Citation

Kawamoto M, Suzuki N, Takasaki M. Anesth. Analg. 1992; 74(5): 747-752.

Copyright

(Copyright © 1992, International Anesthesia Research Society, Publisher Lippincott Williams and Wilkins)

DOI

10.1213/00000539-199205000-00021

PMID

1567044

Abstract

Intravenous liquid halothane causes severe pulmonary edema when administered for suicide attempts. This study was carried out to elucidate the cardiopulmonary effects of intravenous liquid halothane in 14 dogs. Subjects were divided into three groups: group 1 (n = 4) was the control; group 2 (n = 5) received 7.5 mmol intravenous liquid halothane; and group 3 (n = 5) received pretreatment of continuous infusion of prostaglandin E1 at a rate of 0.02 microgram.kg-1.min-1, followed by 7.5 mmol intravenous liquid halothane. Hemodynamic values, extravascular lung water, and arterial blood gas tensions were measured for 240 min. In group 2, thromboxane B2, beta-glucuronidase, and lipid peroxides were measured in four of five dogs. In group 2, intravenous liquid halothane caused pulmonary edema associated with hypoxemia, pulmonary hypertension, and left ventricular dysfunction. In group 3, prostaglandin E1, given to reduce pulmonary vasoconstriction and left ventricular preload, aggravated hypoxemia and pulmonary hypertension and impaired left ventricular contractility, although end-diastolic left ventricular pressure was low. Thromboxane B2 increased, whereas beta-glucuronidase and lipid peroxides did not change after administration of intravenous halothane. We conclude that pulmonary edema induced by intravenous liquid halothane was due to direct pulmonary vascular damage, and that pulmonary vasoconstriction and increased left ventricular preload were not contributory causes.

Language: en

Keywords

Alprostadil; Animals; Dogs; Glucuronidase; Halothane; Hemodynamics; Injections, Intravenous; Lipid Peroxides; Pulmonary Edema; Thromboxane B2