ALTERATION OF SEGMENTAL VASCULAR-RESISTANCE IN THE PULMONARY CIRCULATION OF DIABETIC RATS

Numerous studies have shown that altered plasma glucose and (or) insul in have profound effects on the pulmonary circulation. Recently, we do cumented diminished pressor responses to the synthetic thromboxane ana logue U-46619 (9,11-didexoy-9 alpha,11 alpha-methanoepoxy prostaglandi n F-2 alpha) following short-term streptozotocin-induced diabetes in r ats. However, these earlier studies examined the effects of diabetes o n resistance changes across the entire pulmonary vasculature and made no effort to localize the site(s) of any abnormalities. Thus, in the p resent study we examined segmental pulmonary vascular resistances usin g the double-occlusion method in isolated perfused rat lungs 2 weeks a fter streptozotocin-induced diabetes. Under baseline conditions, total pulmonary vascular resistance (TPVR) did not differ in lungs isolated from control and diabetic animals (0.66 +/- 0.03 vs. 0.85 +/- 0.05 mm Hg . mL(-1). min(-1), respectively (1 mmHg = 133.3 Pa)). However, cont rol animals demonstrated greater arterial (Ra) than venous (Rv) contri bution to TPVR (0.43 +/- 0.02 vs. 0.23 +/- 0.02 mmHg . mL(-1). min(-1) , respectively). This relationship was reversed in diabetic animals (R a = 0.30 +/- 0.02 mmHg . mL(-1). min(-1); Rv = 0.54 +/- 0.04 mmHg .(-1 ). min(-1)). Following constriction with U-46619 this pattern persiste d, although the absolute vasoconstrictor response to the agent was sim ilar in each segment. Likewise, this pattern of resistance was unaffec ted following dilation of the pulmonary vascular bed with arginine vas opressin. These findings illustrate that pulmonary segmental vascular resistances are altered and, more specifically, that pulmonary venous resistance is selectively increased, 2 weeks following the induction o f diabetes.