Recovery of contractile function of postischemic, reperfused myocardium: influence of 2,3-butanedione-2-monoxime. J Cardiovasc Pharmacol 1993 May;21(5):693-700
Date
05/01/1993Pubmed ID
7685437DOI
10.1097/00005344-199305000-00002Scopus ID
2-s2.0-0027506379 (requires institutional sign-in at Scopus site) 8 CitationsAbstract
Inhibition of mechanical activity during ischemia could improve recovery of stunned myocardium. In this study, the effect of 2,3-butanedione-2-monoxime (BDM), an agent that disrupts excitation-contraction coupling, on the time course of recovery of contractile function of postischemic reperfused myocardium was studied in open-chest anesthetized dogs. Ischemia was produced by occluding the left anterior descending coronary artery (LAD) for 15 mins. In separate experimental groups, during the occlusion period, 6 ml of either 100 mM BDM or drug vehicle (0.9% normal saline) was infused into the distal perfusion bed subjected to occlusion. Regional myocardial function (percentages of segment shortening % SS) was assessed by sonomicrometry. LAD occlusion resulted in similar degrees of dyskinesia in both experimental groups. Subsequent recovery of contractile function during reperfusion was evaluated for 3 h. In control experiments, segment shortening remained significantly (p < 0.05) decreased throughout the reperfusion period, returning to only 36.1 +/- 9.2% of the preocclusion value at 3 h postreperfusion. In BDM experiments, regional contractile function returned to 72.4 +/- 11.3% of the preocclusion value at 1 h of reperfusion. Rapid recovery was sustained throughout reperfusion. Regional stroke work area (RSWA) also demonstrated rapid sustained recovery of function after treatment with BDM. RSWA was significantly greater in BDM experiments as compared with control experiments at all times during the reperfusion period. These results demonstrate that selective intracoronary (i.c.) administration of BDM during ischemia markedly enhances postischemic recovery of contractile function. The underlying mechanism for this action may involve modulation of several aspects of impaired cellular function in postischemic tissues.(ABSTRACT TRUNCATED AT 250 WORDS)
Author List
O'Brien P, Bosnjak Z, Warltier DCAuthors
Zeljko Bosnjak PhD, MS Emeritus Professor in the Medicine department at Medical College of WisconsinDavid C. Warltier PhD Emeritus Professor in the Anesthesiology department at Medical College of Wisconsin
MESH terms used to index this publication - Major topics in bold
AnimalsBlood Pressure
Chromogenic Compounds
Diacetyl
Dogs
Electrocardiography
Female
Heart Rate
Male
Myocardial Contraction
Myocardial Ischemia
Myocardial Reperfusion Injury
Stroke Volume
