Study Of Cardiac Damage And Its Mechanism In Rats With Experimental Stroke

Background and Purpose:Clinically, it has been frequently observed that stroke causes cardiac damage that are detrimental to prognosis and may cause death. Its' pathophysiologic mechanism is still unknown. We have developed an experimental model of stroke, a middle cerebral artery occlusion in the rat. The objectives of this study were to study electrocardiographic (ECG), myocardial pathological and autonomic changes associated with our stroke models, and to explore eletrophysiologic and pathologic characteristics of cerebrogenic cardiac damage. Finally, the study was attempt to assess the role of autonomic nervous system ,especially sympathetic transmitters on cardiac damages in rats with experimental stroke.Methods:We established middle cerebral artery occlusion models in the rat with an intraluminal nylon monofilament. The Wistar rats was divided into three experimental groups: sham operation group(Sham), right middle cerebral artery occlusion group(RMCAO) and left middle cerebral artery occlusion group (LMCAO).The ECG monitoring was in the lead â…¡configuration. The ECG were recorded 30 minutes before and at 3-hour, 6-hour, 12-hour and 24-hour intervals after the MCAO or sham operation, and the heart rate variability (HRV) chaotic characteristics was analysed at the same time. At 3-hour and 24-hour intervals after the RMCAO or sham operation the levels of norepinephrine(NE) and neuropeptide Y(NPY)were measured both in plasma and myocardium of rat, and compared to the levels of healthy rats. A histopathologic study of left ventricular myocardium were done at healthy and 24 hours after occlusion or sham occlusion.Results:The incidence of electrocardiographic changes in left hemisphere infarction group is 35%, including elevated ST segments, increased QRS amplitudes and arrhythmias. The incidence of electrocardiographic changes in right hemisphere infarction group is 30%, including supraventricular tachycardia, frequent ventricular premature beats and frequent ectopic beats. FD were suppressed in both left and right hemisphere stroke rats versus controls. The pathological inspection of myocardium showed that there were two abnormal cases in left and right hemisphere infarction group respectively, with features of myocardial fibrous degeneration, it included that disappearance of cross striation, disorder of arrangement of myocardial fibre, foci of dissolution of myocardial cells. Moreover, the change of ultrastructure was significant, including strong contraction of myocardical cells, abnormal contractive belt of muscle cells, remaining of mitochondrial and lysosomes. The levels of NE and NPY of myocardium in hemisphere infarction group were higher significantly than that in sham operation group.Conclusion:1. MCAO models in the rat with an intraluminal nylon monofilament can mimic the brain-heart symdrom observed clinically. It is a convenient and reliable model that can be used for experimental study of cardiac damage caused by cerebral stroke. 2. Left and right hemisphere infarction has been shown to produce differential ECG changes. Left hemisphere infarction is often associated with electrocardiographic (ECG) evidence of cardiac repolarisation abnormalities. Right hemisphere infarction is associated with a greater number of supraventricular tachycardia. 3. Stroke is often associated with myocardial degeneration in the ventricular myocardium. These effects are obviously different from coagulation necrosis of cardiac ischemic disease. 4. Strokeinduces cardiac damage by neurogenic mechanisms mainly. The sympathetic nervous increased discharge of NE and NPY together that may caused cardiac lesion.