AJP - Heart and Circulatory Physiology, Vol 257, Issue 2 571-H580, Copyright © 1989 by American Physiological Society

ARTICLES

Alterations in distribution of cardiac output in experimental diabetes in rats

M. A. Hill and R. G. Larkins
Department of Medicine, University of Melbourne, Royal Melbourne Hospital, Victoria, Australia.

Alterations in blood flow distribution in streptozotocin-induced diabetes in the rat were examined. Blood flow between tissues was estimated by the distribution of radiolabeled microspheres, and a second series of experiments examined skeletal muscle microcirculation by in vivo microscopy. Studies were performed in anesthetized rats 1-8 wk after induction of diabetes. Cardiac index was transiently increased in diabetic animals (29.6 +/- 1.0 ml.min-1.100 g-1) in comparison with control animals (23.0 +/- 1.4 ml.min-1.100 g-1) at 2-wk duration. Cardiac index was similar in both groups of animals at all other time points studied. The increased cardiac index coincided with transiently increased blood flow to diaphragm and abdominal wall and a significant vasodilatation of small cremaster muscle arterioles. Blood flow to skin and some skeletal muscles was thereafter significantly decreased in the diabetic animals. Blood flow (ml.min-1.100 g-1) to the brain and main thoracic and abdominal organs was similar in nonfasting control and diabetic animals throughout the period of study. As a result of hyperplasia, blood flow to the small intestine (%cardiac output) was increased in the diabetic animals (at 4 wk of diabetes, 34.5 +/- 2.1 vs. 17.5 +/- 0.8%, P less than 0.001). Despite reduction in blood flow to the intestine, by dietary restriction, flow to skin and skeletal muscle remained significantly decreased. Insulin treatment, at a dose aimed at preventing body weight loss but maintaining hyperglycemia, led to renal hyperperfusion in comparison with untreated diabetic and control animals. The alterations in regional blood flow appear progressive in nature and are not simply related to each other but may reflect tissue adaptation to the metabolic disorder.

This article has been cited by other articles:

				M. W. Brands, S. M. Fitzgerald, W. H. Hewitt, and A. E. Hailman Decreased cardiac output at the onset of diabetes: renal mechanisms and peripheral vasoconstriction Am J Physiol Endocrinol Metab, May 1, 2000; 278(5): E917 - E924. [Abstract] [Full Text] [PDF]

				F. R. L. Crijns, B. H. R. Wolffenbuttel, J. G. R. de Mey, and H. A. J. S. Boudier Mechanical properties of mesenteric arteries in diabetic rats: consequences of outward remodeling Am J Physiol Heart Circ Physiol, May 1, 1999; 276(5): H1672 - H1677. [Abstract] [Full Text] [PDF]

				M. J. Cipolla, J. M. Porter, G. Osol, and W. G. Mayhan High Glucose Concentrations Dilate Cerebral Arteries and Diminish Myogenic Tone Through an Endothelial Mechanism Stroke, February 1, 1997; 28(2): 405 - 411. [Abstract] [Full Text]