2005Unpublished venueRequires access

Protective Effect of Fluvastatin on Myocardial Ischemia Reperfusion Injury

Dai Shu

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Abstract

Aim To investigate the protective effect of fluvastatin on ischemia reperfusion myocardium in normocholesterolemic rabbit. Methods 24 rabbits were divided into three groups randomly and myocardial ischemia reperfusion model in rabbit was made. Rabbits were subjected to 45 min of regional myocardial ischemia and 3 h of reperfusion. 10 mg/(kg·d) fluvastatin were oral administered for one week. Dynamic index of myocardial function was recorded and analyzed. Serum activity of creatine kinase (CK) and lactate dehydrogenase (LDH) were detected. Infarcted sizes in heart were determined by dual staining with Evans-blue and TTC. The activity of induced nitric oxide sythase (iNOS) and total nitric oxide synthase (tNOS) were detected in ischemic myocardium. Results In comparison with control group, all indexes related to injury, namely left ventricular end-diastolic volume (LVEDP), ±dp/dt max, MB isoenzyme of creatine kinase (CK-MB), LDH-1 and the ratio of myocardial necrosis area, show injury attenuation in fluvastatin group. Increase of activity ratio iNOS/tNOS due to ischemia reperfusion is reduced significantly in fluvastatin group compared with control group (0.25±0.10 vs 0.61±0.13, P0.01). Conclusion Fluvastatin can attenuate myocardial ischemia reperfusion injury in rabbit. Its protective effect may be assoctiated not only with up-regulation of tNOS but also with modulation of iNOS in myocardium.

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Aim To investigate the protective effect of fluvastatin on ischemia reperfusion myocardium in normocholesterolemic rabbit. Methods 24 rabbits were divided into three groups randomly and myocardial ischemia reperfusion model in rabbit was made. Rabbits were subjected to 45 min of regional myocardial ischemia and 3 h of reperfusion. 10 mg/(kg·d) fluvastatin were oral administered for one week. Dynamic index of myocardial function was recorded and analyzed. Serum activity of creatine kinase (CK) and lactate dehydrogenase (LDH) were detected. Infarcted sizes in heart were determined by dual staining with Evans-blue and TTC. The activity of induced nitric oxide sythase (iNOS) and total nitric oxide synthase (tNOS) were detected in ischemic myocardium. Results In comparison with control group, all indexes related to injury, namely left ventricular end-diastolic volume (LVEDP), ±dp/dt max, MB isoenzyme of creatine kinase (CK-MB), LDH-1 and the ratio of myocardial necrosis area, show injury attenuation in fluvastatin group. Increase of activity ratio iNOS/tNOS due to ischemia reperfusion is reduced significantly in fluvastatin group compared with control group (0.25±0.10 vs 0.61±0.13, P0.01). Conclusion Fluvastatin can attenuate myocardial ischemia reperfusion injury in rabbit. Its protective effect may be assoctiated not only with up-regulation of tNOS but also with modulation of iNOS in myocardium.

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Available abstract

Aim To investigate the protective effect of fluvastatin on ischemia reperfusion myocardium in normocholesterolemic rabbit. Methods 24 rabbits were divided into three groups randomly and myocardial ischemia reperfusion model in rabbit was made. Rabbits were subjected to 45 min of regional myocardial ischemia and 3 h of reperfusion. 10 mg/(kg·d) fluvastatin were oral administered for one week. Dynamic index of myocardial function was recorded and analyzed. Serum activity of creatine kinase (CK) and lactate dehydrogenase (LDH) were detected. Infarcted sizes in heart were determined by dual staining with Evans-blue and TTC. The activity of induced nitric oxide sythase (iNOS) and total nitric oxide synthase (tNOS) were detected in ischemic myocardium. Results In comparison with control group, all indexes related to injury, namely left ventricular end-diastolic volume (LVEDP), ±dp/dt max, MB isoenzyme of creatine kinase (CK-MB), LDH-1 and the ratio of myocardial necrosis area, show injury attenuation in fluvastatin group. Increase of activity ratio iNOS/tNOS due to ischemia reperfusion is reduced significantly in fluvastatin group compared with control group (0.25±0.10 vs 0.61±0.13, P0.01). Conclusion Fluvastatin can attenuate myocardial ischemia reperfusion injury in rabbit. Its protective effect may be assoctiated not only with up-regulation of tNOS but also with modulation of iNOS in myocardium.

Key concepts: Fluvastatin, Lactate dehydrogenase, Creatine kinase, Ischemia, Reperfusion injury, Preload, Nitric oxide, Medicine

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