Limits...
Effects of aminoguanidine, a potent nitric oxide synthase inhibitor, on myocardial and organ structure in a rat model of hemorrhagic shock.

Soliman MM - J Emerg Trauma Shock (2014)

Bottom Line: We examined the protective effects of a potent inhibitor of NO synthase, aminoguanidine (AG), on myocardial and multiple organ structure in a rat model of HS.Biopsy samples were taken for light and electron microscopy.AG-treatment decreased the number of inflammatory cells and mitochondrial swollen in myocardial cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, College of Medicine, King Saud University, Riyadh 11461, Saudi Arabia.

ABSTRACT

Background: Nitric oxide (NO) has been shown to increase following hemorrhagic shock (HS). Peroxynitrite is produced by the reaction of NO with reactive oxygen species, leads to nitrosative stress mediated organ injury. We examined the protective effects of a potent inhibitor of NO synthase, aminoguanidine (AG), on myocardial and multiple organ structure in a rat model of HS.

Materials and methods: Male Sprague Dawley rats (300-350 g) were assigned to 3 experimental groups (n = 6 per group): (1) Normotensive rats (N), (2) HS rats and (3) HS rats treated with AG (HS-AG). Rats were hemorrhaged over 60 min to reach a mean arterial blood pressure of 40 mmHg. Rats were treated with 1 ml of 60 mg/kg AG intra-arterially after 60 min HS. Resuscitation was performed in vivo by the reinfusion of the shed blood for 30 min to restore normo-tension. Biopsy samples were taken for light and electron microscopy.

Results: Histological examination of hemorrhagic shocked untreated rats revealed structural damage. Less histological damage was observed in multiple organs in AG-treated rats. AG-treatment decreased the number of inflammatory cells and mitochondrial swollen in myocardial cells.

Conclusion: AG treatment reduced microscopic damage and injury in multiple organs in a HS model in rats.

No MeSH data available.


Related in: MedlinePlus

Effects of in vivo treatment with aminoguanidine (AG) on mean arterial blood pressure in rats (a and b). Recording of arterial blood pressure after 1 h hemorrhages (a) and 30 min of resuscitation (b) in the normotensive group (N), hemorrhage group hemorrhagic shock (HS), hemorrhage group treated with AG (HS-AG). *represents P < 0.05 versus hemorrhagic shock resuscitated group treated and not treated
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4126120&req=5

Figure 1: Effects of in vivo treatment with aminoguanidine (AG) on mean arterial blood pressure in rats (a and b). Recording of arterial blood pressure after 1 h hemorrhages (a) and 30 min of resuscitation (b) in the normotensive group (N), hemorrhage group hemorrhagic shock (HS), hemorrhage group treated with AG (HS-AG). *represents P < 0.05 versus hemorrhagic shock resuscitated group treated and not treated

Mentions: Three experimental groups (n = 6) were assigned for the study [Figure 1]:


Effects of aminoguanidine, a potent nitric oxide synthase inhibitor, on myocardial and organ structure in a rat model of hemorrhagic shock.

Soliman MM - J Emerg Trauma Shock (2014)

Effects of in vivo treatment with aminoguanidine (AG) on mean arterial blood pressure in rats (a and b). Recording of arterial blood pressure after 1 h hemorrhages (a) and 30 min of resuscitation (b) in the normotensive group (N), hemorrhage group hemorrhagic shock (HS), hemorrhage group treated with AG (HS-AG). *represents P < 0.05 versus hemorrhagic shock resuscitated group treated and not treated
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4126120&req=5

Figure 1: Effects of in vivo treatment with aminoguanidine (AG) on mean arterial blood pressure in rats (a and b). Recording of arterial blood pressure after 1 h hemorrhages (a) and 30 min of resuscitation (b) in the normotensive group (N), hemorrhage group hemorrhagic shock (HS), hemorrhage group treated with AG (HS-AG). *represents P < 0.05 versus hemorrhagic shock resuscitated group treated and not treated
Mentions: Three experimental groups (n = 6) were assigned for the study [Figure 1]:

Bottom Line: We examined the protective effects of a potent inhibitor of NO synthase, aminoguanidine (AG), on myocardial and multiple organ structure in a rat model of HS.Biopsy samples were taken for light and electron microscopy.AG-treatment decreased the number of inflammatory cells and mitochondrial swollen in myocardial cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, College of Medicine, King Saud University, Riyadh 11461, Saudi Arabia.

ABSTRACT

Background: Nitric oxide (NO) has been shown to increase following hemorrhagic shock (HS). Peroxynitrite is produced by the reaction of NO with reactive oxygen species, leads to nitrosative stress mediated organ injury. We examined the protective effects of a potent inhibitor of NO synthase, aminoguanidine (AG), on myocardial and multiple organ structure in a rat model of HS.

Materials and methods: Male Sprague Dawley rats (300-350 g) were assigned to 3 experimental groups (n = 6 per group): (1) Normotensive rats (N), (2) HS rats and (3) HS rats treated with AG (HS-AG). Rats were hemorrhaged over 60 min to reach a mean arterial blood pressure of 40 mmHg. Rats were treated with 1 ml of 60 mg/kg AG intra-arterially after 60 min HS. Resuscitation was performed in vivo by the reinfusion of the shed blood for 30 min to restore normo-tension. Biopsy samples were taken for light and electron microscopy.

Results: Histological examination of hemorrhagic shocked untreated rats revealed structural damage. Less histological damage was observed in multiple organs in AG-treated rats. AG-treatment decreased the number of inflammatory cells and mitochondrial swollen in myocardial cells.

Conclusion: AG treatment reduced microscopic damage and injury in multiple organs in a HS model in rats.

No MeSH data available.


Related in: MedlinePlus