Wang TL |
------>authors3_c=None ------>paper_class1=1 ------>Impact_Factor=None ------>paper_class3=2 ------>paper_class2=1 ------>vol=37 ------>confirm_bywho=soulchin ------>insert_bywho=m002183 ------>Jurnal_Rank=None ------>authors4_c=None ------>comm_author= ------>patent_EDate=None ------>authors5_c=None ------>publish_day=None ------>paper_class2Letter=None ------>page2=449 ------>medlineContent= ------>unit=E0110 ------>insert_date=20040419 ------>iam=1 ------>update_date=None ------>author=??? ------>change_event=5 ------>ISSN=None ------>authors_c=None ------>score=500 ------>journal_name=Ann Emerg Med ------>paper_name=Intravenous morphine reduces plasma endothelin 1 concentration through activation of neutral endopeptidase 24.11 in patients with myocardial infarction. ------>confirm_date=20040419 ------>tch_id=092079 ------>pmid=11326179 ------>page1=445 ------>fullAbstract=STUDY OBJECTIVE: Morphine has multiple cardiovascular effects, but its action on hydrolysis of endothelin 1 (ET-1) has not been investigated. METHODS: We measured plasma levels of ET-1, C-terminal degradation products of ET-1, and neutral endopeptidase 24.11 (NEP) in 68 patients with acute Q-wave myocardial infarction and 29 control subjects. All the patients underwent blood sampling at initial presentation and 10 minutes later. Thirty-six of those with Q-wave myocardial infarction intravenously received 3 mg of morphine immediately after the first sampling (group 1), and the other 32 received the same after the second sampling (group 2). Twenty-four of the control subjects (group 3) were randomized to the protocol of group 1, and the remaining 5 subjects (group 4) were randomized to the protocol of group 2. RESULTS: The plasma ET-1 levels were significantly higher in groups 1 and 2 than in groups 3 and 4 (control groups). In group 1, the ET-1 level decreased significantly at second blood samplings (2.5+/-0.4 pmol/L versus 1.7+/-0.6 pmol/L, P <.001), whereas there were no definite changes of ET-1 levels in group 2 (2.5+/-0.5 pmol/L versus 2.6+/-0.6 pmol/L, P =not significant). However, the C-terminal degradation products increased significantly at second blood samplings in group 1 (0.8+/-0.2 pmol/L versus 1.3+/-0.4 pmol/L, P <.001), whereas there were no definite changes in group 2 (0.9+/-0.3 pmol/L versus 0.9+/-0.4 pmol/L, P =not significant). There was no significant difference in baseline NEP activities between groups 1 and 2 (5.02+/-1.30 nmol/mg protein versus 5.06+/-1.48 nmol/mg protein, P =not significant). However, the NEP activities at second blood samplings declined significantly in group 1 (9.76+/-1.76 nmol/mg protein, P <.001 versus baseline), whereas no definite changes were observed in group 2 (5.09+/-1.62 nmol/mg protein, P =not significant versus baseline). CONCLUSION: Intravenous morphine may increase NEP activities to accentuate hydrolysis of ET-1. ------>tmu_sno=None ------>sno=8526 ------>authors2=Chang H ------>authors3= ------>authors4= ------>authors5= ------>authors6= ------>authors6_c=None ------>authors=Wang TL ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=None ------>publish_area=None ------>updateTitle=Intravenous morphine reduces plasma endothelin 1 concentration through activation of neutral endopeptidase 24.11 in patients with myocardial infarction. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2001 ------>submit_flag=None ------>publish_month=None |