Hemodynamic actions of insulin in rat skeletal muscle - Evidence for capillary recruitment

Hemodynamic actions of insulin in rat skeletal muscle - Evidence for capillary recruitment
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DOI:
10.2337/diabetes.46.9.1381
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发表时间:
1997-09-01
期刊:
影响因子:
7.7
通讯作者:
Barrett, EJ
Barrett, EJ
中科院分区:
医学1区
文献类型:
--
作者:
Rattigan, S;Clark, MG;Barrett, EJ

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胰岛素诱导的血流量增加被假设为增强骨骼肌的总体葡萄糖摄取。胰岛素介导的血流变化是否与骨骼肌中血流分布改变和毛细血管募集增加有关尚不清楚。在本研究中,胰岛素对在体Pat骨骼肌血流动力学参数的影响进行了研究。在对照组和正常血糖胰岛素钳夹(10 mU·min(-1)·kg(-1))麻醉大鼠中测量平均动脉血压、心率、股动脉血流、后肢血管阻力和葡萄糖摄取。通过测量I-甲基黄嘌呤(1-MX)(一种外源性添加的毛细血管黄嘌呤氧化酶底物)的代谢来评估后腿肌肉内的血流分布。胰岛素治疗对心率没有影响,但显著增加了动脉血压(12 mmHg)和股动脉血流量(80%),并降低了后腿血管阻力(31%)。变化的幅度和发生时间与人类报告的变化相似。胰岛素治疗增加后腿葡萄糖摄取约四倍,也增加了后腿1-MX代谢50%,表明增加了内皮黄嘌呤氧化酶的暴露。为了确定1-MX代谢的增加是否仅仅是由于股动脉血流量的增加,以与胰岛素诱导的股动脉血流量增加相匹配的剂量(0.125 μ g·min(-1)·kg(-1))输注肾上腺素。该剂量的肾上腺素对动脉血压或心率没有显着影响,但增加股血流量并降低后腿血管阻力,其程度与胰岛素相似。与对照动物相比,肾上腺素没有显著改变I-MX代谢。这些结果表明,胰岛素增加总后腿血流量和1-MX的代谢,表明大鼠后腿中毛细血管血流量的募集不被肾上腺素模拟。
Insulin-induced increases in blood flow are hypothesized to enhance overall glucose uptake by skeletal muscle. Whether the insulin-mediated changes in blood flow are associated with altered blood flow distribution and increased capillary recruitment in skeletal muscle is not known. In the present study, the effects of insulin on hemodynamic parameters in Pat skeletal muscle in vivo were investigated. Mean arterial blood pressure, heart rate, femoral blood flow hind leg vascular resistance, and glucose uptake were measured in control and euglycemic insulin-clamped (10 mU.min(-1).kg(-1)) anesthetized rats. Blood flow distribution within the hind leg muscles was assessed by measuring the metabolism of I-methylxanthine (1-MX), an exogenously added substrate for capillary xanthine oxidase. Insulin treatment had no effect on heart rate but significantly increased arterial blood pressure (12 mmHg) and femoral blood flow (80%) and decreased hind leg vascular resistance (31%). Changes were similar in magnitude and in time of onset to those reported in humans. Insulin treatment increased hind leg glucose uptake approximately fourfold and also increased hind leg 1-MX metabolism by 50%, suggesting increased exposure to endothelial xanthine oxidase. To ascertain whether the increased 1-MX metabolism was simply due to increased bulk femoral blood flow, epinephrine was infused at a dose (0.125 mu g.min(-1).kg(-1)) chosen to match the insulin-induced increase in femoral blood flow. This dose of epinephrine had no significant effects on arterial blood pressure or heart rate but increased femoral blood flow and lowered hind leg vascular resistance to a similar extent as insulin. Epinephrine did not significantly alter I-MX metabolism as compared with control animals. These results demonstrate that insulin increases total hind leg blood flow and metabolism of 1-MX, suggesting a recruitment of capillary blood flow in rat hind leg not mimicked by epinephrine.