LONG-TERM INHIBITION OF Na~+/H~+ EXCHANGE ATTENUATES CARDIAC REMODELING AFTER MYOCARDIAL INFARCTION IN RATS
LONG-TERM INHIBITION OF Na+/H+ EXCHANGE ATTENUATES CARDIAC REMODELING AFTER MYOCARDIAL INFARCTION IN RATS出 版 物：《Journal of Zhejiang University-Science A(Applied Physics & Engineering)》 (浙江大学学报A辑(应用物理与工程)(英文版))
年 卷 期：2001年第4期
页 面：80-85页
核心收录：
学科分类：1007[医学-药学(可授医学、理学学位)] 1006[医学-中西医结合] 100706[医学-药理学] 100602[医学-中西医结合临床] 10[医学]
主 题：myocardial infarction Na\++/H\++ exchange inhibitor remodeling ventricular function
摘 要：Objective: In addition to pH regulation, Na\++/H\++ exchanger (NHE) has been shown to facilitate cell growth and proliferation. However, the effects of long-term inhibition of Na\++/H\++ exchange on cardiac structural and functional remodeling post myocardial infarction (MI) are still controversial. The present study was therefore carried out to further investigate the effects of long-term treatment with cariporide, a specific inhibitor of NHE-1, on cardiac remodeling after MI in rats; Methods: Male Wistar rats that underwent coronary ligation were randomly selected for cariporide treatment starting 6 h after induction of MI or no *** was continued up to 6 weeks post MI, after which, the arterial, venous and left ventricular catheters were chronically implanted. Twenty-four h later, after hemodynamic signals were recorded in conscious rats, they were sacrificed and hearts were taken out for morphological examinations; Results: Cariporide treatment decreased the heart weight and heart weight to body weight ratio (both \%P\%0.05), decreased left ventricular end-diastolic pressure (\%P\%0.001), improved myocardial contractility (d\%P\%/d\%t\%\-\{max\}) (\%P\%0.05) and tended to increase the survival of treated rats compared to that of untreated infarct rats; Conclusion: The results of the present study indicate that the long-term inhibition of NHE with cariporide can attenuate cardiac structural remodeling and improve left ventricular dysfunction in infarcted rats, and suggest that Na\++/H\++ exchange inhibition could be an effective therapeutic strategy for myocardial infarction-induced heart failure.
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