Bhagat B D, Rao P S, Gandhi S S, Cavanagh D
Circ Shock. 1977;4(3):271-8.
Infusion of endotoxin in chemically sympathectomized monkeys caused a fall in the mean aortic pressure, but the cardiac output, stroke volume, and central venous pressure were well maintained. Endotoxin-induced tachycardia in monkeys with functional sympathetics was not seen in the sympathectomized animals. Infusion of dopamine improved the hemodynamic and cardiovascular status, probably by causing vasoconstriction of the splenic and hepatic artery where the pooling of blood is believed to occur in endotoxin shock. However, these beneficial effects were not apparent when dopamine was administered in the chemically sympathectomized animal infused with endotoxin. Since chemical sympathectomy did not affect the endotoxin-induced decline in the systolic and mean aortic pressure or the severity of the endotoxin shock, it is suggested that catecholamines may not be the primary initiator or trigger substances in endotoxin shock.
给化学性交感神经切除的猴子输注内毒素会导致平均主动脉压下降,但心输出量、每搏输出量和中心静脉压保持良好。功能性交感神经存在的猴子中内毒素诱导的心动过速在交感神经切除的动物中未出现。输注多巴胺改善了血流动力学和心血管状态,可能是通过引起脾动脉和肝动脉血管收缩,据信在内毒素休克中血液会在这些部位淤积。然而,当在输注内毒素的化学性交感神经切除动物中给予多巴胺时,这些有益作用并不明显。由于化学性交感神经切除并不影响内毒素诱导的收缩压和平均主动脉压下降或内毒素休克的严重程度,因此提示儿茶酚胺可能不是内毒素休克的主要启动剂或触发物质。