English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

In view of the marked increase in blood flow into the penis during erection and the association of diabetes mellitus with impotence, we used the diabetic rat model to investigate the possibility that: the penis may produce prostacyclin; and prostacyclin secretion may be decreased in diabetes. Rats given a high dose of streptozotocin (120 mg/kg body weight) developed acute ketotic diabetes and were killed after 48 h. Animals given a low dose of streptozotocin (65 mg/kg body weight) developed non-ketonuric diabetes and were killed after 7 or 62 days. Aortic rings and penile tissue discs were incubated in buffer, which was assayed for 6-oxo-prostaglandin F1 alpha, the stable and spontaneous breakdown product of prostacyclin. Penile tissue from control, ketotic and non-ketonuric (7 days) animals released similar quantities of prostacyclin, whereas that from long-term non-ketonuric animals (62 days) produced significantly less prostacyclin. Production of this prostanoid by the aortic rings paralleled these changes. We conclude that: penile tissue releases prostacyclin in quantities comparable to those of the aorta; long-term diabetes leads to diminished prostacyclin release by penile and aortic tissue: the former may contribute to the pathogenesis of diabetic impotence; and since short-term ketotic diabetes does not inhibit aortic or penile prostacyclin release, duration of diabetes rather than its severity is responsible for diminished prostacyclin release.

Experimental diabetes mellitus inhibits prostacyclin synthesis by the rat penis: pathological implications