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

Barmaki B, Khazaei M - Int J Appl Basic Med Res (2015 Jan-Apr)

Bottom Line: 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.No significant differences observed in survival rate between AG-treated and not treated groups.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Zabol University of Medical Sciences, Zabol, Iran.

ABSTRACT

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.

No MeSH data available.


Related in: MedlinePlus

Effect of aminoguanidine on mean arterial pressure and heart rate in normotensive (a and c) and hypertensive (b and d) rats
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Figure 2: Effect of aminoguanidine on mean arterial pressure and heart rate in normotensive (a and c) and hypertensive (b and d) rats

Mentions: Infusion of AG during the shock period in normotensive animals caused a transient increase in MAP, however, after 1-h it returned to the base level [Figure 2a]. In hypertensive animals, AG increased MAP, although it was not statistically significant [Figure 2b]. Administration of AG caused an increase of HR in normotensive and hypertensive animals (P < 0.05) [Figure 2c and d].


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

Barmaki B, Khazaei M - Int J Appl Basic Med Res (2015 Jan-Apr)

Effect of aminoguanidine on mean arterial pressure and heart rate in normotensive (a and c) and hypertensive (b and d) rats
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4318093&req=5

Figure 2: Effect of aminoguanidine on mean arterial pressure and heart rate in normotensive (a and c) and hypertensive (b and d) rats
Mentions: Infusion of AG during the shock period in normotensive animals caused a transient increase in MAP, however, after 1-h it returned to the base level [Figure 2a]. In hypertensive animals, AG increased MAP, although it was not statistically significant [Figure 2b]. Administration of AG caused an increase of HR in normotensive and hypertensive animals (P < 0.05) [Figure 2c and d].

Bottom Line: 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.No significant differences observed in survival rate between AG-treated and not treated groups.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Zabol University of Medical Sciences, Zabol, Iran.

ABSTRACT

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.

No MeSH data available.


Related in: MedlinePlus