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Role of tumor necrosis factor-alpha and interleukin-1beta on lung dysfunction following hemorrhagic shock in rats.
Med Sci Monit. 2008 May; 14(5):BR79-87.MS

Abstract

BACKGROUND

Hemorrhagic shock occasionally causes a fatal outcome following an outbreak of lung dysfunction, but the precise mechanism has not been clearly elucidated. Several studies have indicated that hemorrhagic shock causes a delayed vascular inflammatory decompensation and leads to inflammation-related organ dysfunction. Tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta are known as major proinflammatory cytokines that play an important role in excessive autolytic inflammation, finally inducing organ dysfunctions. In this study, the role of TNF-alpha and IL-1beta on lung dysfunction following hemorrhagic shock was examined by using FR167653, a potent inhibitor of TNF-alpha and IL-1beta production that acts by suppressing p38 mitogen-activated protein kinase (MAPK).

MATERIAL/METHODS

Hemorrhagic shock was induced in anesthetized male rats by bleeding via a common carotid catheter for 20 minutes to 25% of total body blood volume without fluid resuscitation. Mean blood pressure, heart rate and arterial blood gas components were recorded up to 5 hours after the bleeding. The levels of TNF-alpha, IL-1beta and lactic dehydrogenase (LDH)-3 isozyme were measured in the serum of pulmonary venous blood. The lung tissue was excised for the assay of mRNA and for histopathological study.

RESULTS

The expressions of mRNA for TNF-alpha and IL-1beta in the lung tissue and the concentrations of both cytokines in pulmonary serum increased after a hemorrhage. Inflammation-related injuries and function deterioration were observed in the lung following hemorrhagic shock. These hemorrhagic changes were inhibited by pretreatment with FR167653.

CONCLUSIONS

TNF-alpha and IL-1beta play a key role in the development of inflammation-related lung dysfunction following hemorrhagic shock. Our model should be useful to explain the pathogenesis of lung dysfunction following hemorrhagic shock.

Authors+Show Affiliations

Department of Forensic Medicine, School of Medicine, University of Occupational and Environmental Health, Japan. h-sato@med.uoeh-u.ac.jpNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18443542

Citation

Sato, Hiroaki, et al. "Role of Tumor Necrosis Factor-alpha and Interleukin-1beta On Lung Dysfunction Following Hemorrhagic Shock in Rats." Medical Science Monitor : International Medical Journal of Experimental and Clinical Research, vol. 14, no. 5, 2008, pp. BR79-87.
Sato H, Kasai K, Tanaka T, et al. Role of tumor necrosis factor-alpha and interleukin-1beta on lung dysfunction following hemorrhagic shock in rats. Med Sci Monit. 2008;14(5):BR79-87.
Sato, H., Kasai, K., Tanaka, T., Kita, T., & Tanaka, N. (2008). Role of tumor necrosis factor-alpha and interleukin-1beta on lung dysfunction following hemorrhagic shock in rats. Medical Science Monitor : International Medical Journal of Experimental and Clinical Research, 14(5), BR79-87.
Sato H, et al. Role of Tumor Necrosis Factor-alpha and Interleukin-1beta On Lung Dysfunction Following Hemorrhagic Shock in Rats. Med Sci Monit. 2008;14(5):BR79-87. PubMed PMID: 18443542.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of tumor necrosis factor-alpha and interleukin-1beta on lung dysfunction following hemorrhagic shock in rats. AU - Sato,Hiroaki, AU - Kasai,Kentaro, AU - Tanaka,Toshiko, AU - Kita,Toshiro, AU - Tanaka,Noriyuki, PY - 2008/4/30/pubmed PY - 2008/8/12/medline PY - 2008/4/30/entrez SP - BR79 EP - 87 JF - Medical science monitor : international medical journal of experimental and clinical research JO - Med Sci Monit VL - 14 IS - 5 N2 - BACKGROUND: Hemorrhagic shock occasionally causes a fatal outcome following an outbreak of lung dysfunction, but the precise mechanism has not been clearly elucidated. Several studies have indicated that hemorrhagic shock causes a delayed vascular inflammatory decompensation and leads to inflammation-related organ dysfunction. Tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta are known as major proinflammatory cytokines that play an important role in excessive autolytic inflammation, finally inducing organ dysfunctions. In this study, the role of TNF-alpha and IL-1beta on lung dysfunction following hemorrhagic shock was examined by using FR167653, a potent inhibitor of TNF-alpha and IL-1beta production that acts by suppressing p38 mitogen-activated protein kinase (MAPK). MATERIAL/METHODS: Hemorrhagic shock was induced in anesthetized male rats by bleeding via a common carotid catheter for 20 minutes to 25% of total body blood volume without fluid resuscitation. Mean blood pressure, heart rate and arterial blood gas components were recorded up to 5 hours after the bleeding. The levels of TNF-alpha, IL-1beta and lactic dehydrogenase (LDH)-3 isozyme were measured in the serum of pulmonary venous blood. The lung tissue was excised for the assay of mRNA and for histopathological study. RESULTS: The expressions of mRNA for TNF-alpha and IL-1beta in the lung tissue and the concentrations of both cytokines in pulmonary serum increased after a hemorrhage. Inflammation-related injuries and function deterioration were observed in the lung following hemorrhagic shock. These hemorrhagic changes were inhibited by pretreatment with FR167653. CONCLUSIONS: TNF-alpha and IL-1beta play a key role in the development of inflammation-related lung dysfunction following hemorrhagic shock. Our model should be useful to explain the pathogenesis of lung dysfunction following hemorrhagic shock. SN - 1234-1010 UR - https://www.unboundmedicine.com/medline/citation/18443542/Role_of_tumor_necrosis_factor_alpha_and_interleukin_1beta_on_lung_dysfunction_following_hemorrhagic_shock_in_rats_ L2 - https://www.medscimonit.com/download/index/idArt/855744 DB - PRIME DP - Unbound Medicine ER -