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Experimental diabetes: No effects on prostacyclin release from the vessel wall and renal cortex

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Abstract

Diabetes is commonly complicated by thrombosis and atherosclerosis. In humans, diabetes mellitus has been associated with a decreased synthesis of prostacyclin, which could partly explain the prothrombotic state. Experimental diabetes has been diverging in this aspect, and endothelial damage has been proposed to be an early event. To analyse whether the effect of inducing diabetes had any influence on prostacyclin release from diabetic tissue, streptozotocin-induced diabetic rat aortas and renal tissue were incubated in Hank's balanced salt solution. The stable degradation product for prostacyclin 6-keto-PGF1α was determined by radioimmunoassay. There was no difference in the release of 6-keto-PGF1α from aorta and renal tissue in diabetic animals compared to controls, and insulin given to diabetic animals also had no effect.

In order to study only the intraluminal release of prostacyclin, aortas and caval veins from alloxan-diabetic rabbits were perfused for five 15 min periods. Diabetic animals had the same release of 6-keto-PGF1α from the aorta and caval vein as control animals.

Scanning electron microscopy of the luminal side of the perfused vessels revealed the same degree of endothelial coverage with approximately 75% coverage after perfusion.

It is concluded that experimental diabetes of 6 months' duration does not alter the vascular and renal prostacyclin release in response to exogenous trauma like incubation or perfusion.

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  1. Department of Surgery, Lund University, Malmö General Hospital, Sweden

    J. Brunkwall MD PhD & D. Bergqvist

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  1. J. Brunkwall MD PhD
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  2. D. Bergqvist
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Brunkwall, J., Bergqvist, D. Experimental diabetes: No effects on prostacyclin release from the vessel wall and renal cortex. Comp Haematol Int 3, 89–95 (1993). https://doi.org/10.1007/BF00368111

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