1 The acute effects of nicotine, tobacco smoke, and carbon monoxide on myocardial oxygen tension (MPo(2)) were estimated amperometrically in 33 anaesthetized open-chest cats with a glass-insulated 25 mum platinum cathode within a 22-gauge needle implanted in the left ventricular wall.2 MPo(2) was 1.6-60 mmHg (mean 23.5 mmHg) when arterial Po(2) was >80 mmHg. Sequential intravenous infusions of nicotine (2-3 mug/kg every 45 s) or intracheal puffs (3-5 ml) of tobacco smoke commonly produced transitory increases (25-35 mmHg) of arterial pressure and 4-6 mmHg increments of MPo(2). Intratracheal puffs (5 ml) of 5% carbon monoxide sufficient to increase carboxyhaemoglobin from 0.8 to 1.5% to 4-7% had no effect on arterial Po(2) or blood pressure but typically decreased MPo(2) by approximately 1-4 mmHg. Augmentation of MPo(2) often succeeded carbon monoxide administration.3 Arterial hypoxia (arterial Po(2) < 60 mmHg) reduced mean MPo(2) to 14.4 mmHg but anoxic levels were not observed. Pressor responses to nicotine and tobacco smoke were accompanied by small increases (usually 1-3 mmHg) of MPo(2). Puffs of 5% carbon monoxide had less effect than during normoxia. Locations of low MPo(2) (<10 mmHg) were unaffected as carboxyhaemoglobin was raised to 7-11% during hypoxaemia.4 It is concluded that nicotine and tobacco smoke cause augmentation of myocardial oxygen supply, even during moderate hypoxaemia. By contrast, smoking dosages of carbon monoxide have the potential of producing a small reduction of MPo(2) during normoxia, but the effect is negligible during moderate hypoxaemia.