Dobbins D E, Swindall B T, Haddy F J, Dabney J M
Microcirc Endothelium Lymphatics. 1985;2(5):517-49.
The effect of the local intra-arterial infusion of ouabain (11.8 micrograms/min.) on the response of the forelimb to vasoactive agents was examined. In seven dogs, bolus injections of CaCl2, MgSO4, KCl, norepinephrine, adenosine, acetylcholine, PGE1 and saline were made into the forelimb perfused at constant flow before and three times during ouabain infusion. Ouabain blocked potassium vasodilation and changed the response to CaCl2 from vasoconstriction to vasodilation. The response of the forelimb to the other vasoactive agents was initially unaffected by ouabain but with time the forelimb vasculature became less sensitive to all agents studied. These changes were not seen in a series of 5 saline infused control animals. In a third series of animals steady-state dose responses to CaCl2, Ca-gluconate and KCl were explored by infusing solutions intrabrachially at three dosages. Before ouabain, forelimb resistance increased as a function of Ca++ and decreased as a function of K+. Ouabain completely blocked potassium vasodilation and on the average blocked Ca++ vasoconstriction although a number of animals evidenced vasodilation to Ca++ during ouabain infusion. These data indicate that K+ vasodilation is Na+, K+-ATPase dependent and that Na+, K+-ATPase inhibition unmasks a vasodilatory action of locally applied Ca++.
研究了局部动脉内输注哇巴因(11.8微克/分钟)对前肢对血管活性药物反应的影响。在7只狗中,在输注哇巴因之前以及输注过程中3次,以恒定流量向前肢灌注的情况下,分别静脉推注氯化钙、硫酸镁、氯化钾、去甲肾上腺素、腺苷、乙酰胆碱、前列腺素E1和生理盐水。哇巴因阻断了钾引起的血管舒张,并使前肢对氯化钙的反应从血管收缩转变为血管舒张。前肢对其他血管活性药物的反应最初不受哇巴因影响,但随着时间推移,前肢血管系统对所有研究药物的敏感性降低。在一系列5只输注生理盐水的对照动物中未观察到这些变化。在第三组动物中,通过以三种剂量经肱动脉内输注溶液,探究了对氯化钙、葡萄糖酸钙和氯化钾的稳态剂量反应。在使用哇巴因之前,前肢阻力随钙离子浓度升高而增加,随钾离子浓度升高而降低。哇巴因完全阻断了钾引起的血管舒张,平均而言也阻断了钙离子引起的血管收缩,尽管一些动物在输注哇巴因期间出现了对钙离子的血管舒张反应。这些数据表明,钾引起的血管舒张依赖于钠钾ATP酶,并且抑制钠钾ATP酶可揭示局部应用钙离子的血管舒张作用。