交感神经在低体温所致肺动脉高压中的作用

EFFECT OF SYMPATHICUS ON COLD-INDUCE PULMONARY HYPERTENSION

本文观察了低体温对肺循环的影响,并探讨了交感神经在其中的作用。低温时(33.5±0.19℃)动物心输出量下降,肺动脉压升高,肺血管阻力增加51.6％,肺嵌压变化不明显。体温下降时血浆去甲肾上腺素浓度明显升高,但不影响动脉血气值。派唑嗪可以阻止低温引起的肺动脉高压,心得安对低温时肺循环变化无明显影响。结果表明:低温所致肺动脉高压,是由于交感神经兴奋,去甲肾上腺素释放增加,通过α_1肾上腺素能受体,促使肺动脉收缩,导致肺动脉高压形成。

In this study we observed the effect of hypothermia on pulmonary circulation and explored the role of sympothicus.Hy- pothermia induced reduction of cardiac output,and increase of pulmonary artery pressure.Pulmonary vascular resistance in- creased by 51.6%,but no change in pulmonary artery wedge pressure was noticed during hypothermia.The plasma level of norepinephrine increased markedly after blood temperature fell and there was no effect of hypothermia on arterial gas tensions. Prazosin could prevent the pulmonary hypertension induced by hypothermia and propranolol was no effect on pulomnary circu- lation during hypothermia.The results showed that hypothermia-induced pulmmary hypertension was caused by sympathicus, which greatly release norepinephrine and constrict pulmonary artery through α1 adrenoceptor.