BETA-ADRENERGIC STIMULATION OF REPERFUSED MYOCARDIUM AFTER 2-HOUR ISCHEMIA

Postischemic myocardium possesses considerable contractile and metabol ic reserves, but their mobilization could result in increased cell dea th. We tested the hypothesis that beta-adrenergic stimulation of reper fused myocardium would increase segment work more than O-2 consumption , thereby improving efficiency without increased cell death. In 16 ope n-chest anesthetized dogs, the left anterior descending coronary arter y (LAD) was ligated for 2 h; during the reperfusion period, isoprotere nol (ISO; 0.1 mu g/kg/min, i.v.) was administered to nine of the anima ls. Regional myocardial segment length and force were measured in the anterior (LAD) acid posterior circumflex coronary artery (CFX) regions of the left ventricular myocardium. Work was calculated as the integr ated products of force and shortening for each region. Regional myocar dial O-2 consumption was obtained from LAD flow and arterial and local venous O-2 saturations. Infarct Size (tetrazolium) was measured in th e treated and untreated hearts at the end of the experiment. In untrea ted hearts, the first derivative of left ventricular pressure, cardiac output, and external work were significantly depressed during reperfu sion; ISO restored all values to preocclusion levels. Regional myocard ial work in both LAD and CFX regions was significantly increased by IS O (from 564 +/- 207 to 1,635 +/- 543 g/mm/min in LAD, and from 753 +/- 90 to 1,426 +/- 245 g/mm/min in CFX). Efficiency (work/oxygen consump tion) of the reperfused region was similarly increased. LAD flow was s ignificantly increased by ISO, and O-2 extraction was unchanged. Infar ct size was 28.2 +/- 4.7% in untreated hearts and 29.0 +/- 3.5% in ISO hearts. Thus isoproterenol stimulation significantly improved both re gional and global function without subsequent evidence of increased ce ll death.