THE ACUTE EFFECTS OF NICOTINE, TOBACCO SMOKE AND CARBON MONOXIDE ON MYOCARDIAL OXYGEN TENSION IN THE ANAESTHETIZED CAT

Abstract

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 gtm platinum cathode within a 22‐gauge needle implanted in the left ventricular wall. MPo2 was 1.6–60 mmHg (mean 23.5 mmHg) when arterial P02 was >80 mmHg. Sequential intravenous infusions of nicotine (2–3 gg/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. 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. 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. 1978 British Pharmacological Society