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本文介绍家兔油酸型呼吸窘迫综合征时肺动脉血压的变化。静脉注入油酸后,肺血管阻力显著增加,股动脉血压、心率和心输出量均下降;肺动脉压则升高,并经历最初快速升高、相对稳定和后期升高三个时相变化。预先注射神经节阻滞剂六甲双胺或α-受体阻断剂酚妥拉明,然后注射油酸,肺动脉压的最初快速升高期不出现。切断两侧颈动脉窦神经或两侧颈部迷走神经对其并无影响。此外,在后期,六甲双胺及酚妥拉明两者均不能阻断肺动脉压的上升。上述结果表明,动物注射油酸后,肺动脉压的最初快速升高是通过交感神经实现的。肺动脉压的后期升高则是缺氧或其他因素所造成。
This article describes the changes of pulmonary arterial pressure in rabbits with oleic acid type respiratory distress syndrome. Pulmonary vascular resistance was significantly increased after intravenous injection of oleic acid, blood pressure, heart rate and cardiac output of femoral arteries decreased; pulmonary arterial pressure increased, and experienced three rapid changes of initial rapid increase, relative stability and late increase. Pre-injection of the ganglioside blocker hexamethonium or the alpha-blocker phentolamine, followed by oleic acid injection, does not occur at the initial rapid increase in pulmonary arterial pressure. Cut off both sides of the carotid sinus nerve or bilateral cervical vagus nerve has no effect on it. In addition, both hexamidine and phentolamine failed to block the increase in pulmonary arterial pressure late in the day. The above results indicate that the initial rapid increase of pulmonary arterial pressure after the animals injected with oleic acid is achieved by the sympathetic nerve. Late pulmonary hypertension is caused by hypoxia or other factors.