Beckman C B, Ziazi Z, Dietzman R H, Lillehei R C
Circ Shock. 1981;8(2):137-49.
To evaluate the mechanism of protection of epinephrine tolerance in shock, we studied the hemodynamic and regional blood flow response to cardiogenic shock in dogs rendered tolerant to lethal doses of epinephrine. Shock was induced by coronary embolization. Regional organ perfusion was evaluated with radioactive microspheres. The survival of tolerant dogs following embolization was 8/12 (62%) compared to 5/31 (16%) in control dogs (P = 0.008). Heart and adrenal organ weights were significantly greater in the tolerant animals. Ventricular hypertrophy in the tolerant dogs was accompanied by greater myocardial blood flow and greater myocardial contractility both before and during cardiogenic shock. There was significantly greater regional flow to spleen, gastrointestinal tract, and pancreas during shock in the epinephrine-tolerant group.
为评估肾上腺素耐受性在休克中的保护机制，我们研究了对致死剂量肾上腺素产生耐受性的犬在发生心源性休克时的血流动力学及局部血流反应。通过冠状动脉栓塞诱导休克。用放射性微球评估局部器官灌注。栓塞后，耐受性犬的存活率为8/12（62%），而对照犬为5/31（16%）（P = 0.008）。耐受性动物的心脏和肾上腺器官重量显著更大。耐受性犬的心室肥大伴随着心源性休克前及休克期间更大的心肌血流量和更强的心肌收缩力。在休克期间，肾上腺素耐受性组的脾脏、胃肠道和胰腺的局部血流量显著更大。
