ABSTRACT
Objective To investigate the effect of exogenous hydrogen sulfide (H2S) on intestinal mucosal barrier after cardiopulmonary resuscitation (CPR) in cardiac arrest (CA) rabbits. Methods Forty-four male New Zealand rabbits were divided into sham operation group (Sham group, n = 12), post-cardiac arrest syndrome (PCAS) group (n = 16) and H2S intervention group (PCAS+NaHS, n = 16) according to random number table method. The rabbit model of PCAS was established by tracheal clamping and suffocation, and CPR was started at 5 minutes after CA. However, Sham group did not clamp the tracheal intubation after anesthesia, and the other operations were the same as those in PCAS group. In the PCAS+NaHS group, a bolus of NaHS (0.5 mg/kg), a H2S donor, was injected via era vein 1 minute before the start of CPR, followed by a continuous injection of NaHS (1.5 mg·kg-1·h-1) for 3 hours, while the rabbits in other group were intravenously injected with the same volume of normal saline (NaCl 0.9%). Intestinal and portal vein blood samples were collected 24 hours after return of spontaneous circulation (ROSC). The level of serum fluorescein isothiocyanate-dextran (FD-4) was detected by fluorescein isothiocyanate (FITC) labeling method to reflect intestinal mucosal permeability. After hematoxylin-eosin (HE) staining of small intestine tissues, the morphological changes of mucosa were observed under light microscope, and the intestinal mucosa injury score was calculated. The expression of tight junction protein ZO-1 in intestinal mucosa was detected by immunohistochemistry. The content of malondialdehyde (MDA) in small intestinal tissue was determined by thiobarbituric acid chromogenic method, the activity of superoxide dismutase (SOD) was determined by xanthine oxidation method, and the level of myeloperoxidase (MPO) was determined by double antibody sandwich enzyme linked immunosorbent assay (ELISA) to reflect the oxidative stress and inflammatory reaction in small intestinal tissue. The expression of apoptosis protein (caspase-3) and autophagy related protein (Beclin-1, LC3) in small intestine tissue was detected by Western Blot. Results 12, 13 and 14 animals were successfully resuscitated in Sham group, PCAS group and PCAS+NaHS group respectively, while 12 animals in each group survived to the end of experiment. Compared with Sham group, the level of FD-4 in portal vein serum was significantly increased in PCAS group (mg/L: 11.95±0.59 vs. 1.43±0.48, P < 0.05), the pathological injury and inflammation infiltration were obviously aggravated under light microscope, the score of small intestine injury was significantly increased (4.21±0.37 vs. 0.36±0.18, P < 0.05), the expression of tight junction protein ZO-1 in the intestine was visibly down-regulated detected by immunohistochemistry, MDA content and MPO activity were significantly increased [MDA (nmol/mg): 3.65±0.32 vs. 1.54±0.24, MPO (U/g): 362±35 vs. 134±18, both P < 0.05], while SOD activity was significantly decreased (U/mg:78.84±7.49 vs. 115.48±8.48, P < 0.05), the expression levels of cleaved capase-3, Beclin-1 and LC3 proteins in the intestine were significantly increased (caspase-3/β-actin: 1.11±0.08 vs. 0.21±0.02, Beclin-1/β-actin: 2.08±0.11 vs. 0.42±0.03, LC3/β-actin: 1.05±0.07 vs. 0.37±0.05, LC3-Ⅱ/ LC3-Ⅰ: 1.28±0.14 vs. 0.17±0.02, all P < 0.05). Compared with PCAS group, the portal vein serum FD-4 level in PCAS+NAHS group was significantly decreased (mg/L:5.59±0.48 vs. 11.95±0.59, P < 0.05), the intestinal mucosal pathological injury and inflammatory cell infiltration were significantly decreased, the score of small intestine injury was significantly decreased (2.18±0.47 vs. 4.21±0.37, P <0.05), the expression of ZO-1 in intestine was significantly increased, MDA content and MPO activity in intestine were significantly decreased [MDA (nmol/mg): 2.65±0.31 vs. 3.65±0.32, MPO (U/g): 251±21 vs. 362±35, both P < 0.05], while SOD activity was significantly increased (U/mg: 96.86±7.52 vs. 78.84±7.49, P < 0.05), while the expression of activated caspase-3, Beclin-1 and LC3 proteins was significantly decreased (caspase-3/β-actin: 0.72±0.06 vs. 1.11±0.08, Beclin-1/β-actin: 0.96±0.08 vs. 2.08±0.11, LC3/β-actin: 0.72±0.06 vs. 1.05±0.07, LC3-Ⅱ/ LC3-Ⅰ:0.83±0.09 vs. 1.28±0.14, all P < 0.05). Conclusion H2S has a protective effect on intestinal mucosal injury induced by CA/CPR, which may be related to tight junction protein ZO-1 up-regulation, oxidative stress alleviation, inflammation reduction, apoptosis and autophagy inhibition.
ABSTRACT
Objective To observe and assess the effects of full marathon on hemodynamics and cardiac electrophysiology of marathon amateurs without adverse event after the race.Methods Fiftyone subjects were included in the final analysis of the study,blood pressure,heart rate,body surface electrocardiogram (ECG) of all subjects under static status before the race and within (15-30) min after the race were detected,and sufficient amounts of the peripheral blood and the radial arterial blood specimens of all subjects under static status before the race and within (15-30) min after the race were collected instantly.The peripheral blood was used for measuring markers of muscle injury and NT-proBNP,and the radial arterial blood was taken for blood gas analysis.The QTc interval,QRS,PR interval,and QTd interval were recorded from the 12-lead ECG report.Results Compared with those under static status before the race,the systolic blood pressure,diastolic blood pressure,mean arterial blood pressure and heart rate of all the subjects within (15-30) min after the race were significantly higher (P＜0.05).When the markers of striated muscle injury were compared before and after the competition,levels of CK,cTNI,LDH,and myoglobin after the race were significantly increased compared with them under static status before the race (P ＜0.05),and the level of NT-proBNP after the race was also significantly increased compared with it before the race (P＜0.05).When blood gas analysis before the race was compared with that after the race,the PH values after race were significantly lower than it before race (P＜0.05).The level of lactic acid after the race was significantly higher than it before race (P＜0.05).After the race,the levels of PCO2,SBE and HCO3-decreased significantly compared with those before race (P＜0.05),and the QTc and QTd intervals after the race increased significantly compared with those before the race,however,the QTc interval and QTd interval for all subjects before and after the competition were within the normal range.Conclusions Full marathon significantly affect the myocardial electrophysiological markers of healthy amateur athletes without chronic diseases,but those markers fluctuate within the normal range.
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Objective To approach the effects of full Marathon on striated muscle and renal function of Marathon amateurs without complaints. Methods A prospective self-paired design study was conducted. The amateurs without body discomfort, hematuria, brown urine, or persistent muscle pain within 1 week after the 2012 Xiamen International Marathon Race were enrolled voluntarily. The peripheral blood and random urine specimens of all subjects under static status 1 week before the race and after the race instantly (within 10 minutes after finishing the race) were collected to detect markers of renal function and striated muscle injury. Results Sixty-one subjects were included in the final analysis of the study with full Marathon of 42.195 km and mean race time of (297.05± 55.60) minutes. Compared with those under static status before the race, the markers of renal function including the levels of urinary N-acetyl-beta-D-glucusamidase [NAG (U/L): 64.00 (54.50, 85.50) vs. 9.50 (8.10, 11.50)], urinary β2-microspheres protein [β2-MG (μg/L): 261.00 (128.50, 1 608.00) vs. 66.60 (33.75, 123.00)], random urinary creatinine [UCr (μmol/L): 19 066.56±10 938.31 vs. 5 872.52±4 363.20] and serum creatinine [SCr (μmol/L): 129.97±25.84 vs. 97.39±14.51] immediately after the race were significantly increased (all P < 0.01); the markers of muscle injury including the levels of serum creatine kinase [CK (U/L): 864.00 (504.00, 1 644.00) vs. 164.00 (128.00, 256.00)], lactic dehydrogenase [LDH (U/L): 383.26±141.69 vs. 182.23±41.12], myoglobin [Mb (mg/L): 1 880.00 (1 080.00, 3 300.00) vs. 42.00 (36.00, 54.50)], alanine aminotransferase [ALT (U/L): 27.0 (19.5, 38.0) vs. 24.0 (15.0, 29.5)] and aspartate transaminase [AST (U/L): 52.07±25.13 vs. 28.28±11.86] were also significantly increased (all P < 0.01), and the increase in CK, Mb, and LDH were more significant. It was shown by correlation analysis that CK after race was negatively correlated with age (r = -0.352, P = 0.005) and body mass index (r = -0.271, P = 0.035), and it was positively correlated with racing time (r = 0.387, P = 0.002) and urinary β2-MG after the race instantly (r = 0.364, P = 0.004). Mb after race was negatively correlated with body mass index (r = -0.331, P = 0.009), and it was positively correlated with urinary β2-MG after the race instantly (r = 0.315, P = 0.013). LDH after race was negatively correlated with age (r = -0.275, P = 0.032) and body mass index (r = -0.377, P = 0.003), and it was positively correlated with urinary β2-MG after the race instantly (r = 0.424, P = 0.001). Conclusion Full Marathon could significantly impact striated muscle and renal function of Marathon amateurs without complaints.
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Zika virus belongs to Aedes mosquito-borne flavivirus.In response to the current cluster of congenital malformations (microcephaly) and other neurological complications (Guillain-Barré Syndrome) that could be linked to Zika virus infection,WHO declares that Zika virus is of global public health importance.Data sources were from peer review articles and WHO documents.The sources of Zika virus infection would include patients,people with asymptomatic infections and primates.The infectious period of Zika virus remains unclear.However,according to the period that RNA of Zika virus can be positively detected in blood,saliva,urine or semen,we can presume that the communicable period may last for 2 months or even longer.Zika virus is primarily transmitted to humans by infected Aedes spp.mosquitoes.Presumptive vertical,blood or sexual routes of transmission have been reported.More evidence indicated the existence of a cause-effect relationship between Zika virus infection and congenital microcephaly/Guillain-Barre syndrome.Strategies include successful control the amount of mosquitoes and minimize the contacts between mosquitoes and human beings could effectively prevent the Zika virus transmission.Other preventive measures as cutting off vertical,blood or sexual routes of transmission should also be adopted.The epidemiology of Zika virus remains uncertain which calls for further research.