Sympathetic and vascular dysfunction in early experimental juvenile diabetes mellitus.
Sympathetic and vascular dysfunction in early experimental juvenile diabetes mellitus.
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早期实验性青少年糖尿病的交感神经和血管功能障碍。
DOI：
10.1152/ajpheart.1982.243.2.h139
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Ertel,PJ
中科院分区：
文献类型：
--
作者：
Mueller,SM;Mueller,TM;Ertel,PJ
穆勒，〜希尔利·M.，托马斯·穆勒，和〜希利普·J.埃特尔。早期实验性青少年糖尿病的交感神经和血管功能障碍。是。 J.生理学。 243 (Heart Circ. Physiol. 12): H139-H144, 1982.-在糖尿病患者中已分别报道了交感自主神经病变以及小血管病变。为了在未经治疗的严重糖尿病模型（血浆葡萄糖 500 mg/dl）中同时评估这些因素，我们在 4 周龄时给大鼠注射四氧嘧啶，并在 5 周后对其进行研究。皮下麻醉后(平均动脉压：对照，154=t 5；糖尿病，126*6mmHg；P＜0.001)，用含有右旋糖酐的含氧Tyrode溶液以每100g恒定流量通过腹主动脉对10只糖尿病(D)和10只对照(C)大鼠的后躯进行灌注：流出物来自结扎和切断的下静脉卡瓦酒。为了测试产生反射性外周血管收缩的强烈交感刺激的效果，使大鼠的头侧部分迅速出血。 D 组后躯灌注压的增加 (14 & 3 mmHg) 明显低于 C 组 (56= t 5 mmHg) (P.< 0.001)。第二个对照组的后躯灌注压与腰交感链切断后出血时的 D 组相似（增加 6 × 1 mmHg）。为了确定 D 中是否发生外周交感神经去神经支配，确定了对灌注液中去甲肾上腺素的阈值反应。 D 中的阈值显着低于 C（分别为 0.17* 0.03 与 0.49* 0.04 µml，P< 0.001）。用超最大剂量的加压素测试了脉管系统的最大血管收缩能力，D 组显着低于 C 组（分别为 178 t 17 与 262 k 6 mmHg，P < 0.001）。 D 组中用罂粟碱诱导的最大扩张期间的流量-压力曲线显着低于 C 组（P < 0.001）。这些数据表明，交感神经自主神经支配和微血管病理学都存在于氟沙星诱发的糖尿病中，并且可能导致血压控制异常。四氧嘧啶糖尿病大鼠；糖尿病血管病;据报道，高达 50% 的糖尿病患者在采取直立姿势时血压会出现突然性和无代偿性下降 (6)。自主神经病变 (5, 6, 13) 和血管功能障碍 (12, 21) 被认为是导致这种情况的因素之一。尽管对每一种都进行了单独评估，但两者在同一动物中共存的可能性尚未得到证实。本研究的目的是评估早期青少年糖尿病实验模型中的交感自主神经和血管功能。我们在 4 岁的“Sprague-Dawley 大鼠”中诱导糖尿病
MUELLER,~ HIRLEY M., THOMAS M. MUELLER, AND~ HILLIP J. ERTEL. Sympathetic and vascular dysfunction in early experimental juvenile diabetes mellitus. Am. J. Physiol. 243 (Heart Circ. Physiol. 12): H139-H144, 1982.-Sympathetic autonomic neuropathy ‘as well as small vessel angiopathy have separately been reported in diabetic patients. To evaluate these factors concomitantly in a model of severe, untreated diabetes (plasma glucose 500 mg/dl), we administered alloxan to rats at 4 wk of age and studied them 5 wk later. After seconal anesthesia (mean arterial pressure: control, 154= t 5; diabetic, 126* 6 mmHg; P< O. OOl), the hindquarters of 10 diabetic (D) and 10 control (C) rats were perfused at constant flow per 100 g through the abdominal aorta with oxygenated Tyrode solution containing dextran: Efflux was from the ligated and severed inferior vena cava. To test the effect of a strong sympathetic stimulus producing reflex peripheral vasoconstriction, the cephalad portions of the rati were rapidly hemorrhaged. The increase in hindquarter perfusion pressure was markedly less in D (14 & 3 mmHg) than in C (56= t 5 mmHg)(P.< 0.001). The hindquarter perfusion pressure of a second control group was similar to that of D when hemorrhaged after section of the lumbar sympathetic chain (6 t 1 mmHg increase). To determine if peripheral sympathetic denervation occurred in D, the threshold response to norepinephrine in the perfusate was determined. The threshold was significantly lower in D than in C (0.17* 0.03 vs. 0.49* 0.04 &ml, respectively, P< 0.001). The maximum vasoconstrictor capacity of the vasculature was tested with supramaximal doses of vasopressin and was significantly lower in D than in C (178 t 17 vs. 262 k 6 mmHg, respectively, P< 0.001). A flow-pressure curve during maximal dilation, induced with papaverine, was significantly lower in D than in C (P< 0.001). These data suggest that both sympathetic autonomic denervation and microvascular pathology are present in floxan-induced diabetes and can contribute to abnormalities in blood pressure control. alloxan diabetic rats; diabetic angiopathy; diabetic neuropathyANABRUPTANDUNCOMPENSATED decreaseinbloodpressure upon the assumption of upright posture has been reported in up to 50% of diabetic patients (6). Autonomic neuropathy (5, 6, 13) and vascular dysfunction (12, 21) are among the factors thought to contribute to this condition. Though each has been evalauted separately, the possibility that the two coexist in the same animal has not been demonstrated. The purpose of this study was to assess both sympathetic autonomic and vascular function in an experimental model of early juvenile diabetes. We induced diabetes in ‘Sprague-Dawley rats at 4