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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

Electron microscopic analyses. (a-c) Hemorrhage untreated hearts showing mitochondrial swelling with disrupted cristae, ×2000, ×2500, ×800. (d-f) Aminoguanidine treated hearts showing mild mitochondrial swelling with clear cristae, ×2500, ×4000, ×1000
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Figure 5: Electron microscopic analyses. (a-c) Hemorrhage untreated hearts showing mitochondrial swelling with disrupted cristae, ×2000, ×2500, ×800. (d-f) Aminoguanidine treated hearts showing mild mitochondrial swelling with clear cristae, ×2500, ×4000, ×1000

Mentions: Electron microscopy was performed in randomly selected hearts from the in vivo hemorrhage treated and untreated groups [Figure 5]. The hemorrhage group showed prominent I bands and swollen mitochondria with disrupted cristae and amorphous matrix densities. However, no such changes were seen in the treated group. Significant inflammatory cell infiltrates around the coronary vessels was found in the untreated group.


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)

Electron microscopic analyses. (a-c) Hemorrhage untreated hearts showing mitochondrial swelling with disrupted cristae, ×2000, ×2500, ×800. (d-f) Aminoguanidine treated hearts showing mild mitochondrial swelling with clear cristae, ×2500, ×4000, ×1000
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 5: Electron microscopic analyses. (a-c) Hemorrhage untreated hearts showing mitochondrial swelling with disrupted cristae, ×2000, ×2500, ×800. (d-f) Aminoguanidine treated hearts showing mild mitochondrial swelling with clear cristae, ×2500, ×4000, ×1000
Mentions: Electron microscopy was performed in randomly selected hearts from the in vivo hemorrhage treated and untreated groups [Figure 5]. The hemorrhage group showed prominent I bands and swollen mitochondria with disrupted cristae and amorphous matrix densities. However, no such changes were seen in the treated group. Significant inflammatory cell infiltrates around the coronary vessels was found in the untreated group.

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