| Objective To investigate pathological changes of relative encephalic region and heart and to discussion the mechanism of cerebrocardiac syndrome (CCS) caused by acute focal cerebral ischemia–reperfusion injury (CIRI) in rats. To observe the protective effect and analysis the protective mechanism of propyl gallate (PrG) on the brain tissue and the myocardial tissue, which is a 5-LOX/COX-2 double inhibitor.Methods The right middle cerebral artery in rats were occluded by inserting a thread through internal carotid artery for 2h, and then reperfused for 24h. PrG was intraperitoneally injected at 0h and 2h of the reperfusion. The extent of neurological deficits was evaluated by Longer's method. The infarct size of the brain was measured by TTC staining technique. Pathological changes of the cerebral insular lobe in the occluded side and the myocardial tissue were observed by HE staining technique. The changes of theⅡ-lead electrocardiogram (ECG) and the left ventricular functions were monitored by RM6240B typical system of physiological experiment. The contents of TXA2 and PGI2 in blood plasma were measured respectively by radio-immunity method. The content of LTB4 in serum was measured by ELISA method, the activities of MPO, T-AOC, GSH and Na+-K+-ATPase of the myocardium was measured by biochemical method. The expression of iNOS protein of the cerebral insular lobe in the occluded side and the myocardial tissue was measured by immunohistochemistry technique.Results (1) After middle cerebral artery occlussion 2h/reperfusion 24h, the neurological deficits were evidently observed, the white infarct focus were showed on the brain tissue and the pathological changes were appeared in the cerebral insular lobe in the occluded side and the myocardial tissue. The depressed ST segment and T wave were observed in theⅡ-lead ECG. HR and LVEDP were increased and LVSP, +dp/dtmax, -dp/dtmax and t-dp/dtmax were evidently decreased. The content of TXA2 was elevated, the content of PGI2 was decreased and the ratio of TXA2 to PGI2 was disturbed in blood plasma as well as the content of LTB4 was elevated in serum. The activity of MPO was increased and the activities of T-AOC, GSH and Na+-K+-ATPase were decreased in the myocardial tissue. The expressions of iNOS were increased in the cerebral insular lobe in the occluded side and the myocardial tissue. (2) PrG 5, 7.5mg·kg-1 can dramatically improve neurological deficit, minify the infarct size, alleviate the pathological changes in the cerebral insular lobe in the occluded side and the myocardial tissue. PrG 5, 7.5mg·kg-1 can reduce the content of TXA2, increase the content of PGI2, regulate the proportional disbalance of TXA2/ PGI2 in blood plasma as well as reduce the content of LTB4 in serum. PrG 5, 7.5mg·kg-1 can reduce the activity of MPO and increase the activities of T-AOC, GSH and Na+-K+-ATPase in the myocardial tissue. PrG 5, 7.5mg·kg-1 can inhibit the expression of iNOS in the cerebral insular lobe in the occluded side and the myocardial tissue. PrG 7.5mg·kg-1 also can improve the changes of ECG and the left ventricular function.Conclusion (1) CIRI can induce the injuries of the cerebral insular lobe in the occluded side and the myocardial tissue, in which the expressions of iNOS protein were all increased. CIRI can lead to the injured changes of ECG and the left ventricular function and cause the evident inflammatory reaction, oxidative damage and ionic transport disorder in the myocardial tissue. (2) The protective mechanism of PrG maybe related with antiinflammatory, antiplatelet aggregation, elevating the activities of antioxidative erzymes, inbibiting the expression of iNOS and protecting the activity of Na+-K+-ATPase. |
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