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Propofol protects against hemorrhagic shock-induced organ damage in conscious spontaneously hypertensive rats.
Biol Res Nurs. 2009 Oct; 11(2):152-62.BR

Abstract

Patients with hypertension have higher mortality rates from hemorrhagic shock (HS) than normotensive patients. Several inflammatory mediators such as tumor necrosis factor alpha (TNF-alpha) and interleukin 10 (IL-10) can be produced by HS and lead to multiple organ dysfunction and death. We investigated the effects of high dose (10 mg/kg/hr) and low dose (1 mg/kg/hr) propofol treatment after HS in conscious spontaneously hypertensive rats (SHRs). By withdrawing 40% of total blood volume from a femoral arterial catheter (6 ml/100 g body weight [BW]) for more than 30 min, HS was induced. The mean arterial pressure (MAP) and heart rate (HR) were monitored continuously for 24 hr after the start of blood withdrawal. Levels of biochemical parameters, including glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), blood urea nitrogen (BUN), creatinine (Cre), creatine phosphokinase (CPK), and lactic dehydrogenase (LDH) were measured 30 min before and 0, 1, 3, 6, 9, 12, 18, and 24 hr after the 30-min blood withdrawal period. Cytokine levels, including TNF-alpha and IL-10 in the serum, were measured 1 hr after HS. The kidney, liver, and lung were removed for pathology assessment at 48 hr after HS. HS significantly increased blood GOT, GPT, BUN, LDH, CPK, TNF-alpha, and IL-10 levels in conscious SHRs. Posttreatment propofol decreased serum TNF-alpha level, increased serum IL-10 level, attenuated the severity of organ damage, and improved survival rate after HS. This treatment protected SHRs against HS-induced organ damage. Moreover, high-dose propofol had a more protective effect than low-dose propofol against HS in conscious SHRs.

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)

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

Language

eng

PubMed ID

19419978

Citation

Lee, Chung-Jen, et al. "Propofol Protects Against Hemorrhagic Shock-induced Organ Damage in Conscious Spontaneously Hypertensive Rats." Biological Research for Nursing, vol. 11, no. 2, 2009, pp. 152-62.
Lee CJ, Lee RP, Subeq YM, et al. Propofol protects against hemorrhagic shock-induced organ damage in conscious spontaneously hypertensive rats. Biol Res Nurs. 2009;11(2):152-62.
Lee, C. J., Lee, R. P., Subeq, Y. M., Lee, C. C., Peng, T. C., & Hsu, B. G. (2009). Propofol protects against hemorrhagic shock-induced organ damage in conscious spontaneously hypertensive rats. Biological Research for Nursing, 11(2), 152-62. https://doi.org/10.1177/1099800409334750
Lee CJ, et al. Propofol Protects Against Hemorrhagic Shock-induced Organ Damage in Conscious Spontaneously Hypertensive Rats. Biol Res Nurs. 2009;11(2):152-62. PubMed PMID: 19419978.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Propofol protects against hemorrhagic shock-induced organ damage in conscious spontaneously hypertensive rats. AU - Lee,Chung-Jen, AU - Lee,Ru-Ping, AU - Subeq,Yi-Maun, AU - Lee,Chia-Chi, AU - Peng,Tai-Chu, AU - Hsu,Bang-Gee, Y1 - 2009/05/05/ PY - 2009/5/8/entrez PY - 2009/5/8/pubmed PY - 2010/1/12/medline SP - 152 EP - 62 JF - Biological research for nursing JO - Biol Res Nurs VL - 11 IS - 2 N2 - Patients with hypertension have higher mortality rates from hemorrhagic shock (HS) than normotensive patients. Several inflammatory mediators such as tumor necrosis factor alpha (TNF-alpha) and interleukin 10 (IL-10) can be produced by HS and lead to multiple organ dysfunction and death. We investigated the effects of high dose (10 mg/kg/hr) and low dose (1 mg/kg/hr) propofol treatment after HS in conscious spontaneously hypertensive rats (SHRs). By withdrawing 40% of total blood volume from a femoral arterial catheter (6 ml/100 g body weight [BW]) for more than 30 min, HS was induced. The mean arterial pressure (MAP) and heart rate (HR) were monitored continuously for 24 hr after the start of blood withdrawal. Levels of biochemical parameters, including glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), blood urea nitrogen (BUN), creatinine (Cre), creatine phosphokinase (CPK), and lactic dehydrogenase (LDH) were measured 30 min before and 0, 1, 3, 6, 9, 12, 18, and 24 hr after the 30-min blood withdrawal period. Cytokine levels, including TNF-alpha and IL-10 in the serum, were measured 1 hr after HS. The kidney, liver, and lung were removed for pathology assessment at 48 hr after HS. HS significantly increased blood GOT, GPT, BUN, LDH, CPK, TNF-alpha, and IL-10 levels in conscious SHRs. Posttreatment propofol decreased serum TNF-alpha level, increased serum IL-10 level, attenuated the severity of organ damage, and improved survival rate after HS. This treatment protected SHRs against HS-induced organ damage. Moreover, high-dose propofol had a more protective effect than low-dose propofol against HS in conscious SHRs. SN - 1552-4175 UR - https://www.unboundmedicine.com/medline/citation/19419978/Propofol_protects_against_hemorrhagic_shock_induced_organ_damage_in_conscious_spontaneously_hypertensive_rats_ L2 - https://journals.sagepub.com/doi/10.1177/1099800409334750?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -