| Yen MH, Liu YC, Hong HJ, Sheu JR and Wu CC |
------>authors3_c=None ------>paper_class1=1 ------>Impact_Factor=None ------>paper_class3=2 ------>paper_class2=1 ------>vol=60 ------>confirm_bywho=sheujr ------>insert_bywho=??? ------>Jurnal_Rank=None ------>authors4_c=None ------>comm_author=0 ------>patent_EDate=None ------>authors5_c=None ------>publish_day=None ------>paper_class2Letter=None ------>page2=1230 ------>medlineContent= ------>unit=E0100 ------>insert_date=19991209 ------>iam=4 ------>update_date= ------>author=??? ------>change_event=5 ------>ISSN=None ------>authors_c=None ------>score=500 ------>journal_name=Life Sci. ------>paper_name=Role of nitric oxide in lipopolysaccharide-induced mortality from spontaneously hypertensive rats. ------>confirm_date=20020301 ------>tch_id=082005 ------>pmid=9096239 ------>page1=1223 ------>fullAbstract=To investigate whether nitric oxide (NO) contributed to a higher mortality induced by lipopolysaccharide (LPS) in spontaneously hypertensive rats (SHR), NO synthase inhibitors were used to examine the mortality from LPS in SHR and normotensive Wistar-Kyoto (WKY) rats. We evaluated the mortality from LPS in a series of doses (5, 10, or 20 mg/kg, i.v.) in the anesthetized rat. Plasma nitrite was measured before and at 1, 2, and 3 h after treated rats with LPS (5 mg/kg, i.v.). Pressure responses to N omega-nitro-L-arginine methyl ester (L-NAME) and aminoguanidine (AG) were performed in rats treated with or without LPS for 3 h. Thoracic aortic cyclic guanosine 3~,5~-monophosphate (cGMP) levels were also assessed. Our results demonstrated that injection of LPS caused a dose-dependent mortality in both strains, having a more marked effect in SHR. The survival time of rats after injection of LPS (5 mg/kg, i.v.) was much shorter in SHR. A higher basal level of plasma nitrite was observed in SHR and this difference was further augmented by LPS. The administration of L-NAME (3 mg/kg, i.v.) and AG (15 mg/kg, i.v.) 3 h after LPS had no significant effects on the survival time of WKY rats, but significantly prolonged that of SHR to a similar time of WKY rats. The injecton of L-NAME prior to LPS increased blood pressure of WKY rats by 28+/-5 mmHg and increased that of SHR by 38+4 mmHg. At 3 h after LPS, L-NAME had a greater pressor effect in SHR than in WKY rats. By contrast, before rats injected with LPS, AG slightly increased blood pressure of SHR by 7+/-3 mmHg but not of WKY rats (3+/-2 mmHg), whereas it also had a greater pressor effect in SHR than in WKY rats after treated rats with LPS for 3 h. In addition, LPS induced a higher level of cGMP in SHR than in WKY rats, which was attenuated by in vitro treatment of aortic rings from LPS-rats with L-NAME or AG to a similar level in SHR and WKY rats. These results suggest that a higher level of NO evoked by LPS is associated with a higher mortality in SHR and we propose that the elevated NO synthesis in SHR may play an important role in the compensatory mechanisms activated to combat the hypertensive state. ------>tmu_sno=None ------>sno=946 ------>authors2=None ------>authors3=None ------>authors4=None ------>authors5=None ------>authors6=None ------>authors6_c=None ------>authors=Yen MH, Liu YC, Hong HJ, Sheu JR and Wu CC ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=None ------>publish_area=None ------>updateTitle=Role of nitric oxide in lipopolysaccharide-induced mortality from spontaneously hypertensive rats. ------>language= ------>check_flag=0 ------>submit_date= ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho= ------>publish_year=1997 ------>submit_flag= ------>publish_month=None |