ANESTHETIC DEPRESSION OF THE MYOCARDIUM

在麻醉病人中观察到低血压和心脏骤停 吸入麻醉剂氟烷恩氟烷和异氟烷。 这些挥发性 麻醉剂（VA’s）目前在临床上广泛使用。 初步证据 表明VA可能会降低钙的有效性所需的 心脏收缩 该项目旨在研究 上述麻醉剂对心肌细胞中的结构的作用， 调节Ca ~（2+）流量，控制收缩强度。 的元素 将被研究的是：sarolemma（SL），外膜的 肌浆网（SR），一种膜状网络， 控制着肌浆内钙离子的数量， 产生细胞器，该细胞器也用于控制紧张性Ca 2+的可用性， 和肌钙蛋白（Tn），一种通过改变其 形成并启动收缩过程。 实验也将 在分离的乳头肌和肌细胞上进行，以整合 结果发现与孤立的亚细胞结构与系统的更多 生理复杂性 目前的证据表明，SR和SL是 受麻醉剂的影响，可能是改变的主要部位。 收缩性 概述的研究将审查以下因素的相互作用： 氟烷，恩氟烷和异氟烷的亚细胞结构， 观察Ca 2+反应的变化。 结果将量化 每种麻醉剂对每种结构的相对影响以及可能的 将假定作用机制。 获得的数据将有助于 制定药物干预措施，以防止麻醉诱导的 在手术室里心脏抑制。

Hypotension and cardiac arrest have been observed in patients anesthetized with the anesthetics halothane, enflurane, and isoflurane. These volatile anesthetics (VA's) are in wide clinical use today. Preliminary evidence suggests that the VA's might decrease the available of Ca2+ required for cardiac contraction. This project is designed to study the effect of the above mentioned anesthetics on structures in the myocardial cell that regulate Ca2+ flux and control the intensity of contraction. The elements that will be studied are: the sarolemma (SL), the outer membrane of the muscle cell; the sarcoplasmic reticulum (SR), a membranous network that controls the amount of myoplasmic Ca2+; the mitochondrion, the energy generating organelle which also serves to control tonic Ca2+ availability, and troponin (Tn), a protein that responds to Ca2+ binding by changing its shape and initiating the contractile process. Experiments will also be performed on isolated papillary muscles and myocytes to integrate the results found with the isolated subcellular structures with systems of more physiological complexity. Present evidence suggests that the SR and SL are affected by anesthetics and may be the major sites of alteration of contractility. The studies outlined will examine the interaction of halothane, enflurane, and isoflurane with the subcellular structures to observe alterations in Ca2+ response. The results will quantify the relative effect of each anesthetic on each structure and a possible mechanism of action will be postulated. The data obtained will help in formulating pharmacologic interventions to prevent anesthetic-induced cardiac depression in the operating room.