Isoflurane, but not Halothane, Induces Protection of Human Myocardium via  Adenosine A1Receptors and Adenosine Triphosphate–sensitive Potassium Channels

Abstract

This study demonstrates the cardioprotective effects of isoflurane in contrast to the effects of halothane. Furthermore, A1 receptors and KATP channels seem to mediate the beneficial effects of anoxia and isoflurane in human myocardium.

Neuroanesthesia and Intensive Care Isoflurane tolerance against focal cerebral ischemia is attenuated by adenosine A1 receptor antagonists

“…7,13 In our previous study, we found that repeated isoflurane anesthesia induced cerebral ischemic tolerance in rats in a dosedependent manner. 9 Kapinya et al demonstrated that pretreatment with 1.4% isoflurane for three hours at zero, 12, and 24 hr before middle cerebral artery occlusion (MCAO) could induce neuroprotection in a rat focal cerebral ischemia model.…”

“…[21][22][23][24] The possible involvement of adenosine A 1 receptors as mediators of cardiac preconditioning has been proven by studies in several animal models. 7,25,26 It has been suggested that adenosine receptors may be activated by preconditioning and, in turn, activate K ATP channels, possibly through an intermediate such as PKC. 27,28 Whether adenosine receptors play important roles in isoflurane preconditioning in cerebral ischemia is unclear.…”

“…Indeed, the mechanisms underlying isoflurane-induced tolerance are not completely known, but studies of myocardial ischemia have shown that isoflurane-induced tolerance shared several cellular mechanisms with ischemic tolerance including opening of adenosine triphosphate-sensitive potassium channels (K ATP channels), an adenosine receptor-mediated pathway, and a protein kinase C (PKC)-mediated pathway. 7,8 Involvement of adenosine A 1 receptors and K ATP channels in the development of cerebral ischemic tolerance induced by sublethal ischemia has been well studied. In our previous study, we found that glibenclamide, an adenosine triphosphate-regulated potassium channel blocker, abolished the tolerance to focal cerebral ischemia induced by repeated isoflurane anesthesia.…”

Proteção miocárdica pelo pré- e pós-condicionamento anestésico

“…Usando marcadores bioquímicos, esse estudo demonstrou uma melhora pós-operatória significativa nas funções renal e miocárdica nos pacientes que tiveram precondicionamento com sevoflurano. PCA e PCI compartilham a maioria dos passos envolvidos no estabelecimento do estado de precondicionamento, incluindo a ativação dos receptores ligados à proteína G da membrana 26,27 , interação de vários tipos de proteinocinases [28][29][30] , ROS 31 e os canais de KATP dependentes do sarcolema e da mitocôndria como efetores finais da cardioproteção pela regulação do íon Ca ++ . Estudos recentes revelaram diferenças no fenótipo cardioprotetor entre PCA e PCI.…”

“…Using biochemical markers, this study demonstrated significant postoperative improvement in renal and cardiac function in patients undergoing preconditioning with sevoflurane. Anesthetic preconditioning and IPC share most of the steps involved in establishing the state of preconditioning, including the activation of protein G binding receptors in the cell membrane 26,27 , interaction of several types of protein kinases [28][29][30] , ROS 31 , and KATP dependent channels in the sarcolema and mitochondria, as final effectors of cardioprotection by regulating the ion Ca ++ . Recent studies demonstrated differences in the cardioprotective phenotype between ACP and ICP.…”