Propofol but not desflurane maintains rat cerebral arteriolar responses to acetylcholine during acute hyperglycemia

Propofol but not desflurane maintains rat cerebral arteriolar responses to acetylcholine during acute hyperglycemia
复制标题

丙泊酚而非地氟烷在急性高血糖期间维持大鼠脑动脉对乙酰胆碱的反应

DOI:
10.1097/ana.0000000000000632
复制
发表时间:
2019
影响因子:
3.7
通讯作者:
Iida Hiroki
Iida Hiroki
中科院分区:
医学3区
文献类型:
--
作者:
Sakata Koji;Kito Kazuhiro;Tanabe Kumiko;Fukuoka Naokazu;Nagase Kiyoshi;Iida Hiroki

文献摘要

相似文献

背景:急性高血糖可引起包括脑血管在内的多种器官的血管内皮功能障碍。它与围手术期的死亡率和发病率增加有关。麻醉剂对高血糖时脑血管舒张反应的影响尚不清楚。我们研究了在急性高血糖,丙泊酚或地氟醚anesthesia.Materials和方法:一个封闭的颅窗制备的大鼠脑小动脉内皮功能测定软膜小动脉直径的变化引起的局部应用乙酰胆碱(ACh),内皮依赖性血管扩张剂,在大鼠麻醉丙泊酚或地氟醚。在正常血糖和高血糖状态下测量软脑膜微动脉对ACh的反应。然后,我们调查是否丙泊酚麻醉下的脑小动脉急性高血糖的反应与丙泊酚或其车辆,intramedid.Results:乙酰胆碱导致在丙泊酚和地氟烷麻醉在血糖正常的条件下,脑小动脉的剂量依赖性扩张。ACh的血管舒张作用也维持在高血糖条件下丙泊酚麻醉,但血管舒张反应ACh显着受损,在高血糖与normoclonal与地氟烷麻醉相比。ACh的血管舒张作用维持在正常和高血糖的大鼠接受丙泊酚或intramid.Conclusions:大鼠软膜小动脉ACh的反应维持在急性高血糖的条件下,丙泊酚麻醉,但抑制与normoorphine与地氟醚麻醉。
Background:Acute hyperglycemia causes vascular endothelial dysfunction in various organs including the cerebral vessels. It is associated with increased mortality and morbidity in the perioperative period. The impact of anesthetic agents on cerebral vasodilatory responses during hyperglycemia remains unclear. We investigated endothelial function in rat cerebral arterioles during acute hyperglycemia, under propofol or desflurane anesthesia.Materials and Methods:A closed cranial window preparation was used to measure changes in pial arteriole diameter induced by topical application of acetylcholine (ACh), an endothelium-dependent vasodilator, in rats anesthetized with propofol or desflurane. Pial arteriole responses to ACh were measured during normoglycemia and hyperglycemia. We then investigated whether the response of cerebral arterioles to acute hyperglycemia under propofol anesthesia were related to propofol or its vehicle, intralipid.Results:ACh resulted in a dose-dependent dilation of cerebral arterioles during propofol and desflurane anesthesia under normoglycemic conditions. The vasodilatory effects of ACh were also maintained under hyperglycemic conditions during propofol anesthesia, but the vasodilator response to ACh was significantly impaired during hyperglycemia compared with normoglycemia with desflurane anesthesia. The vasodilatory effects of ACh were maintained during normoglycemia and hyperglycemia in rats receiving propofol or intralipid.Conclusions:Rat pial arteriole responses to ACh are maintained during conditions of acute hyperglycemia with propofol anesthesia but suppressed compared with normoglycemia with desflurane anesthesia.