Lidocaine attenuates the hypotensive and inflammatory responses to endotoxemia in rabbits
Taniguchi, T.; Shibata, K.; Yamamoto, K.; Kobayashi, T.; Saito, K.; Nakanuma, Y.
Critical Care Medicine 24(4): 642-646
1996
ISSN/ISBN: 0090-3493 PMID: 8612417 Document Number: 459665
Objective: To assess the effects of lidocaine on the hemodynamic and inflammatory responses to Escherichia coli endotoxemia in rabbits. Design: Prospective, randomized, controlled experimental study. Setting: University laboratory. Subjects: Twenty-seven female Japanese rabbits, anesthetized with urethane and ventilated mechanically. Interventions: Animals were randomly assigned to one of three groups: a) endotoxemic control group (n = 9), receiving intravenous Escherichia coli endotoxin (0.5 mg/kg bolus) via the mesenteric vein; b) laparotomy control group (n = 9), treated identically to the endotoxemic control group, except for substitution of 0.9% saline for endotoxin; and c) lidocaine-treated group (n = 9), treated identically to the endotoxemic controls and additionally, intravenous lidocaine (3 mg/kg bolus, followed by infusion at 2 mg/kg/hr) was administered immediately after endotoxin. Measurements and Main Results: We compared hemodynamics, blood gases, and microscopic findings of lung tissue obtained at necropsy in each group. Laparotomy alone had a minimal effect on the parameters and findings. Endotoxin injection decreased mean systolic arterial pressure from 135 +- 6 (SD) to 95 +- 25 mm Hg (p lt .05) and increased the mean base deficit from -1.2 +- 1.8 to -1 4.4 +- 4.2 mmol/L (p lt .05), and caused the infiltration of neutrophils into the lungs. Lidocaine administration abolished the hypotension and attenuated the increase of bass deficit to -9.5 +- 2.1 mmol/L (p lt .05) and the cellular infiltration in comparison with endotoxemic controls. Conclusions: Lidocaine attenuated the hemodynamic and inflammatory responses to endotoxemia in rabbits. Findings suggest that lidocaine administration may prevent the development of hypotension and metabolic acidosis during endotoxemia.