• W X Wu.
• Frist Affiliated Hospital of Nanjing Medical College.
• Zhonghua Zheng Xing Shao Shang Wai Ke Za Zhi. 1991 Dec 1; 7 (4): 275-7, 318-9.

AbstractAnesthetized dogs were ventilated with 1% carbon monoxide (CO) in air for 10 minutes to produce CO poisoning. They were then ventilated with room air (n = 5) or pure oxygen (n = 5) for 3 hours. They served as controls. Acute lung injury was produced by intratracheal injection of 0.1 N HCl (2 ml/kg) 30 minutes before CO poisoning in another group of dogs. Arterial blood gas and COHb were monitored before and after CO poisoning. Pharmacokinetic analysis was used to find the half-time of COHb elimination (T1/2). Pulmonary shunt was measured before CO poisoning in the injured dogs. Half-time of COHb elimination was prolonged in lung injury dogs resuscitated on air as compared with the control group (275 +/- 28 vs. 203 +/- 24 min, P less than 0.05). Oxygen accelerated COHb excretion in both injured and control animals. No significant correlation was found between T1/2 and Qs/Qt in the injured dogs ventilated with air or oxygen. A negative linear relationship was found between T1/2 of COHb elimination and the pre-CO-poisoning PaO2 (r = -0.98, P less than 0.05) 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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