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Heavy ethanol intoxication increases proinflammatory cytokines and aggravates hemorrhagic shock-induced organ damage in rats.
Mediators Inflamm. 2013; 2013:121786.MI

Abstract

Hemorrhagic shock (HS) following acute alcohol intoxication can increase proinflammatory cytokine production and induce marked immunosuppression. We investigated the effects of ethanol on physiopathology and cytokine levels following HS in acutely alcohol-intoxicated rats. Rats received an intravenous injection of 5 g/kg ethanol over 3 h followed by HS induced by withdrawal of 40% of total blood volume from a femoral arterial catheter over 30 min. Mean arterial pressure (MAP) and heart rate (HR) were monitored continuously for 48 h after the start of blood withdrawal. Biochemical parameters, including hemoglobin, ethanol, glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), blood urea nitrogen (BUN), creatinine (Cre), lactic dehydrogenase (LDH), and creatine phosphokinase (CPK), were measured at 30 min before induction of HS and 0, 1, 3, 6, 9, 12, 18, 24, and 48 h after HS. Serum tumor necrosis factor- α (TNF- α) and interleukin-6 (IL-6) levels were measured at 1 and 12 h after HS. The liver, kidneys, and lungs were removed for pathology at 48 h later. HS significantly increased HR, blood GOT, GPT, BUN, Cre, LDH, CPK, TNF- α , and IL-6 levels and decreased hemoglobin and MAP in rats. Acute ethanol intoxication further increased serum levels of GOT, GPT, BUN, Cre, LDH, CPK, TNF- α and IL-6 elevation following HS. Acutely intoxicated rats exacerbated the histopathologic changes in the liver, kidneys, and lungs following HS.

Authors+Show Affiliations

Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan ; Department of Psychiatry, Yuli Veterans Hospital, Hualien, Taiwan.No affiliation info availableNo 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

24163503

Citation

Hu, Tsung-Ming, et al. "Heavy Ethanol Intoxication Increases Proinflammatory Cytokines and Aggravates Hemorrhagic Shock-induced Organ Damage in Rats." Mediators of Inflammation, vol. 2013, 2013, p. 121786.
Hu TM, Lee RP, Lee CJ, et al. Heavy ethanol intoxication increases proinflammatory cytokines and aggravates hemorrhagic shock-induced organ damage in rats. Mediators Inflamm. 2013;2013:121786.
Hu, T. M., Lee, R. P., Lee, C. J., Subeq, Y. M., Lin, N. T., & Hsu, B. G. (2013). Heavy ethanol intoxication increases proinflammatory cytokines and aggravates hemorrhagic shock-induced organ damage in rats. Mediators of Inflammation, 2013, 121786. https://doi.org/10.1155/2013/121786
Hu TM, et al. Heavy Ethanol Intoxication Increases Proinflammatory Cytokines and Aggravates Hemorrhagic Shock-induced Organ Damage in Rats. Mediators Inflamm. 2013;2013:121786. PubMed PMID: 24163503.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Heavy ethanol intoxication increases proinflammatory cytokines and aggravates hemorrhagic shock-induced organ damage in rats. AU - Hu,Tsung-Ming, AU - Lee,Ru-Ping, AU - Lee,Chung-Jen, AU - Subeq,Yi-Maun, AU - Lin,Nien-Tsung, AU - Hsu,Bang-Gee, Y1 - 2013/09/12/ PY - 2013/04/15/received PY - 2013/07/02/revised PY - 2013/08/13/accepted PY - 2013/10/29/entrez PY - 2013/10/29/pubmed PY - 2014/6/6/medline SP - 121786 EP - 121786 JF - Mediators of inflammation JO - Mediators Inflamm VL - 2013 N2 - Hemorrhagic shock (HS) following acute alcohol intoxication can increase proinflammatory cytokine production and induce marked immunosuppression. We investigated the effects of ethanol on physiopathology and cytokine levels following HS in acutely alcohol-intoxicated rats. Rats received an intravenous injection of 5 g/kg ethanol over 3 h followed by HS induced by withdrawal of 40% of total blood volume from a femoral arterial catheter over 30 min. Mean arterial pressure (MAP) and heart rate (HR) were monitored continuously for 48 h after the start of blood withdrawal. Biochemical parameters, including hemoglobin, ethanol, glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), blood urea nitrogen (BUN), creatinine (Cre), lactic dehydrogenase (LDH), and creatine phosphokinase (CPK), were measured at 30 min before induction of HS and 0, 1, 3, 6, 9, 12, 18, 24, and 48 h after HS. Serum tumor necrosis factor- α (TNF- α) and interleukin-6 (IL-6) levels were measured at 1 and 12 h after HS. The liver, kidneys, and lungs were removed for pathology at 48 h later. HS significantly increased HR, blood GOT, GPT, BUN, Cre, LDH, CPK, TNF- α , and IL-6 levels and decreased hemoglobin and MAP in rats. Acute ethanol intoxication further increased serum levels of GOT, GPT, BUN, Cre, LDH, CPK, TNF- α and IL-6 elevation following HS. Acutely intoxicated rats exacerbated the histopathologic changes in the liver, kidneys, and lungs following HS. SN - 1466-1861 UR - https://www.unboundmedicine.com/medline/citation/24163503/Heavy_ethanol_intoxication_increases_proinflammatory_cytokines_and_aggravates_hemorrhagic_shock_induced_organ_damage_in_rats_ L2 - https://doi.org/10.1155/2013/121786 DB - PRIME DP - Unbound Medicine ER -