兴奋大鼠延髓A1区引起降压、降心率效应的机制

在水合氯醛麻醉、箭毒化、人工呼吸的大鼠,观察到:(1) A_1区注入谷氨酸钠引起明显的血压下降和心率减慢。(2) 切断双侧颈迷走神经明显衰减A_1区的降压,降心率效应。(3) 延髓头端腹外侧区(RVL)预先注射酚妥拉明或心得安,均能明显衰减谷氨酸钠兴奋A_1区的降压效应,A_1区的降心率作用基本不受影响,将纳洛酮注入RVL后,A_1区的降压和降心率效应均无明显变化;注射荷包牡丹碱入RVL则使A_1区的降压、降心率效应反转。(4) RVL内注入酚妥拉明或心得安本身使基础血压降低,注射荷包牡丹碱入RVL则使基础血压升高(提示RVL内的α-,β-受体中介对RVE加压神经元的紧张性兴奋作用,GABA受体中介紧张性抑制作用);另一方面,RVL内注入心得安使基础心率减慢、注入纳洛酮或荷包牡丹碱使基础心率加快(说明β-受体中介紧张性心加速效应,阿片受体和GABA受体中介紧张性心抑制效应)。

MECHANISMS UNDERLYING DEPRESSOR AND BRADYCARDIA EFFECTS OF A_1- EXCITATION IN RATS

In chloral hydrate-anesthetized, tubocurarine-immobilized and artificially ventilated rats, the following results were observed: (1) Microinjection of sodium L-glutamate (Glu) into A1 area induced a significant fall in blood pressure and heart rate. (2) Bilateral vagotomy markedly reduced the magnitude of the depressor and bradycardia effects of Glu-injection into A1. (3) Injection of phentolamine or propranolol into bilateral RVL reduced the depressor effect of Glu-injection into A1. Naloxone-injection into RVL had no significant influence on cardiovascular effects of A1-excitation, but injecting bicuculline into RVL could reverse both depressor and bradycardia effects of A1 area. The results suggest that A1 exerts its cardiovascular effects mainly via RVL, and the alpha-, beta- and GABA-receptors within RVL (but not opiate receptors) mediate the hypotension effect of A1 area, while GABA-receptors play an important role in mediating the bradycardia effect of the A1 area.