This study aimed to determine the effect of long-term (17-20 weeks) st
reptozocin (STZ)-induced diabetes on skeletal muscle vascular transpor
t capacity. Vascular transport capacity was determined from measuremen
ts of pressure-flow relationships, capillary filtration coefficient, a
nd permeability-surface area product (PS) for Cr-51-EDTA in isolated p
erfused 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 d
iabetic rats weighed 42% less than control rats (86 +/- 3 vs. 147 +/-
4 g; P less than or equal to 0.001) because of profound muscle atrophy
. Total hindquarters flow (ml . min(-1) 100 g(-1)) was greater in diab
etic rats (P < 0.001) at perfusion pressures between 23 and 75 mmHg, i
ndicative of an increased flow capacity relative to control rats. Howe
ver, absolute flows (ml/min) were not different between control and di
abetic rats. Neither capillary filtration coefficient (control = 0.024
3 +/- 0.0010 and diabetic = 0.0297 +/- 0.0024 ml . min(-1) . mmHg(-1)
100 g(-1)) nor isogravimetric PS (control = 3.91 +/- 0.31 and diabetic
= 4.39 +/- 0.46 ml . min(-1) 100 . g(-1)) were different in control a
nd diabetic rats. However, absolute values for capillary filtration co
efficient (ml . min(-1) . mmHg(-1)) and PS (ml/min) were less in diabe
tic rats. These results indicate that muscle atrophy in rats with STZ-
induced diabetes is accompanied by a proportional reduction in absolut
e exchange capacity for water (capillary filtration coefficient) and s
mall solutes PS, such that microvascular exchange capacity per tissue
mass is maintained at control levels. In contrast, absolute flow capac
ity is unchanged in diabetic rats such that hindquarters flow capacity
per tissue mass is increased, which results in a greater vascular tra
nsport capacity.