This Article Full Text (PDF) All Versions of this Article: 1099800409334750v1 11/2/152    most recent References Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Scopus Google Scholar Articles by Lee, C.-J. Articles by Hsu, B.-G. PubMed PubMed Citation Articles by Lee, C.-J. Articles by Hsu, B.-G. Social Bookmarking                         What's this?

Propofol Protects Against Hemorrhagic Shock-Induced Organ Damage in Conscious Spontaneously Hypertensive Rats

Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan

Ru-Ping Lee, PhD, RN

Department of Nursing, Tzu Chi University, Hualien, Taiwan

Yi-Maun Subeq, PhD, RN

Department of Nursing, Tzu Chi University, Hualien, Taiwan

Chia-Chi Lee, RN

Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan

Tai-Chu Peng, PhD, RN

Department of Nursing Tzu Chi College of Technology, Hualien, Taiwan

Bang-Gee Hsu, PhD, MD

School of Medicine, Tzu Chi University, Hualien, Taiwan, gee.lily{at}msa.hinet.net, Department of Nephrology Tzu Chi General Hospital, Hualien, Taiwan

Patients with hypertension have higher mortality rates from hemorrhagic shock (HS) than normotensive patients. Several inflammatory mediators such as tumor necrosis factor a (TNF-a) 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-a 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-a, and IL-10 levels in conscious SHRs. Posttreatment propofol decreased serum TNF-a 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.

Key Words: hemorrhagic shock • propofol • hypertension • conscious rat

This version was published on October 1, 2009

Biological Research For Nursing, Vol. 11, No. 2, 152-162 (2009)
DOI: 10.1177/1099800409334750


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?