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Diabetes alters postischemic response to a prostacyclin mimetic
1Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee 53226.
The American Journal of Physiology
|May 1, 1989
Summary
Iloprost (Ilo) reversed postischemic dysfunction in acute diabetic hearts (DH), unlike in control hearts (CH). This suggests Ilo
Area of Science:
- Cardiovascular Physiology
- Metabolic Disease Research
- Eicosanoid Signaling
Background:
- Diabetes mellitus alters eicosanoid metabolism.
- Postischemic cardiac responses to prostacyclin in diabetes remain largely unknown.
Purpose of the Study:
- To investigate the effects of a prostacyclin analogue, iloprost (Ilo), on postischemic cardiac function in diabetic rat hearts.
- To explore the mechanisms underlying Ilo's effects, including endogenous prostacyclin release, calcium ion influx, and free radical production.
Main Methods:
- Utilized isovolumically beating rat hearts subjected to global ischemia and reperfusion.
- Administered iloprost (Ilo) to assess its impact on postischemic cardiac dysfunction.
- Measured endogenous prostacyclin release, and effects of calcium-entry blockers and free radical scavengers.
Main Results:
- Acute diabetic hearts (DH) exhibited severe postischemic dysfunction, completely reversed by Ilo.
- Ilo stimulated endogenous prostacyclin release in control hearts (CH) but not DH.
- Ilo impaired postischemic recovery in CH, an effect mediated by calcium influx and free radical generation, mechanisms apparently depressed in diabetes.
Conclusions:
- Iloprost (Ilo) demonstrates therapeutic potential for acute diabetic heart dysfunction post-ischemia.
- The mechanisms of Ilo action, including calcium ionophoresis and free radical production, are altered in the diabetic heart.
- Diabetes may attenuate the detrimental effects of Ilo in control hearts by impairing these specific pathways.