To determine if inhibition of leukocyte adhesion and aggregation could improve postischemic ventricular dysfunction (“stunning”), a monoclonal antibody (904) that binds to the adhesionpromotingMol glycoprotein on the cell surface of leukocytes was administered intravenously(0.5 mg/kg) to open-chest dogs before a 15-minute coronary occlusion. Ultrasonic crystalsplaced in ischemic and control myocardium were used to measure systolic wall thickeningduring a 15-minute occlusion of the left anterior descending artery and for 3 hours afterreperfusion. Myocardial blood flow was measured with tracer-labeled microspheres beforeocclusion, after 10 minutes of occlusion, 3 minutes of reperfusion, and at 1 and 3 hours afterreperfusion. Six animals receiving anti-Mol antibody had antibody excess demonstrated withimmunofluorescence techniques at 5 minutes and 3 hours of reperfusion; this finding'indicatedsaturation of binding sites. Five animals served as controls and received an antibody (murineimmunoglobulin G) that does not influence neutrophils. The two groups did not differhemodynamically during ischemia and reperfusion. Risk areas and myocardial blood flow werealso not significantly different between the two groups. The main parameter used to defineregional myocardial stunning, percentage systolic wall thickening in the ischemic/reperfusedarea, did not differ significantly between the two groups. Specimens from nonischemicmyocardium were compared with ischemic specimens for myeloperoxldase content There wereno significant differences within or between groups. These data indicate that the anti-Molmonoclonal antibody (904) is not effective in improving the profound myocardial dysfunctionthat persists for 3 hours of reperfusion after IS minutes of ischemia.