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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

Light micrographs of multiple organs from hemorrhagic shocked rats. (a-c) Heart section showing foci of hemorrhage, esoinophilic contraction of some cardiac muscles and a few inflammatory cell infiltrations around blood vessels, H and E, ×200, ×200 and ×400. (d and e) Lung section with evidence of intra-alveolar edema, congested capillaries and expansion of the interstitium, H and E, ×100 and ×400. (f) Intestinal section showing intestinal mucosa revealing hemorrhagic necrosis and infiltration of mucosa by mononuclear cells and eosinophils with congestion of blood vessels, H and E, ×200. (g) Kidney section showing glomerular edema and congestion of blood vessels, H and E, ×400
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Figure 3: Light micrographs of multiple organs from hemorrhagic shocked rats. (a-c) Heart section showing foci of hemorrhage, esoinophilic contraction of some cardiac muscles and a few inflammatory cell infiltrations around blood vessels, H and E, ×200, ×200 and ×400. (d and e) Lung section with evidence of intra-alveolar edema, congested capillaries and expansion of the interstitium, H and E, ×100 and ×400. (f) Intestinal section showing intestinal mucosa revealing hemorrhagic necrosis and infiltration of mucosa by mononuclear cells and eosinophils with congestion of blood vessels, H and E, ×200. (g) Kidney section showing glomerular edema and congestion of blood vessels, H and E, ×400

Mentions: Contraction bands were observed in the H and E-stained sections of the myocardium from hemorrhagic-shocked rats [Figure 3a–c]. This damage was less apparent in sections from hemorrhagic shocked hearts treated with AG [Figure 4a].


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)

Light micrographs of multiple organs from hemorrhagic shocked rats. (a-c) Heart section showing foci of hemorrhage, esoinophilic contraction of some cardiac muscles and a few inflammatory cell infiltrations around blood vessels, H and E, ×200, ×200 and ×400. (d and e) Lung section with evidence of intra-alveolar edema, congested capillaries and expansion of the interstitium, H and E, ×100 and ×400. (f) Intestinal section showing intestinal mucosa revealing hemorrhagic necrosis and infiltration of mucosa by mononuclear cells and eosinophils with congestion of blood vessels, H and E, ×200. (g) Kidney section showing glomerular edema and congestion of blood vessels, H and E, ×400
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 3: Light micrographs of multiple organs from hemorrhagic shocked rats. (a-c) Heart section showing foci of hemorrhage, esoinophilic contraction of some cardiac muscles and a few inflammatory cell infiltrations around blood vessels, H and E, ×200, ×200 and ×400. (d and e) Lung section with evidence of intra-alveolar edema, congested capillaries and expansion of the interstitium, H and E, ×100 and ×400. (f) Intestinal section showing intestinal mucosa revealing hemorrhagic necrosis and infiltration of mucosa by mononuclear cells and eosinophils with congestion of blood vessels, H and E, ×200. (g) Kidney section showing glomerular edema and congestion of blood vessels, H and E, ×400
Mentions: Contraction bands were observed in the H and E-stained sections of the myocardium from hemorrhagic-shocked rats [Figure 3a–c]. This damage was less apparent in sections from hemorrhagic shocked hearts treated with AG [Figure 4a].

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