Faculty Collaboration Database

Diabetes alters postischemic response to a prostacyclin mimetic. Am J Physiol 1989 May;256(5 Pt 2):H1353-60

Date

05/01/1989

Pubmed ID

2470263

DOI

10.1152/ajpheart.1989.256.5.H1353

Scopus ID

2-s2.0-0024352066 (requires institutional sign-in at Scopus site)   13 Citations

Abstract

Eicosanoid metabolism is altered by diabetes. However, postischemic responses of diabetic hearts (DH) to eicosanoids such as prostacyclin are unknown. a prostacyclin analogue iloprost (Ilo) was given to isovolumically beating rat hearts during 20 min of total global ischemia and 30 min of reperfusion. Acute DH (48 h) but not chronic DH (2 mo) had pronounced postischemic dysfunction (developed pressure = 22 +/- 11%), which was completely reversed by 3 X 10(-8) M Ilo (developed pressure = 113 +/- 15%). Ilo also stimulated endogenous prostacyclin release in postischemic control hearts (CH) but not acute or chronic DH. Ilo significantly decreased postischemic recovery in CH (from 67 +/- 11 to 15 +/- 4%), which was partially blocked by the coadministration of the calcium-entry blocker diltiazem or almost completely reversed by the free radical scavengers superoxide dismutase plus catalase (100 U/ml). These data suggest that Ilo may promote functional recovery in DH at concentrations that produce dysfunction in CH. Furthermore, Ilo may induce dysfunction in CH by a calcium ionophoretic action, which appears depressed in diabetes, and by concomitant free radical production (presumably via prostaglandin hydroperoxidases) during Ilo-stimulated endogenous prostacyclin synthesis.

Author List

Pieper GM, Gross GJ

MESH terms used to index this publication - Major topics in bold

Animals
Diabetes Mellitus, Experimental
Dose-Response Relationship, Drug
Drug Resistance
Epoprostenol
Heart
Iloprost
In Vitro Techniques
Male
Myocardial Reperfusion
Prostaglandins, Synthetic
Rats
Rats, Inbred Strains
Reference Values