Meairs S, Weihe E, Mittmann U, Vetter H, Kohler U, Forssmann W G
Lab Invest. 1984 Apr;50(4):469-79.
A sustained and gradual development of hypertension in coronary arteries of 16 foxhounds was induced by afterload stress with supravalvular aortic stenosis. Dogs were perfusion fixed after 4 months and 1 year of stenosis for morphologic analysis of coronary arteries with scanning electron microscopy, transmission electron microscopy, and light microscopy. Mean prestenotic pressures and SD standard deviations in millimeters of mercury for perfusion-fixed foxhounds after 4 months were systolic 141 +/- 14, mean arterial 101 +/- 8, and diastolic 81 +/- 7, and after 1 year systolic 182 +/- 31, mean arterial 128 +/- 22, and diastolic 101 +/- 16. Scanning electron microscopy results of coronary arteries subjected to 4 months of hypertension show little change from normal coronary arteries. Only isolated cases of desquamating endothelial cells were seen directly proximal to ostia of coronary arteries. Transmission electron microscopy showed no ultrastructural changes in this banding group. In four of six foxhounds subjected to 1 year of hypertension, scanning electron microscopy observations of coronary arteries revealed one to five areas of endothelial denudation, typically oriented parallel to the longitudinal axis of the artery, a few cell diameters wide and 100 to 300 microns in length. These lesions were often seen to form narrow channels between two or more branching points, either in a continuous or in series fashion. Platelets, lymphocytes, granulocytes, and monocytes adhered to the subendothelial surface. Occasional denudations were oriented transversely to the longitudinal axis. Denudations were restricted to arteries greater than 1.2 mm in diameter. In the vicinity of denudation lesions, lymphocytes and monocytes adhered to endothelium showing alterations in cell size and shape. Transmission electron and light microscopy of this banding group showed breaks and duplication of the internal elastic lamina and smooth muscle proliferation in the intima. Focal areas of intimal inflammatory reactions, sometimes superimposed upon intimal proliferative changes, were noted in those areas exhibiting luminal cell adherence to endothelium. The results indicate that the morphologic equivalent of hypertension varies depending on the manner in which it is experimentally produced. The findings of intimal proliferation and late endothelial denudation give support to the response-to-injury hypothesis for the pathogenesis of atherosclerosis and suggest a mechanism for the role of hypertension as a risk factor.(ABSTRACT TRUNCATED AT 400 WORDS)
通过主动脉瓣上狭窄造成后负荷应激，诱导16只猎狐犬的冠状动脉持续且逐渐地发生高血压。在狭窄4个月和1年后对犬进行灌注固定，以便用扫描电子显微镜、透射电子显微镜和光学显微镜对冠状动脉进行形态学分析。4个月后灌注固定的猎狐犬，收缩压为141±14毫米汞柱、平均动脉压为101±8毫米汞柱、舒张压为81±7毫米汞柱，1年后收缩压为182±31毫米汞柱、平均动脉压为128±22毫米汞柱、舒张压为101±16毫米汞柱。经历4个月高血压的冠状动脉扫描电子显微镜结果显示与正常冠状动脉相比变化不大。仅在冠状动脉开口直接近端观察到个别内皮细胞剥脱的情况。透射电子显微镜显示该组血管环无超微结构变化。在经历1年高血压的6只猎狐犬中的4只，冠状动脉扫描电子显微镜观察发现有1至5个内皮剥脱区域，通常与动脉纵轴平行，宽几个细胞直径，长100至300微米。这些病变常可见于两个或更多分支点之间形成狭窄通道，呈连续或串联方式。血小板、淋巴细胞、粒细胞和单核细胞黏附于内皮下表面。偶尔有剥脱区域与纵轴呈横向。剥脱限于直径大于1.2毫米的动脉。在剥脱病变附近，淋巴细胞和单核细胞黏附于内皮，呈现细胞大小和形状改变。该组血管环的透射电子显微镜和光学显微镜检查显示内弹性膜断裂和重复以及内膜平滑肌增生。在那些有管腔细胞黏附于内皮的区域，注意到内膜有局灶性炎症反应，有时叠加在内膜增生性改变之上。结果表明，高血压的形态学等效物取决于其实验产生的方式。内膜增生和晚期内皮剥脱的发现支持动脉粥样硬化发病机制的损伤反应假说，并提示高血压作为危险因素的作用机制。（摘要截于400字）
