| Kao SJ |
------>authors3_c=??? ------>paper_class1=1 ------>Impact_Factor=5.594 ------>paper_class3=2 ------>paper_class2=1 ------>vol=38 ------>confirm_bywho=chshih43 ------>insert_bywho=shang-jyh ------>Jurnal_Rank=13.5 ------>authors4_c=??? ------>comm_author= ------>patent_EDate=None ------>authors5_c= ------>publish_day=15 ------>paper_class2Letter=None ------>page2=1788 ------>medlineContent= ------>unit=E0400 ------>insert_date=20060501 ------>iam=1 ------>update_date=None ------>author=??? ------>change_event=6 ------>ISSN= ------>authors_c=??? ------>score=500 ------>journal_name=Clinical Infectious Diseases ------>paper_name=Mechanism of fulminant pulmonary edema caused by Enterovirus 71. ------>confirm_date=20080513 ------>tch_id=092081 ------>pmid=15227628 ------>page1=1784 ------>fullAbstract=Pulmonary edema (PE) may occur with enterovirus 71 (EV71) infection. We monitored arterial pressure (AP) and heart rate (HR) in patients with EV71 infection and analyzed the variability of AP and HR. Sympathetic activity, AP, and HR increased with respiratory stress. Thereafter, parasympathetic activity increased with decreases in AP and HR. The lungs showed edema with inducible nitric oxide synthase (iNOS) expression. Destruction of the medial, ventral, and caudal medulla may lead to sympathetic overactivation, causing blood to shift to the lungs. The pathogenesis of PE may also involve iNOS and nitric oxide. ------>tmu_sno=None ------>sno=13558 ------>authors2=Fwu Yang ------>authors3=Hsu YH ------>authors4=Chen IC ------>authors5= ------>authors6= ------>authors6_c= ------>authors=Kao SJ ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=??? ------>publish_area=0 ------>updateTitle=Mechanism of fulminant pulmonary edema caused by enterovirus 71. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2004 ------>submit_flag=None ------>publish_month=6 |