Wilton N C, Knight P R, Ullrich K, Martin B, Gallagher K P
Department of Anesthesiology, University of Michigan Medical School, Ann Arbor.
Anesthesiology. 1993 Mar;78(3):510-23. doi: 10.1097/00000542-199303000-00015.
The effects of isoflurane on the transmural distribution of myocardial blood flow distal to an acute critical coronary stenosis and the relationship between the changes in regional blood flow and function were studied to determine whether isoflurane can produce a transmural "steal" phenomenon and to assess the role of this phenomenon in producing changes in regional myocardial function.
After production of acute critical coronary stenosis under baseline chloralose and fentanyl anesthesia, the animals were exposed to increasing end-tidal concentrations of isoflurane (0.7%, 1.4%, and 2.1%) without control of the hemodynamic parameters. At 2.1% isoflurane, the blood pressure then was restored to the baseline level by administration of phenylephrine. Changes in the following parameters were assessed: global contractility (measured by changes in pressure with time), regional myocardial function (assessed by systolic wall thickening and measured by sonomicrometers), transmural distribution of myocardial perfusion (measured by the radioactive microsphere method), and regional oxygen consumption and extraction.
Distal to the critical stenosis, a transmural redistribution of myocardial blood flow (endocardial-epicardial ratio < 1) occurred with all concentrations of isoflurane. With higher concentrations (1.4% and 2.1%), a significant decrease in subendocardial blood flow occurred only in the presence of hemodynamic changes and was restored by phenylephrine. In this area, changes in regional myocardial function correlated most strongly with changes in subendocardial perfusion (y = -0.17 + 1.70x -0.58x2, r2 = 0.90). In the stenotic region, oxygen extraction remained stable, but oxygen consumption decreased in parallel with reductions in regional myocardial function. In the normal region, oxygen consumption did not change, but oxygen extraction decreased with increasing isoflurane concentrations.
These results show that isoflurane is a coronary vasodilator able to induce a transmural redistribution of myocardial blood flow distal to an acute critical coronary stenosis. A true transmural steal, however, was not produced reliably in the absence of hemodynamic changes, suggesting that isoflurane either is only a moderate vasodilator, or that the decrease in subendocardial blood flow is offset by the negative inotropic action of the drug. When regional myocardial dysfunction distal to a severe coronary stenosis occurs, this correlates with decreasing subendocardial blood flow during isoflurane anesthesia, suggesting ischemia as the cause.
研究异氟烷对急性严重冠状动脉狭窄远端心肌血流跨壁分布的影响以及局部血流变化与功能之间的关系，以确定异氟烷是否会产生跨壁“窃血”现象，并评估该现象在引起局部心肌功能变化中的作用。
在基线氯醛糖和芬太尼麻醉下造成急性严重冠状动脉狭窄后，在不控制血流动力学参数的情况下，使动物吸入递增的呼气末异氟烷浓度（0.7%、1.4%和2.1%）。在异氟烷浓度为2.1%时，通过给予去氧肾上腺素将血压恢复到基线水平。评估以下参数的变化：整体收缩性（通过压力随时间的变化来测量）、局部心肌功能（通过收缩期室壁增厚评估并由超声微测仪测量）、心肌灌注的跨壁分布（通过放射性微球法测量）以及局部氧耗和氧摄取。
在所有异氟烷浓度下，严重狭窄远端均出现心肌血流的跨壁重新分布（心内膜 - 心外膜比值<1）。在较高浓度（1.4%和2.1%）时，仅在存在血流动力学变化的情况下，心内膜下血流才会显著减少，而去氧肾上腺素可使其恢复。在该区域，局部心肌功能的变化与心内膜下灌注的变化相关性最强（y = -0.17 + 1.70x -0.58x2，r2 = 0.90）。在狭窄区域，氧摄取保持稳定，但氧耗随局部心肌功能的降低而平行下降。在正常区域，氧耗未发生变化，但氧摄取随异氟烷浓度的增加而降低。
这些结果表明，异氟烷是一种冠状动脉血管扩张剂，能够引起急性严重冠状动脉狭窄远端心肌血流的跨壁重新分布。然而，在不存在血流动力学变化的情况下，并未可靠地产生真正的跨壁窃血现象，这表明异氟烷要么只是一种中度血管扩张剂，要么心内膜下血流的减少被该药物的负性肌力作用所抵消。当严重冠状动脉狭窄远端出现局部心肌功能障碍时，这与异氟烷麻醉期间心内膜下血流减少相关，提示缺血是其原因。
