Protective effect of sildenafil citrate on contralateral testis injury after unilateral testicular torsion/detorsion

OBJECTIVES: This study was designed to investigate prevention of contralateral testicular injury with sildenafil citrate after unilateral testicular torsion/detorsion. METHODS: Thirty-seven adult male rats were divided into four groups: sham operated (group 1, n = 7), torsion/detorsion + saline (group 2, n = 10), torsion/detorsion + 0.7 mg of sildenafil citrate (group 3, n = 10) and torsion/detorsion + 1.4 mg of sildenafil citrate (group 4, n = 10). Unilateral testicular torsion was created by rotating the right testis 720º in a clockwise direction for 2 h in other groups, except for group 1, which was served as sham group. After torsion (2 h) and detorsion (2 h) periods, rats were killed. RESULTS: The level of reduced glutathion (GSH) (p<0.05) and the activities of catalase (p<0.01) and glutathione peroxidase (p<0.05) in the contralateral testis from group 2 were significantly lower and nitric oxide (NO) (p<0.05) level in the contralateral testis were significantly higher than those of group 1. Administration of low-dose sildenafil citrate (group 3) prevented the increases in malondialdehyde and NO levels and decreases in glutathione peroxidase activities and GSH values induced by testicular torsion. However, administration of high-dose sildenafil citrate (group 4) had no effect on these testicular parameters (p>0.05). Histopathological changes were detected in groups 2, 3 and 4. CONCLUSION: These results suggest that biochemically and histologically torsion/detorsion injury occurs in the contralateral testis following 2-h torsion and 2-h detorsion and that administration of low-dose sildenafil citrate before detorsion prevents ischemia/reperfusion cellular damage in testicular tissue.

Bilioduodenal anastomosis in rats with extra-hepatic biliary obstruction is followed by lesions ischemia and reperfusion-induced / Lesão de isquemia e reperfusão em ratos com obstrução biliar extra-hepática submetidos à anastomose bilio-duodenal

PURPOSE: The aim of this study was to investigate alterations compatible with hepatic ischemia-reperfusion after bilioduodenal shunt (BD) in rats with obstructive jaundice (OB) . METHODS: Thirty six animals were divided into 6 experimental groups: CO1 and CO2 - control groups, sham-operated (SO) and evaluated 6 and 24 hours after, respectively; OB1 and OB2, - obstructive jaundice groups, sham-operated 15 days after bile duct ligature and evaluated 6 and 24 hours after SO, respectively; DBD1and DBD2 - obstructive jaundice groups evaluated ,respectively, 6 and 24 hours after BD performed 15 days after bile duct ligature. The parameters evaluated were serum total bilirubin, aminotransferase activity (AST, ALT), TNFalpha, liver mitochondrial functions and parenchymatous injury. RESULTS: Bilirubin decreased while aminotransferase activity increased 6 hours after BD (p<0.01); TNFalpha determination at the 6th hour after BD was higher than the one at the 24th hour (p<0.05); oxygen consumption in states 3 and 4 remained elevated in the BD initial phase , and liver cell damage worsened 24 hours after BD. CONCLUSION: The results demonstrated that surgical biliary decompression in obstructive jaundice is followed by alterations related to hepatic ischemia- reperfusion.

OBJETIVO: O objetivo do estudo foi investigar alterações compatíveis com o fenômeno de isquemia-reperfusão hepática em ratos com icterícia obstrutiva (OB) após derivação bilioduodenal (BD). MÉTODOS: Trinta e seis animais foram divididos em seis grupos experimentais: CO1 e CO2 - grupos controle avaliados com 6 e 24 horas após operação simulada (SO), respectivamente; OB1 e OB2 - grupos com obstrução biliar, submetidos a SO 15 dias após ligadura do ducto biliar, e avaliados em 6 e 24 horas após a SO, respectivamente; DBD1 e DBD2 - grupos com 15 dias de obstrução biliar, avaliados em 6 e 24 horas, respectivamente, após BD. Os parâmetros avaliados foram bilirrubinas, aminotranferases (ALT e AST), funções mitocondriais hepáticas, dosagem de TNFalfa e lesão do parênquima hepático. RESULTADOS: As bilirrubinas caíram após BD, enquanto as aminotransferases aumentaram 6 horas após BD (p<0,01). O TNFalfa mensurado na 6ª hora após a BD foi maior que o da 24ª hora (p<0,05). O consumo de oxigênio no estado 3 e 4 mantiveram-se elevados na fase inicial do BD e as lesões celulares hepáticas agravaram-se na 24ª hora pós BD. CONCLUSÃO: Os resultados demonstraram que a descompressão cirúrgica biliar na icterícia obstrutiva foi seguida de alterações que correspondem ao fenômeno de isquemia-reperfusão hepática.

Cerebral protection effect and mechanism of propofol on global cerebral ischemia and reperfusion damage in rats / 中国康复理论与实践

@#ObjectiveTo determine the cerebral protection effect and mechanism of propofol on global cerebral ischemia and reperfusion damage in rats.Methods19 adult male Wistar rats were randomly divided into 3 groups, ischemia group (n=7), propofol group (n=7), and sham injury group (n=5). Global cerebral ischemia and reperfusion model were made by means of Pulsinelli's method. Rats in propofol group were anesthesia with propofol at the dosage of 1.5 ml/h for 30 min at the beginning of reperfusion. Apoptosis and necrosis rate were detected by cytometry. In the same time, bcl-2, Bax and p53 protein expression in hippocampus neurons were detected. ResultsThe apoptosis and necrosis rate in propofol group were significantly decreased as compared with ischemia group ( P<0.05). Bax and p53 protein expression in hippocampus neurons were also significantly decreased as compared with ischemia group (P<0.05), however, no significant findings in bcl-2 protein expression (P>0.05).ConclusionPropofol can decrease apoptosis and necrosis rate in cerebral ischemia reperfusion injured neuron, and the mechanism maybe related to decreasing the expression of Bax, p53 protein.

Protective effect of sivelestat sodium on ischemia reperfusion brain injury in rats / 重庆医科大学学报

Objective:To explore the protective effect of sivelestat sodium on cerebral ischemia reperfusion in rats and its mechanism.Methods:The neurons of neonate rat were cultured in vitro.The protective effects of sivelestat sodium on ischemia injury were observed by treating cells in glucose-free and oxygen-free medium.Results:Sivelestat sodium(10-8、10-7 and 10-6mol/L)increased the activity of neurons,reduced the leakage rate of LDH,increased the activity of SOD and reduced the content of MDA.Conclusion:sivelestat sodium protects the neurons against ischemia injury by suppressing the generation of lipid peroxide.

Protective Effect of Ligustrazin on the Mitochondrial Damage of Myocardium in Ischemiareperfusion Rats / 中国药房

OBJECTIVE:To observe the effect of ligustrazin on the mitochondrial damage of myocardium in ischemia-reperfusion rats and the mechanism involved METHODS:Rat model of myocardial ischemia-reperfusion injury was established by coronary artery ligation and the activities of Ca2+-ATPase,Ca2+?Mg2+-ATPase,succinic dehydrogenase(SDH),cytochrome oxidase(CCO),SOD,GSH-PX and contents of phospholipid(PL),MDA,Cyt aa3 and Cyt C in the myocardial mitochondria were observed RESULTS:As compared with ischemia-reperfusion group(IR),IR+L(ligustrazin)group showed significant increase in the activities of Ca2+-ATPase,Ca2+?Mg2+-ATPase,SDH,CCO,SOD and GSH-PX(P

Effect of Exogenous Adrenomedullin on the Glutathion Levels of Plasma and Brain Tissue in Neonatal Rat with Hypoxic-Ischemia Reperfusion Brain Damage / 实用儿科临床杂志

Objective To explore the effect of exogenous adrenomedullin(ADM) on expressions of glutathion in plasma and brain tissue inneonatal rats with hypoxic-ischemia reperfusion brain damage(HIRBD) and the mechanism of action.Methods Fifty-six cases of 7 d SD rats were randomly divided into 4 groups including normal control group(without any treatment),HIRBD group(the model with hypoxia for 2 h and ischemia for 1 h),primed group(abdomen infusion of ADM at 0.5 h before making model,the other was same to the HIRBD group)and treatment group(abdomen infusion of ADM at onces after making model,the other was same to the HIRBD group).The neonatal rats in 4 groups were derived blood and brain tissue after decapitation at either 4 h or 24 h after reperfusion.The levels of gtutathion(GSH) in plasma and brain tissue were determined by using chromatometry.Results In HIRBD group,the affection areas at 24 h after reperfusion enlarged compared with those at 4 h after reperfusion.Meanwhile,the affection of punctiform degeneration or necrosis at 4 h after reperfusion transformed into the affection of lamellar or diffuse degeneration or necrosis at 24 h after reperfusion.The levels of GSH in plasma and brain tissue in HIRBD group at either 4 h or 24 h after reperfusion were significantly lower than that in normal control group(Pa0.05).Meanwhile the pathology score of brain section in primed group and treatment group were significantly lower than that in HIRBD group at either 4 h or 24 h after reperfusion(Pa0.05).Conclusion Exogenous ADM can induce the neuroprotection in HIRBD by adjusting the expression of GSH.

Protection of ferulic acid compound in ischemia reperfusion brain injury in rats / 重庆医科大学学报

Objective: To explore the protective effect and its mechanism of the traditional Chinese medicine complex, ferulic acid compound, on cerebral ischemia reperfusion in rats. Methods :Experimental cerebral ischemia reperfusion in rats was made by occluding the two- vessel and bleeding from tails. To observe the effect of ferulic acid compound on levels of endothelin - 1 (ET - 1) 、 calcitonin gene- related peptide (CGRP) 、 malonaldehyde (MDA) 、 energy metabolism 、 the expression of heat shock protein 70 (HSP70) and histopathological analysis in brain tissue. Results:Ferulic acid compound can decrease the level of ET- 1 、 MDA and lactic acid in brain after cerebral ischemia reperfusion in rats,and also improve the contents of CGRP 、 ATP and Na+ - K+ - ATPase activity.The effect of ferulic acid compound was related to dosages, and its effect was better than the positive salvia miltiorrhiza. Eerulic acid compound can increase the HSP70 expression significantly and alleviate cerebral ischemic changes histopathologically. Conclusion :The effect of ferulic acid compound in many ways may be related to its protection against ischemia reperfusion brain injury.

Effect of sevoflurance postconditioning on cardiac function and mitochondrial of isolated rat heart with acute myocardial ischemia-reperfusion injury / 中国药理学通报

0.05).After reperfusion,Sevo group and Post group resulted in a significant increase(P