ABSTRACT
ObjectiveTo explore the pharmacodynamic effects of total flavonoids of Paeonia suffruticosa flower （TFPFs） on rats with hyperuricemia and provide scientific data support for the research and development of therapeutic drugs for hyperuricemia. MethodThe hyperuricemia model was induced by adenine combined with ethambutol in rats. The rats were randomly divided into a blank control group， a model group， two positive control groups （allopurinol at 42 mg·kg-1 and Tongfengshu tablets at 600 mg·kg-1）， and high-， medium-， and low-dose TFPFs groups （260， 130， and 65 mg·kg-1）. The general conditions of rats were observed and recorded， and the body weight was recorded once every 5 days. The 24-hour urine volume， water intake， uric acid （UA）， and urinary protein of rats were determined after the last administration. The kidney index was calculated. The pathological changes in thymus and spleen tissues of rats were observed by hematoxylin-eosin （HE） staining. The serum activities of UA， creatinine （Cr）， blood urea nitrogen （BUN）， malondialdehyde （MDA）， superoxide dismutase （SOD）， and total antioxidant capacity （T-AOC） of rats were determined. The xanthine oxidase （XOD） and adenosine deaminase （ADA） activities in the liver were detected. The content of uric acid transporter 1 （URAT1）， organic anion transporter 1 （OAT1）， and glucose transporter 9 （GLUT9） in the kidney was detected by enzyme-linked immunosorbent assay （ELISA）. ResultCompared with the results in the model group， TFPFs could improve the mental state of rats， increase the body weight（P<0.01）， promote UA excretion（P<0.01）， reduce the content of urinary protein（P<0.05）， relieve renal glomerular atrophy， renal tubular epithelial cell status， and urate crystal deposition in renal tubules， dwindle 24-hour urine volume， water intake， kidney index（P<0.05）， serum levels of UA， Cr， BUN， and MDA（P<0.05，P<0.01）， inhibit the activities of XOD（P<0.05） and ADA（P<0.05，P<0.01）in the liver， diminish the expression of GLUT9 in the renal homogenate（P<0.05）， and increase serum SOD and T-AOC activities as well as OAT1 expression（P<0.01） in the kidney. The pathological changes of thymus and spleen were improved. ConclusionTFPFs possess a protective effect on the kidney of rats with hyperuricemia， which is achieved by promoting uric acid excretion， inhibiting oxidation and the activity of key enzymes in uric acid synthesis， and regulating the expression of uric acid transporters.
ABSTRACT
ObjectiveTo explore the pharmacodynamic effects of total flavonoids of Paeonia suffruticosa flower （TFPFs） on rats with hyperuricemia and provide scientific data support for the research and development of therapeutic drugs for hyperuricemia. MethodThe hyperuricemia model was induced by adenine combined with ethambutol in rats. The rats were randomly divided into a blank control group， a model group， two positive control groups （allopurinol at 42 mg·kg-1 and Tongfengshu tablets at 600 mg·kg-1）， and high-， medium-， and low-dose TFPFs groups （260， 130， and 65 mg·kg-1）. The general conditions of rats were observed and recorded， and the body weight was recorded once every 5 days. The 24-hour urine volume， water intake， uric acid （UA）， and urinary protein of rats were determined after the last administration. The kidney index was calculated. The pathological changes in thymus and spleen tissues of rats were observed by hematoxylin-eosin （HE） staining. The serum activities of UA， creatinine （Cr）， blood urea nitrogen （BUN）， malondialdehyde （MDA）， superoxide dismutase （SOD）， and total antioxidant capacity （T-AOC） of rats were determined. The xanthine oxidase （XOD） and adenosine deaminase （ADA） activities in the liver were detected. The content of uric acid transporter 1 （URAT1）， organic anion transporter 1 （OAT1）， and glucose transporter 9 （GLUT9） in the kidney was detected by enzyme-linked immunosorbent assay （ELISA）. ResultCompared with the results in the model group， TFPFs could improve the mental state of rats， increase the body weight（P<0.01）， promote UA excretion（P<0.01）， reduce the content of urinary protein（P<0.05）， relieve renal glomerular atrophy， renal tubular epithelial cell status， and urate crystal deposition in renal tubules， dwindle 24-hour urine volume， water intake， kidney index（P<0.05）， serum levels of UA， Cr， BUN， and MDA（P<0.05，P<0.01）， inhibit the activities of XOD（P<0.05） and ADA（P<0.05，P<0.01）in the liver， diminish the expression of GLUT9 in the renal homogenate（P<0.05）， and increase serum SOD and T-AOC activities as well as OAT1 expression（P<0.01） in the kidney. The pathological changes of thymus and spleen were improved. ConclusionTFPFs possess a protective effect on the kidney of rats with hyperuricemia， which is achieved by promoting uric acid excretion， inhibiting oxidation and the activity of key enzymes in uric acid synthesis， and regulating the expression of uric acid transporters.
ABSTRACT
Objective To explore the short-term hemodynamic change of fluid challenge (FC) with crystalloid or colloid and define fluid responsiveness at the optimal time in patients with septic shock. Methods A prospective observational study was conducted. Septic shock patients monitored with pulmonary catheters admitted to medical intensive care unit (ICU) of the Peking Union Medical College Hospital from July 2016 to December 2018 were enrolled. All included patients received FC and were divided into two groups according to the type of fluid used, i.e. crystalloid group (normal saline for 500 mL) and colloid group (4% succinyl gelatin for 500 mL). The choice of fluid type was decided by the attending physician. Hemodynamic variables were measured at baseline, and 0 (immediately), 10, 30, 45, 60, 90, 120 minutes after FC, included cardiac index (CI), heart rate (HR), mean artery pressure (MAP), central venous pressure (CVP) and pulmonary arterial wedge pressure (PAWP). Fluid responsiveness was defined as CI increased by more than 10% after FC. The data were analyzed by repeated measurements of variance between the two groups as well as responders and nonresponders. Results Forty patients were included, 20 cases each in colloid group and crystalloid group; of whom 26 were fluid responders with 12 of colloid group and 14 of crystalloid group. Of the 14 nonresponders, 8 were of colloid group and 6 of crystalloid group. ① Compared with before FC, CI (mL·s-1·m-2) was significantly increased in crystalloid and colloid groups after FC (71.7±16.7 vs. 65.0±16.7, 68.3±25.0 vs. 63.3±23.3, both P < 0.05). In the colloid group, volume expansion increased the CI to maximum (76.7±18.3) at 30 minutes after FC, at 120 minutes after FC, a significantly higher CI (70.0±16.7) was also observed (P < 0.05), an increased in CI≥10% was observed at 60 minutes after FC. In the crystalloid group, CI was increased to maximum at 10 minutes (73.3±28.3) and decreased to baseline at 60 minutes, an increased in CI≥10% was also observed at 10 minutes after FC. In addition, there was no significant difference in CI changes between colloidal group and crystalloid group at different time points after FC. ② CI did not change over time in nonresponders groups, whereas in responders CI increased parallelly to that in both crystalloid and colloid groups over time. However, an increased in CI≥10% was observed through the 120 minutes after FC in responders of colloid group compared with that of at 30 minutes after FC in crystalloid group. There was significant difference in CI changes between colloidal group and crystalloid group at 30, 45, 60, 90 minutes after FC (mL·s-1·m-2: 18.3±3.3 vs. 8.3±1.7, 18.3±3.3 vs. 5.0±1.7, 13.3±1.7 vs. 3.3±1.7, 11.7±3.3 vs. 3.3±1.7, all P <0.05). ③ The maximal values of CVP and PAWP were observed at the end of FC. In colloid group, both the two variables were notably higher than that before FC over 120 minutes compared with that of only at 10 minutes in crystalloid group. The MAP in colloid increased to maximum immediately at the end of FC and decreased to baseline at 45 minutes, however, the MAP in crystalloid group and HR of both groups showed no differences over 120 minutes. Conclusions Hemodynamic changes were significantly different between crystalloid and colloid after FC in patients with septic shock. Therefore, the timing of fluid responsiveness assessment should be different individually. The assessment time of colloid group may be prolonged to 30 minutes after FC while that of crystal group can be at 10 minute after FC.
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Objective To evaluate the accuracy of central venous-to-arterial carbon dioxide partial pressure difference (Pcv-aCO2) before and after rapid rehydration test (fluid challenge) in predicting the fluid responsiveness in patients with septic shock. Methods A prospective observation was conducted. Forty septic shock patients admitted to medical intensive care unit (ICU) of Peking Union Medical College Hospital from October 2015 to June 2017 were enrolled. All of the patients received fluid challenge in the presence of invasive hemodynamic monitoring. Heart rate (HR), blood pressure, cardiac index (CI), Pcv-aCO2 and other physiological variables were recorded at 10 minutes before and immediately after fluid challenge. Fluid responsiveness was defined as an increase in CI greater than 10% after fluid challenge, whereas fluid non-responsiveness was defined as no increase or increase in CI less than 10%. The correlation between Pcv-aCO2 and CI was explored by Pearson correlation analysis. Receiver operating characteristic (ROC) curves were established to evaluate the discriminatory abilities of baseline and the changes after fluid challenge in Pcv-aCO2 and other physiological variables to define the fluid responsiveness. The patients were separated into two groups according to the initial value of Pcv-aCO2. The cut-off value of 6 mmHg (1 mmHg = 0.133 kPa) was chosen according to previous studies. The discriminatory abilities of baseline and the change in Pcv-aCO2(ΔPcv-aCO2) were assessed in each group. Results A total of 40 patients were finally included in this study. Twenty-two patients responded to the fluid challenge (responders). Eighteen patients were fluid non-responders. There was no significant difference in baseline physiological variable between the two groups. Fluid challenge could increase CI and blood pressure significantly, decrease HR notably and had no effect on Pcv-aCO2 in fluid responders. In non-responders, blood pressure was increased significantly and CI, HR, Pcv-aCO2 showed no change after fluid challenge. Pcv-aCO2 was comparable in responders and non-responders. In 40 patients, CI and Pcv-aCO2 was inversely correlated before fluid challenge (r = -0.391, P = 0.012) and the correlation between them weakened after fluid challenge (r = -0.301, P = 0.059). There was no significant correlation between the changes in CI and Pcv-aCO2 after fluid challenge (r = -0.164, P = 0.312). The baseline Pcv-aCO2 and ΔPcv-aCO2 could not discriminate between responders and non-responders, with the area under ROC curve (AUC) of 0.50 [95% confidence interval (95%CI) =0.32-0.69] and 0.51 (95%CI = 0.33-0.70), respectively. HR and blood pressure before fluid challenge and their changes after fluid challenge showed very poor discriminative performances. Before fluid challenge, 16 patients had a Pcv-aCO2 > 6 mmHg. Their mean CI was significantly lower and Pcv-aCO2 was significantly higher than that in 24 patients whose Pcv-aCO2 ≤6 mmHg [n = 24; CI (mL·s-1·m-2): 48.3±11.7 vs. 65.0±18.3, P < 0.01; Pcv-aCO2 (mmHg): 8.4±1.9 vs. 2.9±2.8, P < 0.01]. Pcv-aCO2was decreased significantly after fluid challenge in patients with an initial Pcv-aCO2 > 6 mmHg and their ΔPcv-aCO2 was notably different as compared with the patients whose baseline Pcv-aCO2≤6 mmHg (mmHg: -3.8±3.4 vs. 0.9±2.9, P < 0.01). 68.8% (11/16) patients responded to the fluid challenge in patients with an initial Pcv-aCO2 > 6 mmHg. The AUC of the baseline Pcv-aCO2 and ΔPcv-aCO2 to define fluid responsiveness was 0.85 (95%CI = 0.66-1.00) and 0.84 (95%CI = 0.63-1.00), respectively, and the positive predictive value was 1 when the cut-off value was 8.0 mmHg and -4.2 mmHg, respectively. 45.8% (11/24) patients responded to the fluid challenge in patients whose baseline Pcv-aCO2≤6 mmHg. There was no predictive value of baseline Pcv-aCO2 and ΔPcv-aCO2 on fluid responsiveness. Conclusion Pcv-aCO2 and its change cannot serve as a surrogate of the change in cardiac output to define the response to fluid challenge in septic shock patients whose baseline Pcv-aCO2≤6 mmHg, while the predictive values of baseline Pcv-aCO2and the change in Pcv-aCO2 are presented in patients with the initial value of Pcv-aCO2 > 6 mmHg. Clinical Trial Registration Clinical Trials, NCT01941472.
ABSTRACT
Objective To study the clincal characters of premature labor compicated with premature rupter of membrance, and how to prevent and treat the complications. Methods Among the 110 cases, according to the nursing routine treatment,we treat 50 of them with 10mg im bid. The rest are treated with 4. 8mg q6h of oral salbu-tamoulum,30-60ml of intravenous drip of 25% of magnesii sulfas per day. lOmg of muscle injection of dexametha-soni acetas. Mean while, observe body temperature, the number of white blood cells, the foetus heartbeat and the shape and property of amniotic fluid. Results The 49 cases are successful.11 of which failure. The death rate of less than 34 weeks is much higher than that of more than 34 weeks. The difference is rery obvious(P