From the above, it appears that the bradycardia observed in HBO is due to two mechanisms: an oxygen-dependent and a non-oxygen-dependent effect. Many authors have tried to determine the processes involved in both these effects, and particularly whether the autonomic nervous system is involved (Daly & Bonduran6, Fagraeus & Linnarson7, Fagraeus8). Fagraeus & Linnarson 7 of the autonomic nervous system using anticholergenic and beta-blocking agents in healthy human beings undergoing a standardized exercise testing in various atmospheres (air at 1 ata, O2 at 1.3 ata and air at 6 ata). Their conclusion was that the oxygen-dependent effect was mainly due to a direct effect of the high pressure of oxygen on the myocardium, combined to a lesser extent with a parasympathetic effect. The non-oxygen-dependent aspect, on the other hand, was mainly related to a decrease in sympathetic heart tone (i.e., a reduced beta effect).
The relative importance of the direct action on the myocardium and of the indirect action of the autonomic nervous system on oxygen-dependent bradycardia has been evaluated. Doubt & Evans9 confirmed the direct action of HBO on the myocardium by demonstrating a specifically oxygen-dependent bradycardia, in cats anaesthetized and curarized at a pressure of 31.3 ata (PO2 = 0.35 ata, PHe = 31 ata). Bergo10, however, reported the disappearance of the oxygen-dependent bradycardia in rats injected with atropine at 5 ata. In fact, apart from the differences in methods and animal models, it seems possible to reconcile the outcome of both studies in differentiating two HBO effects : (1) the bradycardic effect exerted on heart rate both at rest and during exercise and (2) the bradycardia occurring due to a direct effect on myocardial cells at rest, which is oxygen-dependent, appears quickly, is reversible with atropine, and is therefore probably mainly mediated by the parasympathetic system. This parasympathetic effect is brought into play by the baroreceptors stimulated by the hyperoxia-induced arterial hypertension. The effect is further increased because both the activity of the sympathetic system11 and the level of circulating catecholamines12,13decrease due to the hyperoxia.
Another mechanism that has been proposed is a decreased sensitivity of the chemo-receptors to CO2 during hyperoxia14. However, this is not likely to play a significant role if one considers that the time it would take to develop is much longer than the actually observed onset time for the bradycardia. During exercise, the chemo-receptors are stimulated by the increase in pressure of CO2 and although this stimulation is weak, it compensates for the vagotonic action. The bradycardia observed is thus mainly of a direct origin.
Finally, it must be emphasized that the oxygen-dependent bradycardic effect is not a sign of oxygen toxicity. As Matalon15 reported, an increase in heart rate above the baseline takes place before the occurrence of a hyperoxia crisis. Tachycardia rather than bradycardia has long been recognised as a clinical warning sign of an impeding hyperoxic crisis.
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