There is little doubt that the "stunned myocardium" is amenable to therapeutic intervention, as a host of diverse pharmacologic agents have all been shown to improve short-term contractile function of viable, previously ischemic myocardium. However, few studies have addressed the question: Should the stunned myocardium be forced to contract? If the stunned myocardium is a protective mechanism, then acute recruitment could have later deleterious consequences on recovery of contractile function and high-energy phosphate stores. Conversely, acutely "resting" the heart (i.e. by beta-adrenergic blockade) could conceivably enhance or accelerate recovery of the stunned, postischemic tissue. We therefore sought to assess the immediate and longer-term effects of acute recruitment and acute beta-blockade on regional wall thickening (WT: using two-dimensional echocardiography) and adenosine triphosphate (ATP) content in the canine model of the stunned myocardium. Anesthetized open-chest dogs underwent 15 minutes of transient coronary artery occlusion. At 30 minutes following reperfusion, the dogs acutely received either: the ultrashort-acting beta-blocker esmolol, the afterload reducing and cardiostimulatory agent hydralazine, or saline. As anticipated, hydralazine enhanced contractile function of the stunned tissue in the short term: WT at 2 hours after treatment was 53.7 +/- 6.9% versus 7.1 +/- 6.5% in treated versus saline controls (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)