论文部分内容阅读
研究发现吸入麻醉药可保护心肌免受可逆或不可逆的缺血性损伤。吸入麻醉药介导的抗缺血效应可明显影响心血管功能,降低动脉及冠脉灌注压,抑制心肌收缩,舒张冠脉并影响电生理;此外还可不同程度地调节自主神经系统活性。心肌氧供的适度改变、能量依赖性细胞功能的存储以及冠脉血流的增加可部分介导吸入麻醉药的抗缺血效应;但改变心肌代谢与冠脉灌注并非吸入麻醉药抗缺血效应的唯一机制,胞内信号转导通路通过激活 K_(ATP)并诱生活性氧(ROS)而参与抗缺血效应。基础与临床研究表明吸入麻醉药的预处理具有抗心肌缺血损伤
Studies have found that inhaled anesthetics protect the myocardium from reversible or irreversible ischemic injury. Inhalation anesthesia-mediated anti-ischemic effect can significantly affect cardiovascular function, reduce arterial and coronary perfusion pressure, inhibit myocardial contractility, coronary artery relaxation and affect electrophysiology; in addition to varying degrees of regulation of autonomic nervous system activity. Moderate changes in myocardial oxygen supply, storage of energy-dependent cellular functions, and increased coronary blood flow may partially mediate the anti-ischemic effects of inhaled anesthetics; however, changes in myocardial metabolism and coronary perfusion are not an anti-ischemic effect of inhaled anesthetics The only mechanism by which the intracellular signal transduction pathway participates in the anti-ischemic effect by activating K (ATP) and inducing reactive oxygen species (ROS). Basic and clinical studies have shown that inhalation anesthetics pretreatment with anti-ischemic injury