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Isoflurane-induced preconditioning is attenuated by diabetes.

机译:异氟烷诱导的预处理因糖尿病而减弱。

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Volatile anesthetics stimulate, but hyperglycemia attenuates, the activity of mitochondrial ATP-regulated K(+) channels. We tested the hypothesis that diabetes mellitus interferes with isoflurane-induced preconditioning. Acutely instrumented, barbiturate-anesthetized dogs were randomly assigned to receive 0, 0.32, or 0.64% end-tidal concentrations of isoflurane in the absence or presence of diabetes (3 wk after administration of alloxan and streptozotocin) in six experimental groups. All dogs were subjected to a 60-min left anterior descending coronary artery occlusion followed by 3 h of reperfusion. Myocardial infarct size (triphenyltetrazolium staining) was 29 +/- 3% (n = 8) of the left ventricular area at risk in control experiments. Isoflurane reduced infarct size (15 +/- 2 and 13 +/- 1% during 0.32 and 0.64% concentrations; n = 8 and 7 dogs, respectively). Diabetes alone did not alter infarct size (30 +/- 3%; n = 8) but blocked the protective effects of 0.32% (27 +/- 2%; n = 7) and not 0.64% isoflurane (18 +/- 3%; n = 7). Infarct size was directly related to blood glucose concentrations in diabetic dogs, but this relationship was abolished by higher concentrations of isoflurane. The results indicate that blood glucose and end-tidal isoflurane concentrations are important determinants of infarct size during anesthetic-induced preconditioning.
机译:挥发性麻醉剂刺激但线粒体ATP调节的K(​​+)通道的活性,但高血糖会减弱。我们检验了糖尿病干扰异氟烷诱导的预处理的假说。在六个实验组中,在没有糖尿病或存在糖尿病的情况下(用四氧嘧啶和链脲佐菌素给药3周后),将经过严格仪器麻醉的巴比妥酸盐麻醉的狗随机分配为接受0、0.32或0.64%的潮气末异氟烷浓度。对所有的狗进行60分钟的左冠状动脉前降支闭塞,然后再灌注3小时。在对照实验中,心肌梗塞面积(三苯四唑染色)为左心室面积的29 +/- 3%(n = 8)。异氟烷可减少梗塞面积(在0.32和0.64%的浓度下分别为15 +/- 2和13 +/- 1%; n = 8和7只狗)。单独的糖尿病并不能改变梗塞面积(30 +/- 3%; n = 8),但阻断了0.32%(27 +/- 2%; n = 7)的保护作用,而没有阻断0.64%的异氟烷​​(18 +/- 3)的保护作用%; n = 7)。糖尿病犬的梗死面积与血糖浓度直接相关,但异氟烷浓度较高则消除了这种关系。结果表明,在麻醉诱导的预处理过程中,血糖和潮末异氟醚浓度是梗死面积的重要决定因素。

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