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目的:观察大鼠对哌唑嗪的快速耐受性,并探讨其机制.方法:反复iv哌唑嗪诱导大鼠(n=24)对哌唑嗪的降压作用产生快速耐受,对α肾上腺受体的阻滞作用脱敏.结果:等剂量哌唑嗪(50μg/kg)iv4次,清醒大鼠对其降压作用的反应性逐渐减弱,呈明显的递减趋势,哌唑嗪诱导大鼠耐受时,其肛尾肌和主动脉平滑肌α肾上腺受体与去甲肾上腺素(NE)相互作用的pD_2降低,哌唑嗪的拮抗参数pA_2值明显减小;大脑皮层、心脏和脾脏α肾上腺受体与[~3H]prazosin的亲合力下降;但对NE引起的最大反应E_(max)和与[~3H]prazosin相互作用的最大结合容量B_(max)则无明显变化.结论:反复iv哌唑嗪可诱导大鼠对哌唑嗪降压作用产生快速耐受,α肾上腺受体的脱敏是其机制之一.
OBJECTIVE: To observe the rapid tolerance of prazosin in rats and to explore its mechanism.Methods: Rapid iv tolerance to prazosin in rats induced by repeated prazosin (n = 24) Adrenal receptor blockade desensitization.Results: Isoprazole (50μg / kg) iv4 times, awake rat antihypertensive effect gradually weakened, showing a decreasing trend, prazosin induced large In mouse tolerance, the pD_2 of the interaction between α-adrenergic receptor and norepinephrine (NE) in the anus and aortic smooth muscle was decreased and pA_2, an antagonistic parameter of prazosin, was significantly decreased. The cerebral cortex, heart and spleen α The affinity of adrenoceptor to [~ 3H] prazosin decreased, but the maximal response to NE and maximal binding capacity to maximal binding capacity to [~ 3H] prazosin had no significant change.Conclusion: Repeated Prazosin-induced prazosin-induced rapid depressive effects in rats, α-adrenergic receptor desensitization is one of the mechanisms.