Skeletal Muscle Vascular Transport Capacity in Diabetic Rats

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 ≤ 0.001) because of profound muscle atrophy. Total hindquarters flow (ml · min⁻¹ · 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 · 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 and diabetic rats. However, absolute values for capillary filtration coefficient (ml · min⁻¹ · 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. In contrast, absolute flow capacity is unchanged in diabetic rats such that hindquarters flow capacity per tissue mass is increased, which results in a greater vascular transport capacity.