Gutstein W H, Anversa P, Beghi C, Kiu G, Pacanovsky D
Atherosclerosis. 1984 Apr;51(1):135-42. doi: 10.1016/0021-9150(84)90149-7.
Anesthetized rats were sterotaxically implanted with electrodes and electrically stimulated in the lateral hypothalamus. During elevation of the S-T segment on simultaneous precordial electrocardiograms, the heart was perfused with glutaraldehyde-paraformaldehyde fixative and the major coronary arteries prepared for morphometry of luminal dimensions. A similar procedure was performed in a second group receiving intravenous arginine vasopressin (AVP) in place of hypothalamic stimulation. Elevation of the S-T segment was present in these animals as well. Control animals were implanted, not stimulated and otherwise treated in the same way. Morphometry showed that reductions of mean luminal diameter and cross-sectional area of statistical significance occurred in the two experimental groups compared to controls, suggesting that coronary spasm was the cause of the elevated S-T segments. Pooled plasma from separate groups of implanted control and hypothalamically-stimulated animals revealed substantial elevation of AVP levels in the latter raising the possibility that the neuroendocrine was involved in eliciting coronary artery spasm.
将麻醉后的大鼠进行立体定位,植入电极并对下丘脑外侧进行电刺激。在同步胸前心电图S-T段抬高期间,用戊二醛-多聚甲醛固定液灌注心脏,并准备对主要冠状动脉进行管腔尺寸的形态测量。在第二组接受静脉注射精氨酸加压素(AVP)而非下丘脑刺激的动物中进行了类似的操作。这些动物也出现了S-T段抬高。对照组动物进行植入,但不进行刺激,其他处理方式相同。形态测量显示,与对照组相比,两个实验组的平均管腔直径和横截面积均出现了具有统计学意义的减小,提示冠状动脉痉挛是S-T段抬高的原因。来自植入对照组和下丘脑刺激组动物的混合血浆显示,后者的AVP水平大幅升高,这增加了神经内分泌参与引发冠状动脉痉挛的可能性。