Carotid body chemosensory function in prolonged normobaric hyperoxia in the cat

Abstract

The effects of normobaric hyperoxia on carotid body chemosensory function in the cat were studied. The hypothesis was that carotid body chemosensory function would be affected by chronic exposure to 100% O2 at sea level. It was based on the assumptions that carotid body tissue is exposed to high PO2 because of its high blood flow and that its O2 chemosensing mechanism is sensitive to O2 radical-induced reactions. Twelve cats were exposed to 100% O2 for 60-67 h, and 10 control cats were maintained in room air at sea level. They were anesthetized with pentobarbital sodium (Nembutal), and chemosensory afferents from a cut carotid sinus nerve were isolated and identified. The responses of single or a few clearly identifiable chemoreceptor afferents to isocapnic hypoxia and hypercapnia during hyperoxia and to the bolus injections of cyanide, nicotine, and dopamine were studied. We found that chronic hyperoxia severely blunted or eliminated the O2-sensitive response of the carotid chemoreceptors while augmenting the hypercapnic response. The response to cyanide but not to nicotine and dopamine were attenuated. Thus the hypoxic and hypercapnic responses that normally interact were separable. The lack of the cyanide response was consistent with the lack of the hypoxic response, suggesting a possible shared mechanism of carotid chemoreceptor response. Qualitatively normal responses to dopamine and nicotine indicated that the respective receptors were relatively intact after chronic exposure to hyperoxia and that the sensory nerves themselves were not affected by the prolonged O2 exposure.

Level and duration of developmental hyperoxia influence impairment of hypoxic phrenic responses in rats

“…Importantly, the effects of hyperoxia are dose dependent. In the present study, we observed long-term effects after normobaric exposures to as little as 30% O 2 and for durations as short as 1 wk, well below levels of O 2 expected to have toxic effects (14,26,32). However, even 21% O 2 is hyperoxic relative to prenatal conditions, and given its high blood flow relative to metabolic rate, the carotid body may be more susceptible to hyperoxic PaO 2 than other tissues (26,32).…”

“…Although many tissues are susceptible to hyperoxic toxicity (21), including the carotid body (7,26,32), ventilatory control appears normal in rats exposed to 1 mo of 60% O 2 as adults (27,28,30), and newborns may be less sensitive to hyperoxic toxicity than mature mammals, at least in some tissues (14,40). The neural effects of developmental hyperoxia (60% O 2 ) seem specific to the carotid body and related chemoafferent pathways (13), with no effect on the hypercapnic ventilatory response (27) or central neural integration of chemoafferent inputs (16,29).…”

Chemoreceptor plasticity and respiratory acclimation in the zebrafishDanio rerio

“…The continuance of CO 2 sensitivity in the face of a severe blunting or abolishment of the response to hypoxia has led to the idea that hyperoxia in mammals specifically targets O 2 -sensing mechanisms of the carotid body. The carotid body also retains its usual responsiveness to nicotine or dopamine following hyperoxia (Lahiri et al, 1987;Lahiri et al, 1990), further suggesting that the blunting effects of hyperoxia are not caused by general cellular damage. In the present study, the reflex hyperventilatory response to hypercapnia was eliminated (at least statistically; Fig.·7C) by prior exposure to hyperoxia.…”

“…Long-term hyperoxia is known to cause a similar attenuation of the carotid body chemosensitivity to hypoxia and cyanide in cats (Lahiri et al, 1987;Lahiri et al, 1990) and rats (Arieli et al, 1988) but is apparently without effect on humans (Gelfand et al, 1998), even when the levels of hyperoxia approach the limits of toxicity. In those mammals exhibiting a hyperoxic blunting of the ventilatory response to hypoxia, the response to hypercapnia is sustained (Torbati et al, 1989), reduced (Lahiri et al, 1990) or even enhanced (Lahiri et al, 1987). The continuance of CO 2 sensitivity in the face of a severe blunting or abolishment of the response to hypoxia has led to the idea that hyperoxia in mammals specifically targets O 2 -sensing mechanisms of the carotid body.…”

“…Hyperoxia-induced respiratory plasticity has been reported in mammals (Lahiri et al, 1987;Liberzon et al, 1989;Torbati et al, 1989) and is manifested by a reversible blunting of the ventilatory response to hypoxia. To our knowledge, no studies have yet addressed the potential for respiratory plasticity in fish exposed to hyperoxia.…”