Type 1 diabetes was induced in Wistar rats by injection of streptozotocin (STZ). Changes in the myocardial capillary network were examined using the double-staining enzymatic method for alkaline phosphatase (AP) and dipeptidylpeptidase IV (DPPIV) This method allows the identification of the arteriolar (AP-containing) and the venular (DPPIV-containing) portions of the capillary network. In addition, blood plasma was analysed. The AP- and AP/DPPIV-containing capillary portions increased significantly, accompanied by a decrease in the DPPIV-containing portions in 60 days. A significant increase in AP was observed in the plasma. The capillary domain areas of each capillary portion were larger in the STZ-injected group than in the controls. It appears that oxygen transport to the subendocardial myocardial tissues may be decreased in the STZ group. In rats fed with Saji-supplemented chow there was a decrease in plasma AP, with increases in hemoglobin, hematocrit and vitamin C, suggesting a partial improvement of metabolic function and oxygen supply in these diabetic Wistar rats.
In the rat, experimental renal vasoconstriction induced by the use of a Goldblatt clamp caused arterial hypertension, cardiomyocyte hypertrophy and an increased capillary to cardiomyocyte ratio, the latter indicating the formation of new cardiac capillaries. Total capillary density decreased, but capillary portions expressing alkaline phosphatase increased. This suggested a greater arterialization of capillaries which would increase the flow of arterial blood to the myocardial capillary nets. However, the observed increase in the area of the capillary domains means the extra arterialization was not sufficient to compensate for the lengthening of the oxygen diffusion pathway caused by the hypertrophy. Since the effects of renal vasoconstriction were not seen in rats treated with an inhibitor of angiotensin converting enzyme (ACE) it is suggested they are induced by angiotensin II via activation of the renin-angiotensin system (RAS).
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