Johnson G, Henderson D, Bond R F
Circ Shock. 1985;15(2):111-21.
to determine if morphological differences exist between vasculature shown to decompensate, ie, skeletal muscle (SM) and vasculature that maintains the compensatory effort, ie, cutaneous (C).
dogs were anesthetized and subjected to a Wiggers hemorrhagic shock protocol. SM and C flows were monitored using electromagnetic flowmeters. Gracilis (SM) and saphenous (C) arterial segments were removed during: prehemorrhage control, compensation, and decompensation. Segments were fixed at in vivo intraluminal pressures. Both light and EM sections were made from each sample.
During the compensatory phase, both SM and C showed signs of strong vasoconstriction. Even though the amount of endothelial folding was comparable, the C did and the SM did not sustain the vasoconstriction. Vascular diameters of the SM but not C increased during decompensation. Ultrastructural changes consisted of extreme folding of the internal elastic lamina (IEL) during compensation and subsequent flattening out of the IEL during decompensation in the SM but not the C tissues. Cell deformation, damage, and exfoliation were seen in both SM and C tissues.
The data are consistent with the theory that SM vasculature, specifically endothelium, synthesizes an inhibitor of NE release, probably prostaglandins.
确定失代偿的血管系统(即骨骼肌血管)与维持代偿功能的血管系统(即皮肤血管)之间是否存在形态学差异。
对犬进行麻醉,并按照维格斯失血性休克方案进行处理。使用电磁流量计监测骨骼肌和皮肤的血流。在出血前对照、代偿和失代偿期间,切除股薄肌(骨骼肌)和隐静脉(皮肤)动脉段。将动脉段固定于体内管腔内压力状态。对每个样本制作光镜和电镜切片。
在代偿期,骨骼肌和皮肤血管均显示出强烈的血管收缩迹象。尽管内皮褶皱程度相当,但皮肤血管能维持血管收缩,而骨骼肌血管则不能。在失代偿期间,骨骼肌血管直径增加,而皮肤血管直径未增加。超微结构变化包括,在代偿期间骨骼肌组织的内弹性膜极度褶皱,而在失代偿期间内弹性膜变平,皮肤组织则无此现象。在骨骼肌和皮肤组织中均可见细胞变形、损伤及脱落。
这些数据与以下理论相符,即骨骼肌血管系统,特别是内皮,合成了去甲肾上腺素释放的抑制剂,可能是前列腺素。