家兔侧脑室注射组胺对肺动脉血压的影响

ALTERATIONS OF PULMONARY ARTERIAL PRESSURE FOLLOWING INTRAVENTRICULAR INJECTION OF HISTAMINE IN RABBITS

本工作将组胺(HA)注入麻醉家兔侧脑室,观察其对肺动脉血压的影响。结果观察到(1)侧脑室注射HA(50μg)后,肺动脉压和心输出量出现升高、降低和先降后升三种变化,但以升高反应较为多见。发生上述反应时,颈动脉压升高,心率减慢。(2)切断两侧颈部迷走神经或用心脏人工起搏固定心率后,肺动脉压和心输出量均不再下降而出现恒定的升高反应。静脉注射酚妥拉明可部分阻断HA引起的肺动脉和颈动脉升压反应,但不能阻断心输出量的升高。静脉注射心得安能完全阻断HA引起的心输出量升高,但对肺动脉和颈动脉的升压反应无影响。静脉注射六甲双铵或联合应用酚妥拉明和心得安可完全消除HA引起的肺动脉压、颈动脉压和心输出量的升高反应。(3)HA的心血管效应可被H_1受体阻断剂扑尔敏阻断,但不能被H_2受体阻断剂甲氰咪胍阻断。 实验结果表明:家兔侧脑室注射HA后,在中枢H_1受体的介导下,可通过交感神经使心输出量增加,肺血管和外周血管收缩,因而肺动脉压和颈动脉压上升;也可通过迷走神经使心率减慢。而HA引起的肺动脉压下降则是继发性的,是由于心率减慢,心输出量减少所致。

The changes of the pulmonary arterial pressure (PAP) following microinjectionof histamine (HA) into the lateral ventricle in the rabbit were investigated. It wasfound that (1) Intraventricular injection of HA (50 μg) induced either an increase(in the majority) or a decrease in PAP and cardiac output (CO), or a biphasic re-sponse characterized by a decrease followed by an increasc. Slowing down ofheart rate (HR) and elevation of carotid arterial pressure (CAP) were observedaccordingly. (2) After bilateral cervical vagotomy or fixing the heart rate by car-diac pacing, drop in CO and PAP in response to HA was no longer observed. In-stead, they even showed some constant increase. The pressor response of PAPand CAP to HA could be patially blocked by phentolamine applied intravenouslywithout affecting the increment of CO. On the other hand, intravenous injectionof propranolol could totally block the HA-induced increment of CO, but not affectthe pressor responses of PAP and CAP. Intravenous injection of hexamethoniumor combined application of phentolamine and propranolol could completely abolishall the increment responses in CO, PAP and CAP to HA. (3) The cardiovascularresponses to HA could be blocked by the H_1 receptor blocker- chlorpheniramine,but not by H_2 receptor blocker-cimetidine. It is thus assumed that HA applied intraventricularly can activate the centralH_1 receptor, thus inducing an increase in the cardiac output and vasoconstrictionof pulmonary and peripheral vessels giving rise to an elevation of both PAP andCAP by way of sympathetic nerve. Central application of HA also induces bra-dycardia by activating vagus nerve. The drop of PAP observed in responses toHA is thought to be secondary.