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Rosiglitazone protects against severe hemorrhagic shock-induced organ damage in rats.

Yang FL, Subeq YM, Lee CJ, Lee RP, Peng TC, Harn HJ, Hsu BG - Med. Sci. Monit. (2011)

Bottom Line: The molecular mechanism of biologic responses to rosiglitazone has an anti-inflammatory effect.HS significantly increased blood GOT, GPT, BUN, Cre, LDH, CPK, lactate, glucose, TNF-alpha, IL-6 and MCP-1 levels, induced tachycardia, and decreased mean arterial pressure (MAP) in rats.Treatment with rosiglitazone improved survival rate, decreased the markers of organ injury, and suppressed the release of TNF-alpha, IL-6, and MCP-1 after HS in rats.

View Article: PubMed Central - PubMed

Affiliation: School of Medicine, Tzu Chi University, Hualien, Taiwan.

ABSTRACT

Background: Hemorrhagic shock (HS) followed by resuscitation can induce the production of several inflammatory mediators and lead to multiple organ dysfunction. The molecular mechanism of biologic responses to rosiglitazone has an anti-inflammatory effect. The present study was designed to investigate the effects of rosiglitazone on physiopathology and inflammatory mediators after HS in rats.

Material/methods: HS was induced in rats by withdrawing 60% of the total blood volume from a femoral artery catheter, immediately followed by intravenous injection of 0.3 mg/kg rosiglitazone. Mean arterial pressure (MAP) and heart rate (HR) were monitored continuously for 12 h. Levels of biochemical parameters, including GOT, GPT, BUN, Cre, LDH, CPK, and lactate were measured at 30 min before induction of HS and 0, 1, 3, 6, 9, and 12 h after HS, while an equal volume of normal saline was replaced as fluid resuscitation. Inflammatory mediators, including tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1), were measured in serum at 1 and 12 h after HS. The kidneys, liver, lungs, and small intestine were removed for histological assessment by hematoxylin and eosin stained at 48 h after HS.

Results: HS significantly increased blood GOT, GPT, BUN, Cre, LDH, CPK, lactate, glucose, TNF-alpha, IL-6 and MCP-1 levels, induced tachycardia, and decreased mean arterial pressure (MAP) in rats. Treatment with rosiglitazone improved survival rate, decreased the markers of organ injury, and suppressed the release of TNF-alpha, IL-6, and MCP-1 after HS in rats.

Conclusions: Treatment with rosiglitazone suppresses the release of serum TNF-alpha, IL-6 and MCP-1, and ameliorates HS-induced organ damage in rats.

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Related in: MedlinePlus

Survival curves (A), mean artery pressure (MAP) (B) and heart rate (HR) (C) after hemorrhagic shock in rats. *P<0.05 for the HS group compared with the Control group. #P<0.05 for the Rosiglitazone + HS group compared with the HS group.
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f1-medscimonit-17-10-br282: Survival curves (A), mean artery pressure (MAP) (B) and heart rate (HR) (C) after hemorrhagic shock in rats. *P<0.05 for the HS group compared with the Control group. #P<0.05 for the Rosiglitazone + HS group compared with the HS group.

Mentions: All rats were alive at 12 h after induction of HS. However, in the Rosiglitazone + HS group the rats were dead by 18 h after induction of HS, and in the HS group the rats were dead by 24 h after induction of HS. The survival rate at 48 h after induction of HS was 50% in the HS group, 100% in the Control group, 100% in the Rosiglitazone group, and 75% in the Rosiglitazone + HS group (Figure 1A). The mortality rate between groups in the Rosiglitazone + HS group was significantly lower than in the HS groups (log rank test; p=0.021). Mean arterial pressure (MAP) decreased rapidly after withdrawal of 60% of total blood volume from the femoral arterial catheter in rats. MAP stayed relatively low during 12 h after induction of HS (Figure 1B). Compared with the HS group, treatment with rosiglitazone did not affect the MAP after HS (Figure 1B). The heart rate (HR) was significantly increased during HS (Figure 1C). Compared with the HS group, HR in the rosiglitazone + HS group did not change after HS (Figure 1C).


Rosiglitazone protects against severe hemorrhagic shock-induced organ damage in rats.

Yang FL, Subeq YM, Lee CJ, Lee RP, Peng TC, Harn HJ, Hsu BG - Med. Sci. Monit. (2011)

Survival curves (A), mean artery pressure (MAP) (B) and heart rate (HR) (C) after hemorrhagic shock in rats. *P<0.05 for the HS group compared with the Control group. #P<0.05 for the Rosiglitazone + HS group compared with the HS group.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3539481&req=5

f1-medscimonit-17-10-br282: Survival curves (A), mean artery pressure (MAP) (B) and heart rate (HR) (C) after hemorrhagic shock in rats. *P<0.05 for the HS group compared with the Control group. #P<0.05 for the Rosiglitazone + HS group compared with the HS group.
Mentions: All rats were alive at 12 h after induction of HS. However, in the Rosiglitazone + HS group the rats were dead by 18 h after induction of HS, and in the HS group the rats were dead by 24 h after induction of HS. The survival rate at 48 h after induction of HS was 50% in the HS group, 100% in the Control group, 100% in the Rosiglitazone group, and 75% in the Rosiglitazone + HS group (Figure 1A). The mortality rate between groups in the Rosiglitazone + HS group was significantly lower than in the HS groups (log rank test; p=0.021). Mean arterial pressure (MAP) decreased rapidly after withdrawal of 60% of total blood volume from the femoral arterial catheter in rats. MAP stayed relatively low during 12 h after induction of HS (Figure 1B). Compared with the HS group, treatment with rosiglitazone did not affect the MAP after HS (Figure 1B). The heart rate (HR) was significantly increased during HS (Figure 1C). Compared with the HS group, HR in the rosiglitazone + HS group did not change after HS (Figure 1C).

Bottom Line: The molecular mechanism of biologic responses to rosiglitazone has an anti-inflammatory effect.HS significantly increased blood GOT, GPT, BUN, Cre, LDH, CPK, lactate, glucose, TNF-alpha, IL-6 and MCP-1 levels, induced tachycardia, and decreased mean arterial pressure (MAP) in rats.Treatment with rosiglitazone improved survival rate, decreased the markers of organ injury, and suppressed the release of TNF-alpha, IL-6, and MCP-1 after HS in rats.

View Article: PubMed Central - PubMed

Affiliation: School of Medicine, Tzu Chi University, Hualien, Taiwan.

ABSTRACT

Background: Hemorrhagic shock (HS) followed by resuscitation can induce the production of several inflammatory mediators and lead to multiple organ dysfunction. The molecular mechanism of biologic responses to rosiglitazone has an anti-inflammatory effect. The present study was designed to investigate the effects of rosiglitazone on physiopathology and inflammatory mediators after HS in rats.

Material/methods: HS was induced in rats by withdrawing 60% of the total blood volume from a femoral artery catheter, immediately followed by intravenous injection of 0.3 mg/kg rosiglitazone. Mean arterial pressure (MAP) and heart rate (HR) were monitored continuously for 12 h. Levels of biochemical parameters, including GOT, GPT, BUN, Cre, LDH, CPK, and lactate were measured at 30 min before induction of HS and 0, 1, 3, 6, 9, and 12 h after HS, while an equal volume of normal saline was replaced as fluid resuscitation. Inflammatory mediators, including tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1), were measured in serum at 1 and 12 h after HS. The kidneys, liver, lungs, and small intestine were removed for histological assessment by hematoxylin and eosin stained at 48 h after HS.

Results: HS significantly increased blood GOT, GPT, BUN, Cre, LDH, CPK, lactate, glucose, TNF-alpha, IL-6 and MCP-1 levels, induced tachycardia, and decreased mean arterial pressure (MAP) in rats. Treatment with rosiglitazone improved survival rate, decreased the markers of organ injury, and suppressed the release of TNF-alpha, IL-6, and MCP-1 after HS in rats.

Conclusions: Treatment with rosiglitazone suppresses the release of serum TNF-alpha, IL-6 and MCP-1, and ameliorates HS-induced organ damage in rats.

Show MeSH
Related in: MedlinePlus