caspase-3 in myocardial were significantly decreased (GRP78/GAPDH: 0.090±0.070, 0.103±0.060 vs. 0.167±0.090, CHOP/GAPDH: 0.109±0.090, 0.090±0.080 vs. 0.186±0.090, caspase-12/GAPDH: 0.769±0.230, 0.799±0.210 vs. 1.040±0.350, caspase-3/GAPDH: 0.391±0.060, 0.401±0.054 vs. 0.603±0.340), with statistically significant differences (all P < 0.05). There were no significant differences in each indexes between 4-PBA prevention group and 4-PBA treatment group (all P > 0.05). Conclusions ERS is involved in ARDS-related right ventricular dysfunction. 4-PBA can protect the right ventricular function of ARDS rats by inhibiting ERS and alleviating inflammation, and the preventive and therapeutic effects of 4-PBA are similar.
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Right ventricular failure (RVF) is the main cause of death in patients with cardiopulmonary disease, such as pulmonary arterial hypertension (PAH), pulmonary embolism, acute respiratory distress syndrome, and right ventricular infarction. The exact cellular and molecular mechanisms underlying RVF remains unclear. Inflammation may play an important role during the development of RVF, as it does in left heart failure. Cardiac inflammation has been shown in RVF patients and animal models, which played a role in the impairment of the right ventricular contraction and in the maladaptive remodeling. Inflammation plays a dual role in the development of cardiopulmonary disease and its anti-inflammatory therapies may have double benefits for RVF patients. This review summarizes the evidence of inflammation in RVF and research progresses of inflammation in the development of RVF to provide a reference for further exploring the mechanism of inflammation in RVF.
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Objective To explore the effect of acute respiratory distress syndrome (ARDS) induced by endotoxin on the right ventricular function in rats. Methods Sixty male Sprague-Dawley (SD) rats were randomly divided into normal saline (NS) control group and lipopolysaccharide (LPS) model group with 30 rats in each group. The rat model of ARDS was reproduced by intratracheal instillation of LPS 10 mg/kg after tracheotomy, and the rats in NS control group was intratracheally given the same volume of NS instead of LPS. The survival of rats in each group was observed. Right ventricular function was evaluated by echocardiography at 6 hours and 12 hours after instillation of LPS or NS respectively. Then the rats were sacrificed by bloodletting, and the right heart and lung tissue were harvested. The lung wet/dry weight (W/D) ratio was assessed. The pathological changes in cardiopulmonary tissue in rats were observed with hematoxylin and eosin (HE) strain, and the pathological score of lung injury was calculated. Results There was no animal death in NS control group. In LPS model group, there were 3 rats dead at 6 hours, and 4 dead at 12 hours. The pathological manifestations of lung injury were found at 6 hours after instillation of LPS, and the marked pathological changes of ARDS, such as atelectasis and hyaline membranes were observed at 12 hours. There was no obvious abnormality in the lung tissue of the NS control group. Compared with the NS control group, the 12-hour lung W/D ratio and the lung injury pathological score in the LPS model group were significantly increased (lung W/D ratio:7.69±1.02 vs. 4.14±0.48, lung injury pathological score: 8.26±2.12 vs. 1.32±0.94, both P < 0.01). Echocardiography showed that the right heart function of rats was significantly abnormal with the prolongation of LPS induction time, which showed that pulmonary arterial diameter (PAD) and right ventricular diastolic diameter (RVDd) were increased, maximum blood flow velocity of pulmonary artery (PAVmax), maximum pulmonary artery pressure gradient (PAmaxPG),pulmonary artery acceleration time (PAAT) and tricuspid annular plane systolic excursion (TAPSE) were decreased, with significant differences at 12 hours as compared with those of NS normal group [PAD (mm): 2.84±0.31 vs. 2.11±0.37, RVDd (mm): 4.18±0.71 vs. 3.17±0.40, PAVmax (mm/s): 704.00±145.13 vs. 809.59±120.48, PAmaxPG (mmHg, 1 mmHg = 0.133 kPa): 2.07±0.88 vs. 2.73±0.76, PAAT (ms): 23.80±4.87 vs. 30.01±3.02, TAPSE (mm): 2.48±0.45 vs. 3.56±0.40, all P < 0.01]. Pathological examination showed that the cardiac tissue in the LPS model group showed disorder of myocardial cells and scattered inflammatory cells at 6 hours, and cardiomyocyte degeneration, structural destruction and inflammatory cells were found at 12 hours. Conclusion ARDS induced by instillation of LPS at 12 hours causes right ventricular dysfunction in rats.
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Objective To investigate the effect of pre-transplant metabolic syndrome (MS) on new-onset postoperative atrial fibrillation (POAF) in adult liver transplant recipients.Methods Adult patients (age ≥18 years) who underwent primary liver transplantation at the UCLA Medical Center between January 2009 and December 2015 were retrospectively reviewed.Clinical data were collected after obtaining institutional review board approval.MS was defined according to the 2009 harmonized definition.POAF was defined as new-onset atrial fibrillation within 30 days after liver transplantation in patients without chronic persistent atrial fibrillation.Patients were divided into two groups:MS and non-MS groups.Incidence of POAF was compared between two groups.Then,univariate and multivariate logistic regression analyses were performed to assess the relationships between MS and POAF.Results Of 842 patients,prevalence of pre-transplant MS was 29.4％.POAF occurred in 71 patients (8.4％).The incidence of POAF between MS and non-MS groups significantly differed (14.6％ vs.5.9％,P＜0.01).The logistic regression analysis revealed that the presence of MS was significantly associated with POAF [odd ratios (OR) 2.290,95％ CI 1.342-3.907].Other risk factors include recipient age,prior history of AF,and preoperative baseline creatinine (OR 1.030,2.479 and 1.380,respectively,all P＜0.05).Conclusion The presence of pre-transplant MS is an independent risk factor for POAF in liver transplantation patients.Pre-transplant MS should be properly diagnosed and managed before transplantation.
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Right ventricular failure(RVF)is a severe clinical syndrome that affects human health seriously.The establishment and application of experimental animal models are critical to research the pathogenesis, pathophysiology, prevention and treatment of RVF.Recently, numerous researchers have studied the modeling methods and testing indexes of RVF of animal models, which has improved the success rate and quality of the models.However, even if so many models, there is still no widely accepted experimental animal model of RVF because of the different and complex modeling methods, material selection and experimental conditions.This article reviews the methods and mechanism of multiple experimental animal models of RVF and compares them, so as to provide reference for choosing and applying experimental animal models of RVF in the study.
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Acute respiratory distress syndrome (ARDS) is a severe respiratory condition that is characterized by rapidly progressive hypoxemia with noncardiogenic pulmonary edema.Despite the improvement of therapeutic methods,the mortality of ARDS is in the range of 40％-50％ all over the world.Some studies have shown that a significant number of patients with ARDS had acute cor pulmonale (ACP),and ACP is independently associated with the mortality of patients with ARDS,which has attracted wide attention in recent years.This paper reviewed recent related studies,summarized the prevalence,pathogenesis and diagnostic approaches of ACP in ARDS,especially echocardiography which was considered as a cornerstone for ACP diagnosis,and elucidated the beneficial effects of right ventricular protective ventilatory strategy and prone-positioning on the pulmonary vasculature and right heart,in order to provide a novel idea for the therapy of ACP in ARDS.
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Objective To evaluate the diagnostic accuracy of Streptocuccus pneumoniae urinary antigen test (SpUAT) in patients with community acquired Streptocuccus pneumoniae pneumoniae (SPP). Methods The clinical studies relating SpUAT diagnostic accuracy for community acquired Streptocuccus pneumoniae infection were searched via computer and manual screening of Chinese databases including China National Knowledge Internet (CNKI), China Biology Medicine disc, China Technical Journal Full-text Database, and Wanfang Database as well as English databases such as PubMed, EBSCO, Elsevier Science, Ovid Technologies, and Springer. Data were extracted according to appropriate inclusion and exclusion criteria and analyzed with Meta-disc 1.4 and Stata 12.0 software. Pooled sensitivity, specificity, positive likelihood ratio, negative likelihood ratio as well as diagnostic odds ratio (DOR) were calculated, and summary receiver operating characteristic curve (SROC) was plotted and area under SROC (AUC) was calculated to analyze the diagnostic accuracy of SpUAT for adult community acquired SPP. Results A total of 15 studies enrolling 6 866 patients were included, all of which with a quality assessment of diagnostic accuracy studies (QUADAS) score not lower than 10, indicating a high study quality. Random effect model was applied owing to non-threshold effect associated heterogeneity. It was shown by Meta analysis that compared with routine pathogen diagnosis (hemoculture, sputum smears, sputum culture and trachea and bronchus attractive culture), the pooled sensitivity, pooled specificity, pooled positive likelihood ratio, and pooled negative likelihood ratio was 73% [95% confidence interval (95%CI) = 71%-76%,] 91% (95%CI = 90%-92%), 6.97 (95%CI = 4.13-11.77), and 0.30 (95%CI = 0.26-0.34), respectively, pooled DOR was 24.34 (95%CI = 13.14-45.11), and AUC of SROC was 0.8051±0.0362. It was indicated by heterogeneity test that experiment design (prospective or retrospective), sample sizes (lower than 200 or higher than or equal to 200), reference test (fewer than 3 or more than or equal to 3 test methods), or literature language (Hispanic or non-Hispanic) had no effect on study heterogeneity, indicating certain other unknown factors may be involved. Funnel plot suggested that 15 involved studies uniformly distributed along the two sides of regression line, indicating no publication bias. Conclusions The use of SpUAT for the diagnosis of adult community acquired SPP has a moderate sensitivity and high specificity. Although the overall accuracy of SpUAT diagnosis is relatively high, there is significant heterogeneity among the studies, so more high-quality studies are needed.
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Objective To analyze the risk factors of postoperatively prolonged mechanical ventilation (PMV) after liver transplantation.Method The clinical data of 117 patients who received liver transplantation were retrospectively reviewed.According to the duration of postoperative mechanical ventilation (＜24 h or ≥24 h),the patients were divided into two groups.Commonly-used clinical and lab indexes before,during and after operations were analyzed by using single variance logistic regression analysis,and the screened indexes were analyzed by stepwise multiple variance logistic regression analysis.Result Forty-two patients (35.9％) were diagnosed with PMV after liver transplantation.The intensive care unit stay in the control group was (1.60 ± 1.17) days,shorter than in PMV proup (9.35 ± 10.61days).Sixty indexes were analyzed by univarite logistic regression,and 49 indexes showed statistically significant differences (P ＜ 0.2).Multiple variance logistic regression analysis revealed that the levels of preoperative blood glucose,model for end-stage liver disease score (MELD),the blood loss volume during the operation and the levels of glutamic oxalacetic transaminase within 24 h after the operation showed significant difference.Conclusion Preoperative hyperglycemia,high MELD score,excessive intraoperative blood loss volume and the high level of glutamic oxalacetic transaminase after the operation are independent risk factors of PMV.
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Aim To study mRNA and protein expression of eNOS in pulmonary tissue of chronic hypoxic pulmonary hypertension(HPH)rats and chronic hypoxic rats treated with novel KATP opener iptakalim.Methods sixty Sprague-Dawley(SD)male rats were randomly divided into control group, hypoxic group, low dose iptakalim group(0.75 mg·kg~(-1)·d~(-1)), and high dose iptakalim group(1.5 mg·kg~(-1)·d~(-1)).Except the first group, the other three groups were put into hypoxic and normobaric chamber (10%±0.5% O_2,8 h/day and 6 day/week) to establish chronic hypoxic model. After four weeks, the mean pulmonary arterial pressure(mPAP), RV/(LV+S)and the plasma concentration of NO were measured. RT-PCR was performed to analyze the mRNA expression of eNOS in pulmonary tissue. Western blot was performed to analyze the protein expression of eNOS, iNOS in pulmonary tissue. Results ① The level of mPAP and RV/ ( LV + S) were significantly higher in the hypoxic group than those in control group ( P < 0. 05 ) , Low dose iptakalim groupandhighdoseiptakalimgroupdecreased the level of mPAP and RV/( LV + S) significantly (P <0. 05). ② The level of NO was significantly lower in the hypoxic group than those in control group (P<0. 05). Low dose iptakalim group and high dose iptakalim group increased the level of NO significantly (P < 0. 05 ). ③ The mRNA and protein expression of eNOS in the hypoxic group were significantly lower than those in the control group (P < 0. 05 ). Low dose iptakalim group and high dose iptakalim group increased the expression of eNOS significantly ( P < 0. 05). High dose iptakalim group was more significant. Conclusion Pulmonary vascular endothelial dysfunction is induced by chronic hypoxia,and the level of NO, the mRNA and protein expression of eNOS are decreased. Iptakalim can improve the vascular endothelial dysfunction, increase the expression of eNOS and the level of NO and reverse hypoxic pulmonary hypertension.
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Objective To study the effects of electrical stimulation of efferent vagus nerve on the endotoxic shock in rabbits. Method Sixteen Newzealand rabbits were randomly divided into 2 groups, namely group S as the stimulation group and group C as the control group). Rabbits were subjected to bilateral cervical vagotomy and had challenge with intravenous injection of lipopolysaccharide (LPS) (E. COLI O111: B4 , DIFCO, USA) in a dose of 600 μg/kg. The distal end of the left vagus nerve trunk was connected to an electric stimulator with bipolar electrode and controlled by an acquisition system. Stimuli with stable voltage (10 V,5 Hz,5 ms) were applied twice to the nerve for 10 minutes just before and after the administration of LPS in group S. At the time before and after the infusion of LPS 30 min,60 min, 120 min, 180 min,240 min and 300 min respectively, the heart rate(HR)and the mean arterial blood pressure (MABP) in each animal were recorded, and blood samples were taken for measuring serum tumor necrosis factor-αa(TNF-α) and interleukin-10 (IL-10). Results Compared with group C,the electrical stimulation of efferent vagus nerve could significantly attenuated the LPS-induced hypotension and de-creased the contents of TNF-α[(38.12±7.85) pg/mL vs. (55.12±7.89) pg/mL, P <0.01], but increased the contents of IL-10[(55.12±9.37)pg/mL vs. (40.15±5.44) pg/mL, P <0.01]afar LPS challenge. Conclusions The stimulation of the efferent vagus nerve can down-regulate systemic TNF-α, production and attenu-ate the development of shock after LPS challenge.
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AIM: To observe the effects of norepinephrine (NE) on the cardiopulmonary and lung injury in goats with acute respiratory distress syndrome (ARDS) induced by endotoxin. METHODS: A model of septic ARDS was induced by intravenous infusion of low dose endotoxin in six goats. Then 40?10~ -6 NO inhalation was applied to the animals. After 30 min, combined intravenous infusion of NE at concentration of 0.5 mg?kg~ -1 ?min~ -1 was conducted. The dynamic changes in gas exchange and hemodynamics were measured with the aid of Swan-Ganz catheter. Arterial blood gas analysis before and after the onset of ARDS, 30 min after NO inhalation and combined NE was detected. Histology of the lung was also observed. RESULTS: Inhalation of NO rapidly reduced mean pulmonary arterial pressure (MPAP), increased PaO_2, decreased P_ (A-a) O_2 and Qs/Qt in septic ARDS goats. These decrease and increase were more significant than those in NO inhaled alone when animals received NE. The combination of NO inhalation and NE injection resulted in increase in mean arterial pressure. NO inhalation did not ameliorate lung injury and combined NE intravenous injection ameliorated lung injury. CONCLUSION: Injection of low dose norepinephrine improves the beneficial effects of inhaled nitric oxide on lung gas exchange and ameliorates lung injury in goats with acute respiratory distress syndrome induced by endotoxin.