Rat vasopressin cell responses to simulated hemorrhage: stimulus-dependent role for A1 noradrenergic neurons.
Rat vasopressin cell responses to simulated hemorrhage: stimulus-dependent role for A1 noradrenergic neurons.
复制标题
大鼠加压素细胞对模拟出血的反应：A1 去甲肾上腺素能神经元的刺激依赖性作用。
作者：
D. W. Smith;J. Sibbald;S. Khanna;T. Day
通过c-fos表达定位和电生理记录实验，阐明A1去甲肾上腺素能细胞群在脑出血后加压素反应中的作用。在戊巴比妥麻醉的大鼠中，通过短暂闭塞下腔静脉（足以将平均动脉压分别降低至约50或30 mmHg）模拟中度和重度肿胀性脑出血。这两种刺激显着增加了A1区的儿茶酚胺细胞显示Fos样免疫反应，这种效果是最突出的最后区的水平。这两种刺激也增加了视上核加压素细胞显示Fos样免疫反应的数量。因此，涉及单独动物的电生理学研究证实，中度和重度腔静脉闭塞均显著增加了视上核中记录的功能鉴定的加压素细胞的放电。然而，虽然在最后区水平注射γ-氨基丁酸中断A1区神经元功能消除了由中度腔静脉闭塞引起的加压素细胞放电的增加，但它并没有阻止对严重腔静脉闭塞的反应。这些研究结果表明，在大鼠中，加压素对中央血容量急性减少的反应，如出血产生的反应，仅在刺激强度中等时才依赖于A1投射。严重的刺激似乎涉及激活A1投射和绕过A1区的额外加压素刺激通路。
c-fos expression mapping and electrophysiological recording experiments were done to clarify the role of the A1 noradrenergic cell group in the vasopressin response to hypotensive hemorrhage. In pentobarbital-anesthetized rats, moderate and severe hypotensive hemorrhages were simulated by brief occlusion of the inferior vena cava sufficient to reduce mean arterial pressure to approximately 50 or 30 mmHg, respectively. Both stimuli significantly increased the number of A1 region catecholamine cells displaying Fos-like immunoreactivity, this effect being most prominent at the level of the area postrema. Both stimuli also increased the number of supraoptic nucleus vasopressin cells displaying Fos-like immunoreactivity. Accordingly, electrophysiological studies involving separate animals confirmed that both moderate and severe caval occlusion significantly increased the firing of functionally identified vasopressin cells recorded in the supraoptic nucleus. However, although interruption of A1 region neuronal function by injection of gamma-aminobutyric acid at the level of the area postrema eliminated the increase in vasopressin cell firing elicited by moderate caval occlusion, it did not block the response to severe caval occlusion. These findings suggest that, in the rat, the vasopressin response to an acute reduction in central blood volume, such as that produced by hemorrhage, depends on the A1 projection only if the stimulus is of moderate intensity. Severe stimuli appear to involve activation of both the A1 projection and an additional vasopressin-stimulatory pathway that bypasses the A1 region.