Skeletal muscle microvascular recruitment by physiological hyperinsulinemia precedes increases in total blood flow

被引:160
作者
Vincent, MA
Dawson, D
Clark, ADH
Lindner, JR
Rattigan, S
Clark, MG
Barrett, EJ
机构
[1] Univ Virginia, Hlth Sci Ctr, Dept Internal Med, Charlottesville, VA 22908 USA
[2] Univ Tasmania, Sch Med, Div Biochem, Hobart, Tas 7001, Australia
关键词
D O I
10.2337/diabetes.51.1.42
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Supraphysiological doses of insulin enhance total limb blood flow and recruit capillaries in skeletal muscle. Whether these processes change in response to physiological hyperinsulinemia is uncertain. To examine this, we infused either saline (n = 6) or insulin (euglycemic clamp, 3.0 mU (.) min(-1) (.) kg(-1) n = 9) into anesthetized rats for 120 min. Femoral artery flow was monitored continuously using a Doppler flow probe, and muscle microvascular recruitment was assessed by metabolism of infused I-methylxanthine (1-MX) and by contrast-enhanced ultrasound (CEU). Insulin infusion raised plasma insulin concentrations by similar to10-fold. Compared,with saline, physiological hyperinsulinemia increased femoral artery flow (1.02 +/- 0.10 vs. 0.68 +/- 0.09 ml/min; P < 0.05), microvascular recruitment (measured by 1-MX metabolism [6.6 +/- 0.5 vs. 4.5 +/- 0.48 nmol/min; P < 0.05] as well as by CEU [167.0 +/- 39.8 vs. 28.2 +/- 13.8%; P < 0.01]), and microvascular flow velocity (beta, 0.14 +/- 0.02 vs. 0.09 +/- 0.02 s(-1)). Subsequently, we studied the time dependency of insulin's vascular action in a second group (n = 5) of animals. Using CEU, microvascular volume was measured at 0, 30, and 90 min of insulin infusion. Insulin augmented microvascular perfusion within 30 min (52.8 +/- 14.8%), and this persisted at 90 min (64.6 +/- 9.9%). Microvascular recruitment occurred without changes to femoral artery flow or P. We conclude that insulin increases tissue perfusion by recruiting microvascular beds, and at physiological concentrations this precedes increases in total muscle blood flow by 60-90 min.
引用
收藏
页码:42 / 48
页数:7
相关论文
共 31 条
[1]   SKELETAL-MUSCLE BLOOD-FLOW - A POSSIBLE LINK BETWEEN INSULIN RESISTANCE AND BLOOD-PRESSURE [J].
BARON, AD ;
BRECHTELHOOK, G ;
JOHNSON, A ;
HARDIN, D .
HYPERTENSION, 1993, 21 (02) :129-135
[2]   MECHANISM OF INSULIN RESISTANCE IN INSULIN-DEPENDENT DIABETES-MELLITUS - A MAJOR ROLE FOR REDUCED SKELETAL-MUSCLE BLOOD-FLOW [J].
BARON, AD ;
LAAKSO, M ;
BRECHTEL, G ;
EDELMAN, SV .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1991, 73 (03) :637-643
[3]   REDUCED POSTPRANDIAL SKELETAL-MUSCLE BLOOD-FLOW CONTRIBUTES TO GLUCOSE-INTOLERANCE IN HUMAN OBESITY [J].
BARON, AD ;
LAAKSO, M ;
BRECHTEL, G ;
HOIT, B ;
WATT, C ;
EDELMAN, SV .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1990, 70 (06) :1525-1533
[4]   Role of blood flow in the regulation of muscle glucose uptake [J].
Baron, AD ;
Clark, MG .
ANNUAL REVIEW OF NUTRITION, 1997, 17 :487-499
[5]   Interaction between insulin sensitivity and muscle perfusion on glucose uptake in human skeletal muscle - Evidence for capillary recruitment [J].
Baron, AD ;
Tarshoby, M ;
Hook, G ;
Lazaridis, EN ;
Cronin, J ;
Johnson, A ;
Steinberg, HO .
DIABETES, 2000, 49 (05) :768-774
[6]   Role of tissue-specific blood flow and tissue recruitment in insulin-mediated glucose uptake of human skeletal muscle [J].
Bonadonna, RC ;
Saccomani, MP ;
Del Prato, S ;
Bonora, E ;
DeFronzo, RA ;
Cobelli, C .
CIRCULATION, 1998, 98 (03) :234-241
[7]   SKELETAL-MUSCLE IS A PRIMARY SITE OF INSULIN RESISTANCE IN ESSENTIAL-HYPERTENSION [J].
CAPALDO, B ;
LEMBO, G ;
NAPOLI, R ;
RENDINA, V ;
ALBANO, G ;
SACCA, L ;
TRIMARCO, B .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1991, 40 (12) :1320-1322
[8]   Insulin stimulates laser Doppler signal by rat muscle in vivo, consistent with nutritive flow recruitment [J].
Clark, ADH ;
Barrett, EJ ;
Rattigan, S ;
Wallis, MG ;
Clark, MG .
CLINICAL SCIENCE, 2001, 100 (03) :283-290
[9]  
DAWSON D, IN PRESS AM J PHYSL
[10]   HETEROGENEITY OF INSULIN ACTION IN MUSCLE - INFLUENCE OF BLOOD-FLOW [J].
JAMES, DE ;
BURLEIGH, KM ;
STORLIEN, LH ;
BENNETT, SP ;
KRAEGEN, EW .
AMERICAN JOURNAL OF PHYSIOLOGY, 1986, 251 (04) :E422-E430