Hill M A, Meininger G A
Department of Medical Physiology, College of Medicine, Texas A&M University, College Station.
Diabetes. 1993 Sep;42(9):1226-32. doi: 10.2337/diab.42.9.1226.
Hyperperfusion and an increase in capillary pressure has been implicated in the pathogenesis of diabetic microangiopathy. The existence of such alterations suggests that the myogenic response to increased intravascular pressure may be altered in diabetes. To examine this, in vivo studies were performed on the rat cremaster muscle microcirculation of age-matched control and STZ-induced (65 mg/kg) diabetic rats (3-4 wk of diabetes). Anesthetized rats were enclosed in an airtight Plexiglas box with the cremaster muscle exteriorized into an organ bath containing Krebs' solution. To study myogenic responsiveness, box pressure was increased in steps of 10 mmHg from 0 to 30 mmHg for 2 min. Third-order arterioles of the control animals (lumen diameter 18 +/- 2 microns) responded to increased pressure with a rapid onset vasoconstriction. In contrast, the rate of development of the constriction was markedly attenuated in similar vessels (15 +/- 1 micron) of the diabetic animals, despite their ability to exhibit a similar maximal arteriolar constriction to that of the control animals. When 20 mmHg pressure steps were applied for only 10 s, arterioles of the diabetic animals constricted minimally, whereas those of the control animals constricted to 75% of the maximal response expected for that pressure increase (P < 0.01). Second-order arterioles of both groups of animals responded with a primarily passive distension to increased intravascular pressure suggesting that the impaired responsiveness of the third-order arterioles is not compensated for by an increase in the myogenic responsiveness of upstream vessels. Basal intravascular pressures, measured in first-, second-, and third-order arterioles, were similar in control and diabetic animals.(ABSTRACT TRUNCATED AT 250 WORDS)
高灌注和毛细血管压力升高与糖尿病微血管病变的发病机制有关。这种改变的存在表明，糖尿病患者对血管内压力升高的肌源性反应可能发生改变。为了对此进行研究，我们对年龄匹配的对照大鼠和链脲佐菌素诱导（65mg/kg）的糖尿病大鼠（糖尿病病程3 - 4周）的提睾肌微循环进行了体内研究。将麻醉的大鼠置于一个密闭的有机玻璃盒中，将提睾肌暴露于含有 Krebs 溶液的器官浴中。为了研究肌源性反应性，将盒内压力从0逐步升至30 mmHg，每次升高10 mmHg，持续2分钟。对照动物的三级小动脉（管腔直径18±2微米）对压力升高的反应是迅速发生血管收缩。相比之下，糖尿病动物类似血管（15±1微米）的收缩发展速率明显减弱，尽管它们能够表现出与对照动物相似的最大小动脉收缩。当以20 mmHg的压力步长仅施加10秒时，糖尿病动物的小动脉收缩极小，而对照动物的小动脉收缩至该压力升高预期最大反应的75%（P<0.01）。两组动物的二级小动脉对血管内压力升高的反应主要是被动扩张，这表明三级小动脉反应性受损并未被上游血管肌源性反应性增加所代偿。在一级、二级和三级小动脉中测量的基础血管内压力在对照动物和糖尿病动物中相似。（摘要截短于250字）
