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.