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糖尿病大鼠骨骼肌的血管运输能力

Skeletal muscle vascular transport capacity in diabetic rats.

作者信息

Sexton W L

机构信息

Department of Physiology, Kirksville College of Osteopathic Medicine, Missouri 63501.

出版信息

Diabetes. 1994 Feb;43(2):225-31. doi: 10.2337/diab.43.2.225.

DOI:10.2337/diab.43.2.225
PMID:8288047
Abstract

This study aimed to determine the effect of long-term (17-20 weeks) streptozocin (STZ)-induced diabetes on skeletal muscle vascular transport capacity. Vascular transport capacity was determined from measurements of pressure-flow relationships, capillary filtration coefficient, and permeability-surface area product (PS) for 51Cr-EDTA in isolated perfused hindquarters of control (n = 7) and diabetic (n = 6; 65 mg/kg STZ intraperitoneally) rats. Hindquarters were perfused with Tyrode's solution containing albumin (5 g/dl) and horse serum (10% vol/vol) and were maximally vasodilated with papaverine (30 mM). Hindquarters of diabetic rats weighed 42% less than control rats (86 +/- 3 vs. 147 +/- 4 g; P < or = 0.001) because of profound muscle atrophy. Total hindquarters flow (ml.min-1 x 100 g-1) was greater in diabetic rats (P < 0.001) at perfusion pressures between 23 and 75 mmHg, indicative of an increased flow capacity relative to control rats. However, absolute flows (ml/min) were not different between control and diabetic rats. Neither capillary filtration coefficient (control = 0.0243 +/- 0.0010 and diabetic = 0.0297 +/- 0.0024 ml.min-1 x mmHg-1 x 100 g-1) nor isogravimetric PS (control = 3.91 +/- 0.31 and diabetic = 4.39 +/- 0.46 ml.min-1 x 100 g-1) were different in control and diabetic rats. However, absolute values for capillary filtration coefficient (ml.min-1 x mmHg-1) and PS (ml/min) were less in diabetic rats. These results indicate that muscle atrophy in rats with STZ-induced diabetes is accompanied by a proportional reduction in absolute exchange capacity for water (capillary filtration coefficient) and small solutes PS, such that microvascular exchange capacity per tissue mass is maintained at control levels.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

本研究旨在确定长期(17 - 20周)链脲佐菌素(STZ)诱导的糖尿病对骨骼肌血管运输能力的影响。通过测量压力 - 流量关系、毛细血管滤过系数以及51Cr - EDTA在对照大鼠(n = 7)和糖尿病大鼠(n = 6;腹腔注射65 mg/kg STZ)分离灌注后肢中的通透表面积乘积(PS)来确定血管运输能力。后肢用含白蛋白(5 g/dl)和马血清(10%体积/体积)的台氏液灌注,并用罂粟碱(30 mM)使其最大程度血管舒张。由于严重的肌肉萎缩,糖尿病大鼠的后肢重量比对照大鼠轻42%(86±3 vs. 147±4 g;P≤0.001)。在23至75 mmHg的灌注压力下,糖尿病大鼠的后肢总血流量(ml·min-1×100 g-1)更大(P < 0.001),表明相对于对照大鼠,其血流能力增加。然而,对照大鼠和糖尿病大鼠的绝对血流量(ml/min)并无差异。对照大鼠和糖尿病大鼠的毛细血管滤过系数(对照 = 0.0243±0.0010,糖尿病 = 0.0297±0.0024 ml·min-1×mmHg-1×100 g-1)和等重量PS(对照 = 3.91±0.31,糖尿病 = 4.39±0.46 ml·min-1×100 g-1)均无差异。然而,糖尿病大鼠的毛细血管滤过系数(ml·min-1×mmHg-1)和PS(ml/min)的绝对值较低。这些结果表明,STZ诱导的糖尿病大鼠的肌肉萎缩伴随着水(毛细血管滤过系数)和小分子溶质PS的绝对交换能力成比例降低,从而使每组织质量的微血管交换能力维持在对照水平。(摘要截断于250字)

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