Endothelin alters central sympathetic responses, but the resultant effects on arrhythmogenesis are unknown. We examined ventricular tachyarrhythmias after endothelin receptor-A blockade in the brain of Wistar rats with acute myocardial infarction. For this aim, BQ-123 (n=6) or phosphate-buffered saline (n=6) were injected intracerebroventricularly. After 10 min, the left coronary artery was ligated, followed by implantation of telemetry transmitters. Electrocardiography and voluntary activity (as a surrogate of acute left ventricular failure) were continuously monitored for 24 h. Infarct-size was similar in the two groups. There were fewer episodes of ventricular tachyarrhythmias of shorter average duration in treated rats, leading to markedly shorter total duration (12.3+/-8.9 s), when compared to controls (546.2+/-130.3 s). Voluntary activity increased in treated rats during the last hours of recording, but bradyarrhythmic episodes were comparable between the two groups. Endothelin receptor-A blockade in the brain of rats decreases the incidence of ventricular tachyarrhythmias post-ligation, without affecting bradyarrhythmic episodes. These findings call for further research on the pathophysiologic role of endothelin during acute myocardial infarction.

• MeSH
• antagonisté endotelinového receptoru A aplikace a dávkování   MeSH
• cyklické peptidy aplikace a dávkování   MeSH
• infarkt myokardu farmakoterapie   komplikace   metabolismus   patofyziologie   MeSH
• injekce intraventrikulární MeSH
• komorová tachykardie etiologie   metabolismus   patofyziologie   prevence a kontrola   MeSH
• komorové extrasystoly etiologie   metabolismus   patofyziologie   prevence a kontrola   MeSH
• modely nemocí na zvířatech MeSH
• mozkové komory metabolismus   patofyziologie   účinky léků   MeSH
• potkani Wistar MeSH
• receptor endotelinu A metabolismus   účinky léků   MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

Perinatal hypoxemia may have serious long-term effects on the adult cardiovascular system and may lead to sex-dependent changes in cardiac tolerance to acute ischemia in adult life. The aim of the study was to answer the question whether gonadectomy of the male and female rats in the early phase of ontogenetic development affects the late effect of perinatal hypoxia. Pregnant Wistar rats were placed into a normobaric hypoxic chamber (12 % O2) 7 days before the expected date of delivery. Newborn pups were kept in the chamber with their mothers for another 5 days after birth. After hypoxic exposure all animals were kept for 3 months in room air. Some of the pups were gonadectomized right after removal from the hypoxic chamber. Ventricular arrhythmias were assessed on isolated perfused hearts. Castration did not influence arrhythmogenesis in the adult normoxic or perinatally hypoxic female hearts. Nevertheless, the number of arrhythmias was decreased in perinatally hypoxic gonadectomized males. In conclusion, we have shown that perinatal normobaric hypoxia increased cardiac tolerance to acute ischemia in adult male rats; however, it had no late effect in females. Gonadectomy did not affect arrhythmogenesis in both normoxic and hypoxic female hearts, whereas in males significantly decreased the number of arrhythmias.

• MeSH
• časové faktory MeSH
• financování organizované MeSH
• hypoxie komplikace   patofyziologie   MeSH
• komorová tachykardie etiologie   patofyziologie   prevence a kontrola   MeSH
• komorové extrasystoly etiologie   patofyziologie   prevence a kontrola   MeSH
• krysa rodu rattus MeSH
• modely nemocí na zvířatech MeSH
• novorozená zvířata MeSH
• orchiektomie MeSH
• ovarektomie MeSH
• potkani Wistar MeSH
• reperfuzní poškození myokardu etiologie   patofyziologie   prevence a kontrola   MeSH
• sexuální faktory MeSH
• srdce embryologie   patofyziologie   růst a vývoj   MeSH
• stárnutí MeSH
• těhotenství MeSH
• věkové faktory MeSH
• zpožděný efekt prenatální expozice MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• těhotenství MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• srovnávací studie MeSH

Ischemic preconditioning (I-PC) induced by brief episodes of ischemia and reperfusion (I/R) protects the heart against sustained I/R. Although activation of mitochondrial K(ATP) channels (mitoK(ATP)) interacting with reactive oxygen species (ROS) has been proposed as a key event in this process, their role in the antiarrhythmic effect is not clear. This study was designed: 1) to investigate the involvement of mito K(ATP) opening in the effect of I-PC (1 cycle of I/R, 5 min each) on ventricular arrhythmias during test ischemia (TI, 30-min LAD coronary artery occlusion) in Langendorff-perfused rat hearts and subsequent postischemic contractile dysfunction, and 2) to characterize potential mechanisms of protection conferred by I-PC and pharmacological PC induced by mito K(ATP) opener diazoxide (DZX), with particular regards to the modulation of ROS generation. Lipid peroxidation (an indicator of increased ROS production) was determined by measurement of myocardial concentration of conjugated dienes (CD) and thiobarbituric acid reactive substances (TBARS) in non-ischemic controls, non-preconditioned and preconditioned hearts exposed to TI, I-PC alone, as well as after pretreatment with DZX, mito K(ATP) blocker 5-hydroxydecanoate (5-HD) and antioxidant N-acetylcysteine (NAC). Total number of ventricular premature beats (VPB) that occurred in the control hearts (518+/-71) was significantly (P<0.05) reduced by I-PC (195+/-40), NAC (290+/-56) and DZX (168+/-22). I-PC and NAC suppressed an increase in CD and TBARS caused by ischemia indicating lower production of ROS. On the other hand, I-PC and DZX themselves moderately enhanced ROS generation, prior to TI. Bracketing of I-PC with 5-HD suppressed both, ROS production during PC and its cardioprotective effect. In conclusion, potential mechanisms of protection conferred by mito K(ATP) opening in the rat heart might involve a temporal increase in ROS production in the preconditioning phase triggering changes in the pro/antioxidant balance in the myocardium and attenuating ROS production during subsequent prolonged ischemia.

• MeSH
• acetylcystein farmakologie   MeSH
• antiarytmika farmakologie   MeSH
• antioxidancia farmakologie   MeSH
• blokátory draslíkových kanálů farmakologie   MeSH
• časové faktory MeSH
• diazoxid farmakologie   MeSH
• draslíkové kanály metabolismus   účinky léků   MeSH
• financování organizované MeSH
• funkce levé komory srdeční účinky léků   MeSH
• hydroxykyseliny farmakologie   MeSH
• ischemické přivykání MeSH
• komorové extrasystoly metabolismus   patofyziologie   prevence a kontrola   MeSH
• kontrakce myokardu účinky léků   MeSH
• krysa rodu rattus MeSH
• kyseliny dekanové farmakologie   MeSH
• látky reagující s kyselinou thiobarbiturovou metabolismus   MeSH
• obnova funkce MeSH
• oxidační stres MeSH
• perfuze MeSH
• peroxidace lipidů MeSH
• potkani Wistar MeSH
• reaktivní formy kyslíku metabolismus   MeSH
• reperfuzní poškození myokardu metabolismus   patofyziologie   prevence a kontrola   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH

• MeSH
• adrenalin aplikace a dávkování   škodlivé účinky   terapeutické užití   MeSH
• antiarytmika aplikace a dávkování   škodlivé účinky   terapeutické užití   MeSH
• atropin škodlivé účinky   terapeutické užití   MeSH
• infarkt myokardu * diagnóza   komplikace   MeSH
• komorové extrasystoly * diagnóza   mortalita   prevence a kontrola   MeSH
• lidé MeSH
• náhlá srdeční smrt * etiologie   prevence a kontrola   MeSH
• presoreceptory fyziologie   patofyziologie   MeSH
• statistika jako téma MeSH
• Check Tag
• lidé MeSH