Please use this identifier to cite or link to this item: https://doi.org/10.1016/S0024-3205(03)00510-1
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dc.titleThe role of inducible nitric oxide synthase inhibitor on the arteriolar hyporesponsiveness in hemorrhagic-shocked rats
dc.contributor.authorMd, S.
dc.contributor.authorMoochhala, S.M.
dc.contributor.authorSiew-Yang, K.L.
dc.date.accessioned2014-11-20T05:58:30Z
dc.date.available2014-11-20T05:58:30Z
dc.date.issued2003-08-22
dc.identifier.citationMd, S., Moochhala, S.M., Siew-Yang, K.L. (2003-08-22). The role of inducible nitric oxide synthase inhibitor on the arteriolar hyporesponsiveness in hemorrhagic-shocked rats. Life Sciences 73 (14) : 1825-1834. ScholarBank@NUS Repository. https://doi.org/10.1016/S0024-3205(03)00510-1
dc.identifier.issn00243205
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/108065
dc.description.abstractHemorrhagic shock (HS) has been implicated in the induction of inducible nitric oxide synthase (iNOS) that leads to increase production of nitric oxide (NO). Recently, NO has been implicated to cause hyporesponsiveness of blood vessel in vitro towards vasoconstrictors in refractory (decompensated) HS. In our in vivo model, we examined the effects of aminoguanidine (AG), a known iNOS inhibitor, with angiotensin II (ANG II), a vasoconstrictor, following hemorrhagic shock decompensatory phase (HSDP) on percentage survival, vascular responsiveness, mean arterial blood pressure (MABP), heart rate and mean nitrate/nitrite levels in anaesthetized rats. HSDP (3 h) was achieved via constant pressure method (40-45 mmHg). MABP and heart rate was measured via the left carotid artery. Plasma collected from HSDP rats was used to measure nitrate/nitrite levels. Vascular hyporeactivity to ANG II was carried out using HSDP aortic strips, precontracted with KCl and noradrenaline. Sham-operated rats served as controls. HSDP rats decreased percentage survival, vascular contractility to ANG II and noradrenaline, MABP, heart rate while showing increased levels of nitrate/nitrite. Infusion of AG with ANG II, increased percentage survival and had reversed these cardiovascular effects of HSDP rats. This study indicates that excessive NO formation from iNOS activity induces vascular hyporeactivity and decompensation in HSDP. This might suggest that selective NOS inhibitor, AG, when coupled with ANG II, show reduction in NO's effect in HSDP. © 2003 Elsevier Inc. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/S0024-3205(03)00510-1
dc.sourceScopus
dc.subjectAngiotensin II
dc.subjectIn vitro
dc.subjectiNOS
dc.subjectNitric oxide
dc.subjectNoradrenaline
dc.typeArticle
dc.contributor.departmentPHARMACOLOGY
dc.description.doi10.1016/S0024-3205(03)00510-1
dc.description.sourcetitleLife Sciences
dc.description.volume73
dc.description.issue14
dc.description.page1825-1834
dc.description.codenLIFSA
dc.identifier.isiut000184526400008
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