In models of regional ischemia, hypertonic mannitol has been shown to increase myocardial blood flow and reduce experimental infarct size. To determine the effects of mannitol in a model of global ischemia simulating ischemic arrest during cardiac surgery, 32 isolated isovolumic feline hearts were subjected to 1 hour of normothermic (37°C) ischemic arrest and 45 minutes of reperfusion (37°C). Group A hearts received no mannitol and served as controls. In group B, infusion of mannitol at a rate sufficient to raise coronary sinus osmolality from 310 ± 4 to 354 ± 8 mOsm was begun immediately prior to aortic cross clamping and continued during reperfusion. Mannitol infusion was begun at the start of reperfusion in group C or after 15 minutes of reperfusion in group D. Recovery of ventricular performance (maximum developed pressure and dP/dt) was significantly better in group C than in control hearts (group A) or in mannitol-treated hearts in groups B and D. During reperfusion all hearts had elevated left ventricular end-diastolic pressure and reduced coronary flow, but these changes were least marked in group C. Quantitative morphologic studies demonstrated that only group C hearts, in which mannitol infusion was begun at the onset of reflow, had an injury score significantly lower than control (P<0.05 versus group A). Mannitol reduced the severity of myocardial edema, as evidenced by water content and morphology, independent of the time of administration. In contrast, mannitol resulted in sustained improvement in coronary flow and myocardial contractility only when it was given at the onset of reperfusion. Thus, following ischemic arrest and reperfusion, the timing of administration of a hyperosmolar agent, such as mannitol, appears critical in order for it to have a beneficial effect on myocardial structure and function.
|Original language||English (US)|
|Number of pages||10|
|State||Published - 1981|
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