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The Effects of Interleukin-10 in Hemorrhagic Shock

Identifieur interne : 002510 ( Main/Merge ); précédent : 002509; suivant : 002511

The Effects of Interleukin-10 in Hemorrhagic Shock

Auteurs : Stavros Karakozis ; Mcdonna Hinds ; James W. Cook ; Donald Kim ; Haydee Provido ; John R. Kirkpatrick

Source :

Journal of Surgical Research [ 0022-4804 ] ; 2000.

RBID : ISTEX:7AA610992D793397E490617B1E1CBF9BFDFE13D3

English descriptors

KwdEn :
- cytokine, inflammatory, sepsis, systemic, tumor necrosis factor.
Teeft :
- Academic press, Antigen expression, Arterial pressure, Baseline, Cannula, Carotid, Carotid cannula, Cytokine, Cytokine release, Equal volume, Experimental group, Experimental groups, Hemorrhagic, Hemorrhagic shock, Immunol, Interleukin, Kupffer cell antigen presentation, Lactate, Lactate levels, Medstar research institute, Necrotizing pancreatitis, Resuscitation, Sepsis, Septic complications, Serum lactate, Severe hemorrhagic shock, Shock period, Surgical, Surgical research, Survival rate, Trauma, Tumor necrosis factor, Wilcoxon test.

Abstract

Abstract: Background. Interleukin-10 (IL-10) counteracts the effects of the proinflammatory cytokines interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor (TNF). Experimental data suggest that inhibition of these proinflammatory cytokines improves outcome in sepsis, endotoxemia, necrotizing pancreatitis, and other severe inflammatory states. We hypothesized that the administration of IL-10 would attenuate the release of proinflammatory cytokines after severe hemorrhagic shock. Methods. To test our hypothesis, male Sprague–Dawley rats (N = 20) were divided into control and experimental groups. We induced hemorrhagic shock by removing a sufficient quantity of blood to maintain a mean arterial pressure of 50 mm Hg or less for 120 min. The animals were then resuscitated with shed blood and an equal volume of 0.9% saline. The experimental group received 10,000 units of IL-10 at the initiation of shock. Serum IL-1, IL-6, TNF, and lactate were measured at baseline, after 120 min of shock, and 60 min after resuscitation. The rats were followed for 72 h to calculate survival. Results. Similar levels of hypoperfusion were obtained in both groups as demonstrated by lactate levels and amount of shed blood. The survival rate (70%) was the same in both groups. Serum levels of IL-1 and IL-6 were not significantly different between the two groups, although there was a trend toward IL-6 suppression. TNF, however, was significantly lower in the IL-10-treated group at the end of shock (Wilcoxon test, P < 0.025). Conclusion. Administration of IL-10 suppresses the TNF surge observed after severe hemorrhagic shock.

Url:

https://api.istex.fr/ark:/67375/6H6-SFWBH29G-V/fulltext.pdf

DOI: 10.1006/jsre.2000.5860

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ISTEX:7AA610992D793397E490617B1E1CBF9BFDFE13D3

Le document en format XML

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<keywords scheme="Teeft" xml:lang="en"><term>Academic press</term>
<term>Antigen expression</term>
<term>Arterial pressure</term>
<term>Baseline</term>
<term>Cannula</term>
<term>Carotid</term>
<term>Carotid cannula</term>
<term>Cytokine</term>
<term>Cytokine release</term>
<term>Equal volume</term>
<term>Experimental group</term>
<term>Experimental groups</term>
<term>Hemorrhagic</term>
<term>Hemorrhagic shock</term>
<term>Immunol</term>
<term>Interleukin</term>
<term>Kupffer cell antigen presentation</term>
<term>Lactate</term>
<term>Lactate levels</term>
<term>Medstar research institute</term>
<term>Necrotizing pancreatitis</term>
<term>Resuscitation</term>
<term>Sepsis</term>
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<term>Shock period</term>
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<front><div type="abstract" xml:lang="en">Abstract: Background. Interleukin-10 (IL-10) counteracts the effects of the proinflammatory cytokines interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor (TNF). Experimental data suggest that inhibition of these proinflammatory cytokines improves outcome in sepsis, endotoxemia, necrotizing pancreatitis, and other severe inflammatory states. We hypothesized that the administration of IL-10 would attenuate the release of proinflammatory cytokines after severe hemorrhagic shock. Methods. To test our hypothesis, male Sprague–Dawley rats (N = 20) were divided into control and experimental groups. We induced hemorrhagic shock by removing a sufficient quantity of blood to maintain a mean arterial pressure of 50 mm Hg or less for 120 min. The animals were then resuscitated with shed blood and an equal volume of 0.9% saline. The experimental group received 10,000 units of IL-10 at the initiation of shock. Serum IL-1, IL-6, TNF, and lactate were measured at baseline, after 120 min of shock, and 60 min after resuscitation. The rats were followed for 72 h to calculate survival. Results. Similar levels of hypoperfusion were obtained in both groups as demonstrated by lactate levels and amount of shed blood. The survival rate (70%) was the same in both groups. Serum levels of IL-1 and IL-6 were not significantly different between the two groups, although there was a trend toward IL-6 suppression. TNF, however, was significantly lower in the IL-10-treated group at the end of shock (Wilcoxon test, P < 0.025). Conclusion. Administration of IL-10 suppresses the TNF surge observed after severe hemorrhagic shock.</div>
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The Effects of Interleukin-10 in Hemorrhagic Shock

The Effects of Interleukin-10 in Hemorrhagic Shock

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Abstract

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