• W X Wu.
• First Affiliated Hospital of Nanjing Medical College.
• Zhonghua Nei Ke Za Zhi. 1992 Nov 1; 31 (11): 689-91, 730.

AbstractAnesthetized dogs were ventilated with 1% carbon monoxide (CO) in air for 10 minutes to produce CO poisoning and then with room air (n = 5) or pure oxygen (n = 5) for 3 hours as control. Acute lung injury was produced by intratracheal injection of 0.1 N HCl (2 ml/kg) 30 minutes before CO poisoning in another 10 experimental dogs. Arterial blood gas and carboxyhemoglobin (COHb) were monitored before and after CO poisoning. Pharmacokinetic analysis was used to find the half-time of COHb elimination (T 1/2 beta). Pulmonary shunt was measured before CO poisoning in the injured dogs. Half-time of COHb elimination was prolonged in the injured dogs resuscitated with air as compared with dogs in the control group (275% +/- 28 vs. 203 +/- 24 min., P < 0.05); Oxygen accelerated COHb excretion in both injured and control animals. No significant correlation was found between T 1/2 beta and Qs/Qt in the injured dogs ventilated with air or oxygen. A negative linear relationship was found between T 1/2 beta of COHb elimination and the pre-CO-poisoning PaO2 (r = -0.98, P < 0.005) in the injured dogs treated with oxygen. The data suggest that hypoxemia may represent the underlying mechanism of altered COHb kinetics in acute inhalation lung injury.

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