Effects of propofol on hemodynamic and inflammatory responses to endotoxemia in rats.

Abstract:

OBJECTIVE:To document the effects of propofol on the hemodynamic and inflammatory responses to endotoxemia in an animal model. DESIGN:Randomized, prospective laboratory study. SETTING:University experimental laboratory. SUBJECTS:Thirty-two male rats. INTERVENTIONS:The animals were randomly assigned to one of four groups: a) endotoxemia group (n = 8), which received intravenous Escherichia coli endotoxin (15 mg/kg over 2 mins); b) control group (n = 8), which was treated identically to the endotoxemia group except for the substitution of 0.9% saline for endotoxin; c) propofol group (n = 8), which was treated identically to the control group but also received propofol (10 mg/kg bolus, followed by infusion at 10 mg/kg/hr) immediately after the injection of 0.9% saline; and d) propofol-endotoxemia group (n = 8), which was treated identically to the endotoxemia group with the additional administration of propofol (10 mg/kg bolus, followed by infusion at 10 mg/kg/hr) immediately after endotoxin injection. MEASUREMENTS AND MAIN RESULTS:Hemodynamics, arterial blood gases, and acid-base status were recorded and the blood propofol concentrations and plasma cytokine concentrations were measured during the 5-hr observation. Microscopic findings of lung tissue for each group were obtained at necropsy. The systolic arterial pressure and heart rate of the propofol-endotoxemia group were similar to those of the endotoxemia group. The increases in the plasma cytokine (tumor necrosis factor, interleukin-6, and interleukin-10) concentrations, in the base deficit, and in the infiltration of neutrophils in the air space or vessel walls of the lungs were attenuated in the propofol-endotoxemia group compared with the endotoxemia group. CONCLUSIONS:Propofol attenuated cytokine responses, base deficit, and activation of neutrophils to endotoxemia. These findings suggest that propofol may inhibit inflammatory response and prevent the development of metabolic acidosis during endotoxemia.

journal_name

Crit Care Med

journal_title

Critical care medicine

authors

Taniguchi T,Yamamoto K,Ohmoto N,Ohta K,Kobayashi T

doi

10.1097/00003246-200004000-00032

subject

Has Abstract

pub_date

2000-04-01 00:00:00

pages

1101-6

issue

4

eissn

0090-3493

issn

1530-0293

journal_volume

28

pub_type

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