6533b7ddfe1ef96bd1275469

RESEARCH PRODUCT

0110 : Experimental cerebral ischemia in rats increases myocardial vulnerability to ischemia-reperfusion injury ex vivo

subject

description

For years, the relationship between cardiac and neurological ischemic events has been mainly attributed to overlapping pathophysiological mechanisms and common risk factors. However, acute stroke may induce dramatic alterations of cardiovascular function. The aim of this work was to evaluate how prior cerebrovascular lesions affect myocardial function in vivo and ex vivo , as well as myocardial vulnerability to ischemic injury. Cerebral embolization was performed in adult Wistar male rats by the injection of microspheres into the left internal carotid artery. Left ventricular function, investigated in vivo using echocardiography (1 hour, 24 hours and 7 days after the embolization), was not significantly impaired; however, the heart rate was significantly increased in the stroke group (+7.2%). Epinephrine (E) and norepinephrine (NE) plasma levels increased in rats from the stroke group (E: 47.3±2.1 vs. 24.3±8.7 and NE: 22.7±4.2 vs. 10.9±3.7). One hour after stroke or sham embolization, hearts were isolated and perfused ex vivo in the Langendorff mode. In hearts from the stroke group, the baseline left ventricular developed pressure was diminished (-11%); moreover, a greater myocardial vulnerability to ischemic injury was observed, with impaired coronary flow recovery after 40 minutes of total global normothermic ischemia. Our study provides original exciting data indicating that myocardial vulnerability to ischemia can be worsened by prior ischemic stroke, a situation that does not agree with the concept of remote preconditioning. The underlying molecular mechanisms of the stroke-induced myocardial alterations after cerebral embolization remain to be established, insofar as they may involve the sympathetic nervous system. The author hereby declares no conflict of interest