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Role of p38 mitogen-activated protein kinase on cardiac dysfunction after hemorrhagic shock in rats.
Shock. 2007 Sep; 28(3):291-9.S

Abstract

Cardiac dysfunction is a well-known complication of hemorrhagic shock as a consequence of local inflammatory response. Several studies have indicated that p38 mitogen-activated protein kinase (MAPK) is a key mediator in organ dysfunction that is associated with the inflammatory state through the activation of proinflammatory cytokines such as TNF-alpha and IL-1beta. Whether the same applies to cardiac dysfunction after hemorrhagic shock has not been clearly determined. Therefore, in this study, the role of p38 MAPK on cardiac dysfunction after hemorrhagic shock was studied up to 5 h after a hemorrhage using FR167653, a specific inhibitor of p38 MAPK phosphorylation. The p38 MAPK phosphorylation, the cardiac mRNA expressions of TNF-alpha and IL-1beta, and intracardiac serum concentrations of each cytokine and creatine phosphokinase-MB isozyme increased after a hemorrhage. Activated neutrophil accumulation in the heart, histological inflammation-related injuries, and frequent ventricular arrhythmia were observed in the late phase after hemorrhagic shock. FR167653 inhibited these hemorrhagic changes except the induction of the primary hypotensive state. These results demonstrate that p38 MAPK phosphorylation in hemorrhagic shock plays an important role in the cardiac expression of the proinflammatory cytokines and in the development of cardiac dysfunction relative to the inflammatory responses.

Authors+Show Affiliations

Department of Forensic Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, Kitakyushu, 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

17545949

Citation

Sato, Hiroaki, et al. "Role of P38 Mitogen-activated Protein Kinase On Cardiac Dysfunction After Hemorrhagic Shock in Rats." Shock (Augusta, Ga.), vol. 28, no. 3, 2007, pp. 291-9.
Sato H, Tanaka T, Kasai K, et al. Role of p38 mitogen-activated protein kinase on cardiac dysfunction after hemorrhagic shock in rats. Shock. 2007;28(3):291-9.
Sato, H., Tanaka, T., Kasai, K., Kita, T., & Tanaka, N. (2007). Role of p38 mitogen-activated protein kinase on cardiac dysfunction after hemorrhagic shock in rats. Shock (Augusta, Ga.), 28(3), 291-9.
Sato H, et al. Role of P38 Mitogen-activated Protein Kinase On Cardiac Dysfunction After Hemorrhagic Shock in Rats. Shock. 2007;28(3):291-9. PubMed PMID: 17545949.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of p38 mitogen-activated protein kinase on cardiac dysfunction after hemorrhagic shock in rats. AU - Sato,Hiroaki, AU - Tanaka,Toshiko, AU - Kasai,Kentaro, AU - Kita,Toshiro, AU - Tanaka,Noriyuki, PY - 2007/6/5/pubmed PY - 2007/10/16/medline PY - 2007/6/5/entrez SP - 291 EP - 9 JF - Shock (Augusta, Ga.) JO - Shock VL - 28 IS - 3 N2 - Cardiac dysfunction is a well-known complication of hemorrhagic shock as a consequence of local inflammatory response. Several studies have indicated that p38 mitogen-activated protein kinase (MAPK) is a key mediator in organ dysfunction that is associated with the inflammatory state through the activation of proinflammatory cytokines such as TNF-alpha and IL-1beta. Whether the same applies to cardiac dysfunction after hemorrhagic shock has not been clearly determined. Therefore, in this study, the role of p38 MAPK on cardiac dysfunction after hemorrhagic shock was studied up to 5 h after a hemorrhage using FR167653, a specific inhibitor of p38 MAPK phosphorylation. The p38 MAPK phosphorylation, the cardiac mRNA expressions of TNF-alpha and IL-1beta, and intracardiac serum concentrations of each cytokine and creatine phosphokinase-MB isozyme increased after a hemorrhage. Activated neutrophil accumulation in the heart, histological inflammation-related injuries, and frequent ventricular arrhythmia were observed in the late phase after hemorrhagic shock. FR167653 inhibited these hemorrhagic changes except the induction of the primary hypotensive state. These results demonstrate that p38 MAPK phosphorylation in hemorrhagic shock plays an important role in the cardiac expression of the proinflammatory cytokines and in the development of cardiac dysfunction relative to the inflammatory responses. SN - 1073-2322 UR - https://www.unboundmedicine.com/medline/citation/17545949/Role_of_p38_mitogen_activated_protein_kinase_on_cardiac_dysfunction_after_hemorrhagic_shock_in_rats_ L2 - https://doi.org/10.1097/SHK.0b013e3180326e3d DB - PRIME DP - Unbound Medicine ER -