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|Title:||The role of selective nitric oxide synthase inhibitor on nitric oxide and PGE 2 levels in refractory hemorrhagic-shocked rats|
|Authors:||Md, S. |
|Source:||Md, S., Moochhala, S.M., Yang, K.L.S., Lu, J., Anuar, F., Mok, P., Ng, K.C. (2005-02). The role of selective nitric oxide synthase inhibitor on nitric oxide and PGE 2 levels in refractory hemorrhagic-shocked rats. Journal of Surgical Research 123 (2) : 206-214. ScholarBank@NUS Repository. https://doi.org/10.1016/j.jss.2004.07.243|
|Abstract:||The up-regulation of nitric oxide (NO) and cyclooxgenase-2 (COX-2) has been implicated in the pathophysiology of hemorrhagic shock. We examined the effects of aminoguanidine (AG), which is a known inducible nitric oxide synthase (iNOS) inhibitor, and NS-398, a known COX-2 inhibitor, in our rat model of refractory hemorrhagic shock (RHS). We measured tissue iNOS and COX-2 protein expression, brain and plasma nitrate/nitrite and prostaglandin E 2 (PGE 2) levels, plasma creatinine and glutamic oxalacetic transaminase (GOT) levels, quantified the histological damages in kidney, liver, lung, and brain, survival rate, and mean arterial blood pressure (MABP) in RHS rats. Semiquantitative analysis of tissues showed iNOS protein was not detected in AG + RHS rats but was detected in normal saline and NS-398 RHS rats. Tissue COX-2 protein was not detected in AG and NS-398 RHS rats but was detected in normal saline + RHS rats. The levels of brain and plasma nitrate/nitrite and PGE 2 and plasma creatinine and GOT were significantly lower in the AG + RHS rat group when compared with the normal saline RHS rat group. Histological examinations also showed a reduction in organ damage for AG + RHS rats when compared with treated RHS rats. AG + RHS rats showed significantly increased survival and MABP level when compared with treated RHS rats. Our present findings suggest that NO produced by iNOS might result in organ damages. This in turn might lead to COX-2 up-regulation, and it increases the production of reactive oxygen species and toxic prostanoids. NO-mediated organ damage might be one way in which toxic products of COX-2 might further contribute to NO's deleterious effect in the later stages of RHS. It is therefore suggested that treatment of AG via inhibition of NO might contribute to improved physiological parameters and survival rates following RHS. © 2004 Elsevier Inc. All rights reserved.|
|Source Title:||Journal of Surgical Research|
|Appears in Collections:||Staff Publications|
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