摘要
The Section of Cardiology, Department of Medicine (Cherng WJ, Wang CH, Chen SF and Chen JJ), Department of Pathology (Lee N), Chang Gung Medical College, Chang Gung Memorial Hospital, Keelung, Taiwan, China Address for reprints: Wen jin Cherng, MD, Chang Gung Memorial Hospital, 222 Mai Chin Road, Keelung, Taiwan, China. Objectives There is little information available regarding local vasomotor regulating processes in chronic heart failure. In this study, we tested the hypothesis that chronic heart failure impaired the endothelial function, and long term captopril treatment might reverse endothelial activity through tissue endothelin (ET) pathway. Methods Forty Spraque Dawley rats were divided into 4 groups including 15 rats in each of the sham operated with or without captopril treated groups and 5 rats in each of large infarcted with or without captopril treated groups. Results Concentration response curves obtained in aortic rings without endothelium revealed no difference in nitroprusside induced relaxation. With endothelium, rightward shifting was noted only in the untreated large infarct group during acetylcholine induced relaxation. As compared to the non treated group, plasma ET 1 concentrations were lower in the captopril treated with or without large infarct groups. However, endothelin like immunoreactivity in endothelial cells and cytoplasma of smooth muscle cells of the media of the aorta were lower only in the non treated large infarct group. Conclusions Endothelial function was impaired in the chronic heart failure model. Coverting enzyme inhibitor might improve endothelial function through the Local endothelin pathway.
The Section of Cardiology, Department of Medicine (Cherng WJ, Wang CH, Chen SF and Chen JJ), Department of Pathology (Lee N), Chang Gung Medical College, Chang Gung Memorial Hospital, Keelung, Taiwan, China Address for reprints: Wen jin Cherng, MD, Chang Gung Memorial Hospital, 222 Mai Chin Road, Keelung, Taiwan, China. Objectives There is little information available regarding local vasomotor regulating processes in chronic heart failure. In this study, we tested the hypothesis that chronic heart failure impaired the endothelial function, and long term captopril treatment might reverse endothelial activity through tissue endothelin (ET) pathway. Methods Forty Spraque Dawley rats were divided into 4 groups including 15 rats in each of the sham operated with or without captopril treated groups and 5 rats in each of large infarcted with or without captopril treated groups. Results Concentration response curves obtained in aortic rings without endothelium revealed no difference in nitroprusside induced relaxation. With endothelium, rightward shifting was noted only in the untreated large infarct group during acetylcholine induced relaxation. As compared to the non treated group, plasma ET 1 concentrations were lower in the captopril treated with or without large infarct groups. However, endothelin like immunoreactivity in endothelial cells and cytoplasma of smooth muscle cells of the media of the aorta were lower only in the non treated large infarct group. Conclusions Endothelial function was impaired in the chronic heart failure model. Coverting enzyme inhibitor might improve endothelial function through the Local endothelin pathway.
