Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.resuscitation.2004.01.005
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dc.titleInfluence of selective nitric oxide synthetase inhibitor for treatment of refractory haemorrhagic shock
dc.contributor.authorShirhan, Md.
dc.contributor.authorMoochhala, S.M.
dc.contributor.authorKerwin, S.-Y.L.
dc.contributor.authorNg, K.C.
dc.contributor.authorLu, J.
dc.date.accessioned2014-11-20T05:58:27Z
dc.date.available2014-11-20T05:58:27Z
dc.date.issued2004-05
dc.identifier.citationShirhan, Md., Moochhala, S.M., Kerwin, S.-Y.L., Ng, K.C., Lu, J. (2004-05). Influence of selective nitric oxide synthetase inhibitor for treatment of refractory haemorrhagic shock. Resuscitation 61 (2) : 221-229. ScholarBank@NUS Repository. https://doi.org/10.1016/j.resuscitation.2004.01.005
dc.identifier.issn03009572
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/108060
dc.description.abstractObjective: Haemorrhagic shock (HS) is implicated in the induction of inducible nitric oxide synthase that leads to increased production of nitric oxide (NO). We investigated the influence of aminoguanidine (AG), a selective iNOS inhibitor, N G-nitro-L-arginine methyl ester (L-NAME), a non-selective inhibitor and S-Nitroso-N-acetylpenicillamine (SNAP), a NO donor, each of which was given with (+) or without (-) angiotensin II (ANGII), a vasoconstrictor, on the survival rate of HS decompensatory phased (HSDP) rats. Materials and methods: HSDP was achieved via a constant pressure method. Organs were harvested and analyzed from rats sacrificed 72 h after HSDP or upon death. Plasma collected from HSDP rats were used to measure nitrate/nitrite, GOT and creatinine levels. Results: AG+ANGII-treated rats had significantly higher survival rates compared to the other treatment groups, 72 h following HSDP. A marked increase in MABP level was observed in AG+ANGII-treated rats when compared to other treatment groups. Histological examinations also showed a reduction of organ damage in AG+ANGII-treated rats compared to other treatment groups. Nitrate/nitrite level, glutamic oxalacetic transaminase (GOT) level and creatinine level were also significantly improved in AG+ANGII-treated rats compared to the other groups. Conclusions: A greater beneficial effect was achieved with treatment by the AG+ANGII combination. Our experiments showed that the inhibition of excessive NO formation that occurred during HSDP, had augmented the vascular responsiveness effect of ANGII following protracted HS. © 2004 Elsevier Ireland Ltd. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.resuscitation.2004.01.005
dc.sourceScopus
dc.subjectAminoguanidina
dc.subjectAminoguanidine
dc.subjectChoque hemorrágico
dc.subjectHaemorrhagic shock
dc.subjectNitric oxide
dc.subjectOxido nítrico
dc.subjectRat
dc.subjectrata
dc.subjectRatos
dc.subjectSOC hemorrágico
dc.typeArticle
dc.contributor.departmentPHARMACOLOGY
dc.description.doi10.1016/j.resuscitation.2004.01.005
dc.description.sourcetitleResuscitation
dc.description.volume61
dc.description.issue2
dc.description.page221-229
dc.description.codenRSUSB
dc.identifier.isiut000221681400014
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