Characterization of Myocardial Ischemia in Shock by NADH Fluorescence

为了阐明休克时心肌缺血的特点，通过调整与锁骨下动脉相连的储血器的水平，在犬模型中实验性地诱导低血压。将跳动的心脏快速横切并原位冷冻夹持以获得冷冻的心脏切片。当主动脉平均压降低到40 mmHg或更低时，NADH荧光照相提供了心肌缺血的可视化，其主要局限于内膜下。冠状动脉血流量减少取决于低冠状动脉灌注压和休克时心室的工作，然而，冠状动脉储备得以维持，如稳定的冠状动脉阻力、左心室中的心内膜心外膜组织流量比和冠状动脉闭塞后反应性充血的保存所示。血浆肾上腺素和去甲肾上腺素浓度升高表明交感神经张力增强，可能在休克时收缩冠状动脉血管中起重要作用。右心室也与左心室同时参与心肌缺血，例如当主动脉压为40 mmHg或更低时，右心室可见心肌缺血。L-NAME预处理增加了休克时的缺血面积，给予L-NAME后，休克时冠状动脉血流量进一步减少。提示休克时释放的血管活性物质的缩血管和扩血管作用对休克时心肌缺血的发生起重要作用。在休克状态下，血管紧张素和NO可能是影响冠状动脉循环的候选者。

To clarify the characteristics of myocardial ischemia in the shock, hypotension was experimentally induced in the canine model by adjusting the level of the reservoir connected to the subclavian artery. The beating hearts were rapidly cross-sectioned and freeze-clamped in situ to obtain frozen heart slices. When aortic mean pressure was lowered to 40 mmHg or less, NADH fluorescence photography provided visualization of myocardial ischemia which was localized dominantly in the subendocardium. Coronary blood flow was reduced depending on the low coronary perfusion pressure and also the work of the ventricle in the shock, however, coronary reserve was maintained as shown by stable coronary resistance, endocardial epicardial tissue flow ratio in the left ventricle, and preservation of reactive hyperemia following coronary occlusion. Augmented sympathetic tone, indicated by elevated plasma epinephrine and norepinephrine concentrations, is likely to take a significant role to constrict coronary vessels in the shock.Right ventricle was also involved in myocardial ischemia simultaneously with the left ventricle, e.g.myocardial ischemia was visualized in the right ventricle when aortic pressure was at 40 mmHg or less.Pretreatment with L-NAME increased ischemic area in the shock, and coronary blood flow in the shock was further reduced following L-NAME administration. It is indicated that both vasoconstricting and vasodilating effect s of vasoactive substances released in the shock take significant roles to generate myocardial ischemia in the shock. Cathecolamines and NO are possible candidates to affect coronary circulation in the shock.