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ORIGINAL ARTICLE
Year : 2015  |  Volume : 5  |  Issue : 1  |  Page : 12-17

Effect of aminoguanidine on cardiovascular responses and survival time during blood loss: A study in normotensive and deoxycorticosterone acetate-salt hypertensive rats


1 Department of Physiology, Zabol University of Medical Sciences, Zabol, Iran
2 Department of Physiology, Isfahan University of Medical Sciences, Isfahan; Department of Physiology, Mashhad University of Medical Sciences, Mashhad, Iran

Correspondence Address:
Majid Khazaei
Department of Physiology, Isfahan University of Medical Sciences, Hezar Jarib Ave., Isfahan
Iran
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Source of Support: The Isfahan University of Medical Sciences supported this study (Grant No: 387413), Conflict of Interest: None


DOI: 10.4103/2229-516X.149222

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Introduction: Hemorrhagic shock causes more circulatory disturbances and mortality in hypertensive than normotensive subjects. In the late phase of hemorrhagic shock, nitric oxide (NO) overproduction leads to vascular decompensation. In this study, we evaluated the effect of inducible NO synthase (iNOS) inhibitor, aminoguanidine (AG), on hemodynamic parameters and serum nitrite concentration in decompensated hemorrhagic shock model in normotensive and hypertensive male rats. Materials and Methods: Twenty-four male rats were divided into hypertensive and normotensive groups (n = 12 each). Hypertension was induced by subcutaneous injection of deoxycorticoesterone acetate (DOCA), 30 mg/kg in uninephrectomized rats. Decompensated hemorrhagic shock was induced by withdrawing blood until the mean arterial pressure (MAP) reached 40 mmHg. After 120 min, each group was assigned to aminguanidine (100 mg/kg) and control group. Hemodynamic parameters were monitored for next 60 min. Blood samples were taken before and after shock period and 60 min after treatment. Survival rate was monitored for 72 h. Results: Infusion of AG in normotensive animals caused a transient increase in MAP and increase of heart rate, whereas it did not affect those parameters in hypertensive animals. Hemorrhagic shock caused a significant rise in serum nitrite concentration in normotensive and hypertensive rats and infusion of AG did not significantly change it in both groups. No significant differences observed in survival rate between AG-treated and not treated groups. Conclusion: It seems that inhibition of iNOS with AG does not have beneficial effects on hemodynamatic parameters and survival rate during decompensated hemorrhagic shock in normotensive and hypertensive animals.


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