Wiener J, Giacomelli F
Am J Pathol. 1973 Aug;72(2):221-31.
Acute hypertension was produced in rats by the infusion of angiotensin amide for 2 to 4 hours. These animals were injected intravenously prior to sacrifice with either colloidal carbon or iron dextran particles. The mesenteric vessels from hypertensive and control animals were processed for electron microscopy. Ultrastructural alterations are found in dilated segments of small arteries. Initially there is severe contraction of medial smooth muscle cells and the formation of processes of smooth muscle cytoplasm. This is followed by lysis of cell processes and bodies, and passage of plasma and colloidal iron into the media. Subsequently, carbon, platelets, fibrin and cellular debris are seen within these foci of medial necrosis. These changes appear as a sequence whose severity reflects the duration of the angiotensin infusion and degree of elevation of the systolic pressure. The morphologic alterations are discussed in relation to the generalized increase in vascular permeability that is associated with the hypertensive state.
通过输注血管紧张素酰胺2至4小时在大鼠中诱发急性高血压。在处死这些动物之前,静脉注射胶体碳或右旋糖酐铁颗粒。对高血压动物和对照动物的肠系膜血管进行电子显微镜检查。在小动脉扩张段发现超微结构改变。最初,内侧平滑肌细胞严重收缩,平滑肌细胞质形成突起。随后,细胞突起和细胞体溶解,血浆和胶体铁进入中膜。随后,在这些中膜坏死灶内可见碳、血小板、纤维蛋白和细胞碎片。这些变化呈现出一种序列,其严重程度反映了血管紧张素输注的持续时间和收缩压升高的程度。结合与高血压状态相关的血管通透性普遍增加来讨论形态学改变。