Effect of reduction in myocardial edema on myocardial blood flow and ventricular function after coronary reperfusion.

The contribution of myocardial edema to the no-reflow phenomenon, left ventricular functional recovery, and infarct size after coronary occlusion and reperfusion is uncertain. To examine this, we studied 26 open-chest dogs after coronary occlusion and reperfusion. Twelve dogs received hypertonic mannitol 30 min before reperfusion, which increased serum osmolality (P less than 0.01 vs. control). Fourteen control dogs received a similar volume of saline that had no effect on serum osmolality. Tissue biopsies of central ischemic and normal myocardial areas were analyzed by proton nuclear magnetic resonance relaxation spectroscopy to assess edema content. Hypertonic mannitol resulted in a significant decrease in ischemic tissue T1 (767.0 +/- 16.3 vs. 818.6 +/- 19.0 ms, P less than 0.05) compared with the control group. Despite this, no significant differences were found between the mannitol and control groups in 4-h reperfusion subendocardial blood flow or left ventricular wall thickening. In addition, mannitol administered before reperfusion did not modify infarct size compared with the control group (infarct/risk area, 41.0 +/- 1.4 vs. 37.9 +/- 1.9%, P not significant). In conclusion, no benefit is produced in reperfusion blood flow or functional recovery by reducing edema in postischemic myocardial tissue. This suggests that mechanisms other than myocardial edema are responsible for myocardial no reflow and contractile dysfunction after coronary reperfusion. Furthermore, hypertonic mannitol administered before reperfusion does not reduce infarct size.