マスイ ト シュウジュツキ シンキン キョケツ
Anesthetic Management and Perioperative Myocardial Ischemia
Prevention and adequate treatment of perioperative myocardial ischemia has been an important subject of anesthetic practice. Potent coronary vasodilators, including dipyridamole, have been shown to cause myocardial ischemia via a "coronary steal" mechanism, which is defined as marked redistribution of myocardial blood flow from ischemic to normal zones or from subendocardial to subepicardial areas during constant aortic perfusion pressure and heart rate. The hypothesis that inhalation agents, e.g., isoflurane and sevoflurane, may cause coronary steal in humans remained controversial. By using the myocardial contrast echocardiography, however, it was showed that sevoflurane did not cause transmural coronary steal or intercoronary steal in dogs with acute coronary artery stenosis and in patients with multivessel coronary artery disease.
Ischemic preconditioning, which is defined as previous exposure to transient cardiac ischemia, provides protection from subsequent myocardial infarction. Administration of volatile anesthetics including sevoflurane also improves myocardial function and reduces myocardial infarct size after ischemia-reperfusion in vitro and in vivo. This phenomenon is called anesthetic-induced preconditioning. Activation of mitochondrial adenosine triphosphate-regulated potassium (KATP) channels and inhibition of the opening of the mitochondrial permeability pore, through multiple signaling pathways including protein kinase C, has been implicated as a pivotal mechanism mediating ischemic- and anesthetic-induced preconditioning.
Several prospective, randomized, clinical trials provided evidence that perioperative beta-adrenergic receptor blockade reduced postsurgical mortality in patients at risk for myocardial ischemia and infarction. Consequently the American Heart Association and American College of Cardiology issued the guidelines that made appropriate perioperative beta-adrenergic receptor blockade a standard of care.
In the heart, sublethal heat stress induces heat shock protein (Hsp) 70 synthesis. The resulting increased level of Hsp 70 has been shown to enhance myocardial tolerance to subsequent ischemia-reperfusion injury. It has been reported that administration of the anti-gastric ulcer drug geranylgeranylacetone (GGA) before ischemia induced Hsp 70 expression and resulted in myocardial protection against ischemia and reperfusion injury. This cardioprotective effect of GGA was negated by administration of 5-hydroxydecanoate. These results suggest that the mechanism of GGA-induced myocardial protection may involve mitochondrial KATP channels.
A more detailed knowledge of different mechanisms in myocardial protection can allow effective strategy of cardioprotection in perioperative anesthetic protocols.
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