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. 1978 Apr;62(4):591–597. doi: 10.1111/j.1476-5381.1978.tb07766.x

The acute effects of nicotine, tobacco smoke and carbon monoxide on myocardial oxygen tension in the anaesthetized cat

Richard D Rink
PMCID: PMC1668045  PMID: 656704

Abstract

1 The acute effects of nicotine, tobacco smoke, and carbon monoxide on myocardial oxygen tension (MPo2) were estimated amperometrically in 33 anaesthetized open-chest cats with a glass-insulated 25 μm platinum cathode within a 22-gauge needle implanted in the left ventricular wall.

2 MPo2 was 1.6-60 mmHg (mean 23.5 mmHg) when arterial Po2 was >80 mmHg. Sequential intravenous infusions of nicotine (2-3 μg/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 MPo2. 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 Po2 or blood pressure but typically decreased MPo2 by approximately 1-4 mmHg. Augmentation of MPo2 often succeeded carbon monoxide administration.

3 Arterial hypoxia (arterial Po2 < 60 mmHg) reduced mean MPo2 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 MPo2. Puffs of 5% carbon monoxide had less effect than during normoxia. Locations of low MPo2 (<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 MPo2 during normoxia, but the effect is negligible during moderate hypoxaemia.

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Selected References

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