| Tsung-Ming Lee |
------>authors3_c= ------>paper_class1=1 ------>Impact_Factor=3.560 ------>paper_class3=2 ------>paper_class2=1 ------>vol=294 ------>confirm_bywho=ncchang ------>insert_bywho=tmlee ------>Jurnal_Rank=15.3 ------>authors4_c= ------>comm_author= ------>patent_EDate=None ------>authors5_c= ------>publish_day=15 ------>paper_class2Letter=None ------>page2=H1879 ------>medlineContent= ------>unit=E0100 ------>insert_date=20080415 ------>iam=1 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN= ------>authors_c= ------>score=500 ------>journal_name=AJP - Heart and Circulatory Physiology ------>paper_name=Effect of endothelin receptor antagonists on ventricular susceptibility in postinfarcted rats ------>confirm_date=20080415 ------>tch_id=093042 ------>pmid=18281380 ------>page1=H1871 ------>fullAbstract=This study investigated whether selective endothelin (ET) type A (ET(A)) or nonselective ET(A)/ET(B) receptor blockade exerted antiarrhythmic effects through attenuated sympathetic reinnervation after infarction. Twenty-four hours after ligation of the left anterior descending artery, male Wistar rats received either vehicle, ABT-627 (selective ET(A) receptor antagonist), bosentan (nonselective ET(A)/ET(B) receptor antagonist), or hydralazine for 4 wk. The measurement of myocardial ET-1 levels at the remote zone revealed a significant increase in vehicle-treated infarcted rats compared with sham-operated rats, consistent with increased activities of ET-1 after infarction. Sympathetic nerve function changes assessed by the norepinephrine content of myocardium and the dialysate and plasma dihydroxyphenylglycol levels were parallel to ET-1 levels. Immunohistochemical analysis for tyrosine hydroxylase, growth-associated protein 43, and neurofilament also confirmed the change of nerve function. This was accompanied with a significant upregulation of nerve growth factor protein expression and mRNA in the vehicle-treated infarcted rats, which reduced after the administration of either ET(A) or ET(A)/ET(B) blockade to a similar extent. The beneficial effects of ET receptor antagonists on sympathetic nerve function and structures were dissociated from their blood pressure-lowering effect because ET receptor antagonists and hydralazine reduced arterial pressure similarly. Arrhythmic severity during programmed stimulation in ET receptor antagonists-treated rats was significantly lower than that in vehicle-treated infarcted rats. Our data indicate that the ET system, especially via ET(A) receptors, plays an important role in attenuating sympathetic reinnervation after infarction. Independent of their hemodynamic effects, a chronic use of either ET(A) or ET(A)/ET(B) antagonists may modify the arrhythmogenic response to programmed electrical stimulation. ------>tmu_sno=None ------>sno=17505 ------>authors2=Chien-Chang Chen ------>authors3=Mei-Shu Lin ------>authors4=Nen-Chung Chang ------>authors5= ------>authors6= ------>authors6_c= ------>authors=Tsung-Ming Lee ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c= ------>publish_area=0 ------>updateTitle=Effect of endothelin receptor antagonists on ventricular susceptibility in postinfarcted rats. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2008 ------>submit_flag=None ------>publish_month=2 |