Effect of cooling on cutaneous microvascular adrenoceptors in vivo in the rabbit ear.
Effect of cooling on cutaneous microvascular adrenoceptors in vivo in the rabbit ear.
复制标题
冷却对兔耳体内皮肤微血管肾上腺素受体的影响。
DOI：
10.1002/jor.1100160206
复制
发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Smith,TL
中科院分区：
文献类型：
--
作者：
Li,Z;Koman,LA;Rosencrance,E;Pollock,DC;Smith,BP;Strandhoy,JW;Smith,TL
先前的研究表明，适度的冷却会增加血管α2-肾上腺素受体的反应性。然而，有限的信息是可用的，记录温度变化对体温调节器官的微血管系统中肾上腺素受体反应的影响（例如，人的手指和兔耳）经受宽范围的温度。在本研究中，局部冷却（24°C）对雄性新西兰白色兔（共66只耳）耳内皮肤微血管肾上腺素受体的影响在体内进行了研究。在温控组织浴中研究兔耳;耳制备物用特拉唑嗪（α1-肾上腺素受体拮抗剂）（10− 5 M）或特拉唑嗪（10 − 5 M）和普萘洛尔（β-肾上腺素受体拮抗剂）（10− 6 M）的组合进行预处理。然后分别在24或34°C下测定耳朵对去甲肾上腺素（10-l1 - 10 - 4 M）的微血管直径反应，以确定低温对肾上腺素受体对去甲肾上腺素刺激反应的影响。结果表明，低浓度的去甲肾上腺素可引起小动脉血管舒张和动静脉硬化。在34°C下，在α1-肾上腺素能阻滞的动物中，血管舒张后血管收缩，去甲肾上腺素浓度增加。适度的组织冷却可增加兔耳微血管对去甲肾上腺素的最大反应，并可消除低浓度去甲肾上腺素引起的血管舒张作用。在同时阻断α1-肾上腺素受体和β-肾上腺素受体后，两种温度条件下对去甲肾上腺素的微血管反应无显著差异。本研究的数据表明，适度冷却不会增强α2-肾上腺素受体对去甲肾上腺素的反应性。相反，冷却降低去甲肾上腺素刺激后小动脉和动静脉栓塞的β-肾上腺素能活性。
Previous studies have suggested that moderate cooling increases the responsiveness of vascular α2‐adrenoceptors. However, limited information is available documenting the influence of temperature changes on adrenoceptor responses in the microvasculature of thermoregulatory organs (e.g., the human digit and the rabbit ear) subjected to a wide range of temperatures. In the present study, the effect of local cooling (24°C) on cutaneous microvascular adrenoceptors in the ear was observedin vivoin male New Zealand White rabbits (total: 66 ears). The rabbit ear was studied in a temperature‐controlled tissue bath; the ear preparation was pretreated with terazosin (an α1‐adrenoceptor antagonist) (10−5M) or a combination of terazosin (10−5M) and propranolol (a β‐adrenoceptor antagonist) (10−6M). The microvascular diameter responses of the ear to norepinephrine (10−l1‐10−4M) then were determined at 24 or 34°C, respectively, to determine the influences of low temperature on adrenoceptor responses to norepinephrine stimulation. The results demonstrated that low concentrations of norepinephrine induced vasodilation in arterioles and arteriovenous anastomoses. This vasodilation was followed by vasoconstriction with an increased concentration of norepinephrine in animals with α1‐adrenergic blockade at 34°C. Moderate tissue cooling increased the microvascular maximal response of the rabbit ear to norepinephrine and abolished the vasodilatation induced by a low concentration of norepinephrine. There was no significant difference in the microvascular response to norepinephrine between the two temperature conditions after simultaneous blockade of α1‐adrenoceptors and β‐adrenoceptors. Data from the present study indicate that moderate cooling does not enhance the responsiveness of α2‐adrenoceptors to norepinephrine. In contrast, cooling reduced the β‐adrenergic activity of arterioles and arteriovenous anastomoses after norepinephrine stimulation.