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Fluvastatin attenuates severe hemorrhagic shock-induced organ damage in rats.
Resuscitation. 2009 Mar; 80(3):372-8.R

Abstract

OBJECTIVES

Multiple organ dysfunction resulting from hemorrhagic shock (HS) and subsequent resuscitation was mediated by several inflammatory factors such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10). The present study was designed to investigate the protective effects of fluvastatin on these mediators after HS in rats.

METHODS

The experimental rats were randomly divided into three groups. The vehicle group received only vitamin K without HS, the HS-control group received vitamin K and HS, and the HS-experimental group received both vitamin K and fluvastatin (1mg/kg) before HS. HS was produced by bleeding from a femoral arterial catheter to remove 60% of total blood volume (6ml/100g BW) over 30min. The mean arterial pressure (MAP) and heart rate (HR) were monitored continuously for 12h after the start of blood withdrawal. The biochemical parameters, including arterial blood gas, glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), blood urea nitrogen (BUN), creatinine (Cre), lactic dehydrogenase (LDH), creatine phosphokinase (CPK), and lactate were obtained at 30min before induction of HS and at 0, 1, 3, 6, 9 and 12h after HS. Equal volume of normal saline was given to replace blood volume loss. Cytokine levels including TNF-alpha and IL-10 in serum were measured at 1h after HS. Kidney, liver, lung and small intestine were removed for pathology examination at 48h after HS.

RESULTS

HS significantly increased HR, blood GOT, GPT, BUN, Cre, LDH, CPK, lactate, TNF-alpha and IL-10 levels, and also induced metabolic acidosis and decreased MAP in rats. Pre-treatment with fluvastatin was found to improve survival rate, preserved MAP, decreased the markers of organ injury, suppressed the release of TNF-alpha and increased IL-10 after HS in rats.

CONCLUSION

Pre-treatment with fluvastatin can suppress the release of serum TNF-alpha and can also increase serum IL-10 level to protect HS-induced multi-organ damage in rats.

Authors+Show Affiliations

Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

19150166

Citation

Lee, Chia-Chi, et al. "Fluvastatin Attenuates Severe Hemorrhagic Shock-induced Organ Damage in Rats." Resuscitation, vol. 80, no. 3, 2009, pp. 372-8.
Lee CC, Lee RP, Subeq YM, et al. Fluvastatin attenuates severe hemorrhagic shock-induced organ damage in rats. Resuscitation. 2009;80(3):372-8.
Lee, C. C., Lee, R. P., Subeq, Y. M., Lee, C. J., Chen, T. M., & Hsu, B. G. (2009). Fluvastatin attenuates severe hemorrhagic shock-induced organ damage in rats. Resuscitation, 80(3), 372-8. https://doi.org/10.1016/j.resuscitation.2008.12.003
Lee CC, et al. Fluvastatin Attenuates Severe Hemorrhagic Shock-induced Organ Damage in Rats. Resuscitation. 2009;80(3):372-8. PubMed PMID: 19150166.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fluvastatin attenuates severe hemorrhagic shock-induced organ damage in rats. AU - Lee,Chia-Chi, AU - Lee,Ru-Ping, AU - Subeq,Yi-Maun, AU - Lee,Chung-Jen, AU - Chen,Tse-Min, AU - Hsu,Bang-Gee, Y1 - 2009/01/15/ PY - 2008/05/26/received PY - 2008/11/30/revised PY - 2008/12/03/accepted PY - 2009/1/20/entrez PY - 2009/1/20/pubmed PY - 2009/4/9/medline SP - 372 EP - 8 JF - Resuscitation JO - Resuscitation VL - 80 IS - 3 N2 - OBJECTIVES: Multiple organ dysfunction resulting from hemorrhagic shock (HS) and subsequent resuscitation was mediated by several inflammatory factors such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10). The present study was designed to investigate the protective effects of fluvastatin on these mediators after HS in rats. METHODS: The experimental rats were randomly divided into three groups. The vehicle group received only vitamin K without HS, the HS-control group received vitamin K and HS, and the HS-experimental group received both vitamin K and fluvastatin (1mg/kg) before HS. HS was produced by bleeding from a femoral arterial catheter to remove 60% of total blood volume (6ml/100g BW) over 30min. The mean arterial pressure (MAP) and heart rate (HR) were monitored continuously for 12h after the start of blood withdrawal. The biochemical parameters, including arterial blood gas, glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), blood urea nitrogen (BUN), creatinine (Cre), lactic dehydrogenase (LDH), creatine phosphokinase (CPK), and lactate were obtained at 30min before induction of HS and at 0, 1, 3, 6, 9 and 12h after HS. Equal volume of normal saline was given to replace blood volume loss. Cytokine levels including TNF-alpha and IL-10 in serum were measured at 1h after HS. Kidney, liver, lung and small intestine were removed for pathology examination at 48h after HS. RESULTS: HS significantly increased HR, blood GOT, GPT, BUN, Cre, LDH, CPK, lactate, TNF-alpha and IL-10 levels, and also induced metabolic acidosis and decreased MAP in rats. Pre-treatment with fluvastatin was found to improve survival rate, preserved MAP, decreased the markers of organ injury, suppressed the release of TNF-alpha and increased IL-10 after HS in rats. CONCLUSION: Pre-treatment with fluvastatin can suppress the release of serum TNF-alpha and can also increase serum IL-10 level to protect HS-induced multi-organ damage in rats. SN - 0300-9572 UR - https://www.unboundmedicine.com/medline/citation/19150166/Fluvastatin_attenuates_severe_hemorrhagic_shock_induced_organ_damage_in_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0300-9572(08)00835-6 DB - PRIME DP - Unbound Medicine ER -