Maximov M J, Brody M J
Am J Cardiol. 1976 Jan;37(1):26-32. doi: 10.1016/0002-9149(76)90495-1.
The possibility that failure of vascular resistance to increase during hypotension in cardiogenic shock is a generalized phenomenon affecting many vascular beds was investigated in anesthetized dogs subjected to coronary arterial embolization. Blood flow in the carotid, mesenteric and renal vascular beds was monitored. Efferent vagus nerve stimulation, which, through bradycardia, produces hypotension of cardiac origin without myocardial damage, was associated with reflex vasoconstrictor responses in the carotid and mesenteric vascular beds; no change in resistance occurred in the renal vascular bed. In marked contrast, vasoconstriction failed to occur in any of the vascular beds in response to the hypotension produced by coronay embolization. These responses to cardiogenic shock mimicked those seen after ganglionic blockade, in which hypotension of partly cardiac origin was produced and reflex vasoconstriction blocked. The data support the previous hypothesis that myocardial infarction is associated with reflex inhibition of the reflex vasoconstrictor response to hypotension.
在接受冠状动脉栓塞的麻醉犬中，研究了心源性休克时低血压期间血管阻力未能增加这一情况是否为影响多个血管床的普遍现象。监测了颈动脉、肠系膜和肾血管床的血流。通过心动过缓产生无心肌损伤的心脏源性低血压的传出迷走神经刺激，与颈动脉和肠系膜血管床的反射性血管收缩反应相关；肾血管床的阻力未发生变化。与之形成显著对比的是，对冠状动脉栓塞所致低血压，任何血管床均未出现血管收缩。这些对心源性休克的反应与神经节阻断后所见相似，神经节阻断会产生部分心脏源性低血压并阻断反射性血管收缩。这些数据支持了先前的假设，即心肌梗死与对低血压的反射性血管收缩反应的反射抑制有关。
