Ischaemia-reperfusion Dotaz Zobrazit nápovědu
European heart journal, ISSN 1520-765X vol. 3, suppl. C, June 2001
C73 s. : tab., grafy ; 30 cm
- MeSH
- endotel MeSH
- farmakoterapie metody MeSH
- ischemie MeSH
- neutrofily MeSH
- reaktivní formy kyslíku MeSH
- reperfuzní poškození MeSH
- tkáně patologie MeSH
- Publikační typ
- přehledy MeSH
The aim of the study was to analyse protective effects of different doses of pomiferin in therapy of reperfusion injury. Rats were randomly divided into five groups (n=10). One group was intact. Three medicated groups and one placebo group were subjected to ischaemia and reperfusion of the left kidney. Pomiferin was administrated by single gastric gavage in 2 ml of 0.5% Avicel solution in doses of 5, 10 and 20 mg/kg. The placebo group was given only Avicel solution. On day 15, all the animals were exsanguinated and the reperfused kidneys were recovered. Selected biochemical markers were assessed in blood: antioxidative enzymes, total antioxidative capacity, malondialdehyde, creatinine, urea and uric acid. Creatinine, urea and total proteins were analysed in urine and 24-hour diuresis was recorded. The kidney tissue samples were used for histopathological examination. The results confirmed the expected protective effects of pomiferin. Pomiferin supported defensive reactions of the body against free radicals (increased levels of superoxide dismutase, total antioxidative capacity), decreased lipid peroxidation (decreased malondialdehyde) and contributed to the recovery of kidney functions (creatinine and urea in blood). The best biochemical and histopathological results were achieved after pomiferin administration in the dose of 5 mg/kg.
Cíl. Cílem práce bylo zjistit, zda použití S-adenosylmethioninu (SAMe) vede ke snížení ischemicko-reperfuzního poškození u jaterních štěpů s vysokým procentem steatózy při transplantaci jater na potkanovi. Materiál a metodika. K pokusu jsme použili zdravé potkany typu Lewis a potkany s vyvinutou steatózou jater. Potkani byly rozděleni do 4 skupin. Ia skupina: sedmi zdravým potkanům byl transplantován steatotický jaterní štěp. Při odběru jaterního štěpu byl do perfuzního roztoku přidán SAMe. Ib skupina: sedmi zdravým potkanům byl transplantován steatotický jaterní štěp, bez aplikace SAMe. IIa skupina: sedmi zdravým potkanům byl transplantován normální jaterní štěp s přidáním SAMe. IIb skupina: sedmi zdravým potkanům byl transplantován normální jaterní štěp bez aplikace SAMe. Odběry krve byly prováděny 1., 3. a 14. den po transplantaci. Sledovány byly markery ischemicko-reperfuzního poškození: ALT, AST, GSH. Výsledky. Hodnoty ALT 14. pooperační den v Ia skupině: 1,75 ± 1,10 µkat/l. V Ib. skupině 1,91 ± 1,41 µkat/l. Hodnoty ALT 14. pooperační den v IIa. skupině 2,13 ± 1,85 µkat/l, v IIb. skupině 2,08 ± 1,35 µkat/l. Signifikantně se hodnoty nelišily. Hodnoty GSH 14. pooperační den v Ia skupině 44,90 ± 8,61 µM/mg, v Ib skupině 43,82 ± 8,58 µM/mg. V IIa skupině 41,65 ± 4,87 µM/mg, u kontrolní skupiny IIb 42,71 ± 4,17 µM/mg. Koncentrace GSH se u všech skupin signifikantně nelišila. Závěr. Laboratorní známky ischemicko-reperfuzního poškození při transplantaci steatotického jaterního štěpu, který je více náchylný k ischemicko-reperfuznímu poškození, se v případě použití SAMe signifikantně neliší od skupiny bez jeho použití. Naše studie neprokazuje pozitivní vliv SAMe na snížení ischemicko-reperfuzního poškození při transplantaci jater na malém laboratorním zvítřeti.
The aim of the study. The aim of our study was to determine whether the use of S-adenosylmethionine reduces ischaemia-reperfusion injury in hepatic grafts with a high degree of steatosis during liver transplantation in rats. Materials and methods. we used healthy Lewis rats and rats with liver steatosis in our experiment. Rats were divided into four groups of seven animals: Ia: steatotic liver grafts were transplanted into seven healthy rats; S-adenosylmethionine was added to the perfusion solution used during removal of the liver grafts prior to transplantation; Ib: steatotic liver grafts were transplanted into seven healthy rats; S-adenosylmethionine was not used; IIa: normal liver grafts were transplanted into seven healthy rats; S-adenosylmethionine was added to the perfusion solution; IIb: normal liver grafts were transplanted into seven healthy rats; no S-adenosylmethionine was added to the perfusion solution. Blood samples were taken after transplantation at days 1, 3 and 14. The following markers of ischaemia-reperfusion injury were examined: ALT, AST and GSH. Results. The following ALT values were determined after transplantation at day 14: 1.75 ± 1.10 µkat/l (in group Ia), 1.91 ± 1.41 µkat/l (in group Ib), 2.13 ± 1.85 µkat/l (in group IIa) and 2.08 ± 1.35 µkat/l (in group IIb). There were no significant differences between these values. GSH values at day 14 post-transplantation were: 44.90 ± 8.61 µM/mg (in group Ia), 43.82 ± 8.58 µM/mg (in group Ib), 41.65 ± 4.87 µM/mg (in group IIa) and 42.71 ± 4.17 µM/mg (in control group IIb). Conclusion. Laboratory markers of ischaemia-reperfusion injury proved the liability of steatotic liver graft to ischaemia-reperfusion injury but no significant differences were demonstrated between groups using S-adenosylmethionine and the control group. Our study didn’t demonstrated the positive effect of S-adenosylmethionine on ischaemia-reperfusion injury during liver transplantation in rats.
Dexrazoxane (DEX), an inhibitor of topoisomerase II and intracellular iron chelator, is believed to reduce the formation of reactive oxygen species (ROS) and protects the heart from the toxicity of anthracycline antineoplastics. As ROS also play a role in the pathogenesis of cardiac ischaemia/reperfusion (I/R) injury, the aim was to find out whether DEX can improve cardiac ischaemic tolerance. DEX in a dose of 50, 150, or 450 mg·(kg body mass)(-1) was administered intravenously to rats 60 min before ischaemia. Myocardial infarct size and ventricular arrhythmias were assessed in anaesthetized open-chest animals subjected to 20 min coronary artery occlusion and 3 h reperfusion. Arrhythmias induced by I/R were also assessed in isolated perfused hearts. Only the highest dose of DEX significantly reduced infarct size from 53.9% ± 4.7% of the area at risk in controls to 37.5% ± 4.3% without affecting the myocardial markers of oxidative stress. On the other hand, the significant protective effect against reperfusion arrhythmias occurred only in perfused hearts with the dose of DEX of 150 mg·kg(-1), which also tended to limit the incidence of ischaemic arrhythmias. It is concluded that DEX in a narrow dose range can suppress arrhythmias in isolated hearts subjected to I/R, while a higher dose is needed to limit myocardial infarct size in open-chest rats.
- MeSH
- akutní nemoc MeSH
- elektrokardiografie MeSH
- infarkt myokardu etiologie metabolismus prevence a kontrola MeSH
- kardiovaskulární látky aplikace a dávkování terapeutické užití MeSH
- krysa rodu rattus MeSH
- modely nemocí na zvířatech MeSH
- perfuze MeSH
- potkani Wistar MeSH
- razoxan aplikace a dávkování terapeutické užití MeSH
- reaktivní formy kyslíku metabolismus MeSH
- reperfuzní poškození myokardu komplikace farmakoterapie metabolismus MeSH
- srdeční arytmie etiologie metabolismus prevence a kontrola MeSH
- techniky in vitro MeSH
- výsledek terapie MeSH
- vztah mezi dávkou a účinkem léčiva MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
To observe the protective effects of L-citrulline on the renal I/R injury and elucidate the mechanisms involved, 48 rats were randomized into eight groups: Group 1: sham operated; Group 2: I/R (45 min renal ischaemia and 24 h reperfusion); Group 3: I/R + L-citrulline (300 mg/kg, i.g.); Group 4: I/R + L-citrulline (600 mg/kg, i.g.); Group 5: I/R + L-citrulline (900 mg/kg, i.g.); Group 6: I/R + normal saline (NS, i.g.); Group 7: I/R + N sup ω nitro-L-arginine ester (L-NAME, 20 mg/kg, i.p.); Group 8: I/R + L-citrulline (900 mg/kg, i.g.) + L-NAME (20 mg/ kg, i.p.). At the end of the reperfusion period, serum was collected and the kidneys underwent histological and biochemical examinations. Our results showed that pre-treatment with L-citrulline (300, 600, and 900 mg/kg) significantly ameliorated the renal injury caused by I/R. Moreover, L-citrulline prevented induction of lipid peroxidation and increased the activity of superoxide dismutase and the levels of glutathione and nitric oxide. The I/R-induced decreases in total nitric oxide synthase activity, inducible nitric oxide activity, constitutive nitric oxide activity and endothelial nitric oxide protein expression in the renal cortex were significantly prevented. However, the L-citrulline-mediated protection was significantly antagonized by co-administration of L-NAME. These results suggested that L-citrulline administration exhibited significant protection against renal I/R injury. This protective effect, at least in part, via up-regulation of the endothelial nitric oxide protein expression and constitutive nitric oxide synthase activity, maintained production of nitric oxide at the basal level.
- MeSH
- citrulin farmakologie terapeutické užití MeSH
- krysa rodu rattus MeSH
- oxid dusnatý metabolismus MeSH
- reperfuzní poškození farmakoterapie metabolismus MeSH
- signální transdukce účinky léků MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
