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目的 探讨侧脑室注射 (icv)组胺 (HA)对升高血压、减慢心率的作用机制。方法 实验用乌拉坦麻醉、肌肉松弛、人工呼吸的家兔 ,观察在icvHA之前和之后血压和心率的变化。结果 icvHA (5 0 μg)可引起血压升高、心率减慢。预先icvH1受体阻断剂扑尔敏或α1受体阻断剂哌唑嗪 ,或静脉注射酚妥拉明或六甲双铵均可阻断HA的中枢升压反应。预先icvH2 受体阻断剂甲氰咪胍 ,或α2 受体阻断剂Yohinbin(育亨宾 )对HA的中枢心血管效应均无影响。切断两侧颈部迷走神经 ,再icvHA ,心率减慢作用消失。结论 家兔icvHA后 ,可通过交感神经使血压升高 ,通过迷走神经使心率减慢 ,并与中枢H1受体有关。此外 ,在中枢HA能的升压作用中也有α1肾上腺素能受体的参与。
Objective To investigate the mechanism of intracerebroventricular (icv) histamine (HA) on blood pressure and heart rate. Methods Experiments were performed with urethane anesthetized, muscle-relaxed, and resuscitated rabbits to observe changes in blood pressure and heart rate before and after icvHA. Results icvHA (50 μg) caused an increase in blood pressure and a decrease in heart rate. Pre-icvH1 receptor blocker chlorpheniramine or α1 receptor blocker prazosin, or intravenous injection of phentolamine or hexamethonium can block the HA central vasopressor response. Pre-icvH2 receptor blocker cimetidine, or α2-receptor blocker Yohinbin (yohimbine), had no effect on the central cardiovascular effects of HA. Cut off both sides of the neck vagus nerve, then icvHA, heart rate slowed down disappear. Conclusion After icvHA in rabbits, blood pressure can be increased by sympathetic nerves, heart rate slowed by the vagus nerve and related to central H1 receptor. In addition, central HA potentiates the effects of α1 adrenergic receptors.