Background: Mitochondrial adenosine triphosphate-sensitive potassium (mitoKATP) channels play a pivotal role in mediating cardiac preconditioning. The effects of intravenous anesthetics on this protective channel have not been investigated so far, but would be of importance with respect to experimental as well as clinical medicine.
Methods: Live cell microscopy was used to visualize and measure autofluorescence of flavoproteins, a direct reporter of mitoKATP channel activity, in response to the direct and highly selective mitoKATP channel opener diazoxide, or to diazoxide following exposure to various anesthetics commonly used in experimental and clinical medicine. A cellular model of ischemia with subsequent hypoosmolar trypan blue staining served to substantiate the effects of the anesthetics on mitoKATP channels with respect to myocyte viability.
Results: Diazoxide-induced mitoKATP channel opening was significantly inhibited by the anesthetics R-ketamine, and the barbiturates thiopental and pentobarbital. Conversely, urethane, 2,2,2-trichloroethanol (main metabolite of [alpha]-chloralose and chloral hydrate), and the opioid fentanyl potentiated the channel-opening effect of diazoxide, which was abrogated by coadministration of chelerythrine, a specific protein kinase C inhibitor. S-ketamine, propofol, xylazine, midazolam, and etomidate did not affect mitoKATP channel activity. The significance of these modulatory effects of the anesthetics on mitoKATP channel activity was substantiated in a cellular model of simulated ischemia, where diazoxide-induced cell protection was mitigated by R-ketamine and the barbiturates, while urethane, 2,2,2-trichloroethanol, and fentanyl potentiated myocyte protection. 相似文献
目的:报道1例因双眼脉冲幅度(OPA)增加发现动脉反流的病例,而后者正是引起OPA增加的原因。设计:病例报道。方法:偶然发现双眼OPA增高,由此发现脉压增高和动脉反流。患者接受动脉瓣膜手术,待动脉脉压恢复正常后评价OPA。结果:动脉脉压高时的双眼OPA为9mmHg,动脉脉压恢复正常后的双眼OPA为3mmHg。结论:动脉脉压增高可以导致OPA增高。眼脉冲幅度增加提示动脉反流@McKee H.D.R.$Hull and East Yorkshire Eye Hospital, Fountain Street, Hull, Uni ted Kingdom
@Saldaa M.
@Ahad M.A.
@张少娟… 相似文献