Previous studies have demonstrated that crystalloid coronary perfusion can cause myocardial edema, but the time required for resolution of this edema has not been defined. Accordingly, studies were conducted in 30 rats. Myocardial edema was induced by coronary perfusion with 20 cc/kg of Plegisol (294 mOsm/liter) during aortic occlusion, which produced diastolic arrest. This was followed by whole blood reperfusion, which restored normal contractile function. Duration of reperfusion in minutes was zero (group 0, n = 6), one (group 1, n = 6), five (group 5, n = 6), or fifteen (group 15, n = 6). A control group (n = 6) was studied without edema or reperfusion. Data included heart weight and myocardial water content. Left ventricular pressure-volume curves were measured in groups 1, 5, and 15. Myocardial water content increased significantly from 75.7 ± 0.5% (SD) in the control group to 79.7 ± 1.1% (P < 0.05) in group 0 and then decreased significantly to 77.3 ± 0.7, 75.2 ± 1.4, and 75.3 ± 1.6% in groups 1, 5, and 15, respectively. Water content in group 1 was also significantly greater than in groups 5 and 15. Heart weight changes were not statistically significant. Normalized pressure-volume relationships shifted rightward with increasing reperfusion time, but changes were not statistically significant. We conclude that edema induced by crystalloid coronary perfusion of the arrested heart resolves in the beating heart after less than 5 min of blood reperfusion.
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