The role of branchial and orobranchial O2 chemoreceptors in the control of aquatic surface respiration in the neotropical fish tambaqui (Colossoma macropomum): progressive responses to prolonged hypoxia.

The present study examined the role of branchial and orobranchial O(2) chemoreceptors in the cardiorespiratory responses, aquatic surface respiration (ASR), and the development of inferior lip swelling in tambaqui during prolonged (6 h) exposure to hypoxia. Intact fish (control) and three groups of denervated fish (bilateral denervation of cranial nerves IX+X (to the gills), of cranial nerves V+VII (to the orobranchial cavity) or of cranial nerves V alone), were exposed to severe hypoxia (Pw(O)2=10 mmHg) for 360 min. Respiratory frequency (fr) and heart rate (fh) were recorded simultaneously with ASR. Intact (control) fish increased fr, ventilation amplitude (V(AMP)) and developed hypoxic bradycardia in the first 60 min of hypoxia. The bradycardia, however, abated progressively and had returned to normoxic levels by the last hour of exposure to hypoxia. The changes in respiratory frequency and the hypoxic bradycardia were eliminated by denervation of cranial nerves IX and X but were not affected by denervation of cranial nerves V or V+VII. The V(AMP) was not abolished by the various denervation protocols. The fh in fish with denervation of cranial nerves V or V+VII, however, did not recover to control values as in intact fish. After 360 min of exposure to hypoxia only the intact and IX+X denervated fish performed ASR. Denervation of cranial nerve V abolished the ASR behavior. However, all (control and denervated (IX+X, V and V+VII) fish developed inferior lip swelling. These results indicate that ASR is triggered by O(2) chemoreceptors innervated by cranial nerve V but that other mechanisms, such as a direct effect of hypoxia on the lip tissue, trigger lip swelling.

Cardiorespiratory reflexes and aquatic surface respiration in the neotropical fish tambaqui (Colossoma macropomum): acute responses to hypercarbia.

We examined the cardiorespiratory responses to 6 h of acute hypercarbia (1, 2.5, and 5% CO(2)) in intact and gill-denervated (bilateral denervation of branchial branches of cranial nerves IX and X) tambaqui, Colossoma macropomum. Intact fish exposed to 1 and 2.5% CO(2) increased respiratory frequency ( f(R)) and ventilation amplitude ( V(AMP)) slowly over a 1- to 3-h period. Denervated fish did not show this response, suggesting that tambaqui possess receptors in the gills that will produce excitatory responses to low levels of hypercarbia (1 and 2.5% CO(2)) if the exposure is prolonged. The cardiac response to stimulation of these receptors with this level of CO(2) was a tachycardia and not a bradycardia. During exposure to 5% CO(2), intact fish increased f(R) and V(AMP), and showed a pronounced bradycardia after 1 h. After 2 h, the heart rate ( f(H)) started to increase, but returned to control values after 6 h. In denervated fish, the increase in f(R) was abolished. The slow increase in V(AMP) and the bradycardia were not abolished, suggesting that these changes arose from extra-branchial receptors. Neither intact nor denervated fish developed the swelling of the lower lip or performed aquatic surface respiration, even after 6 h, suggesting that these are unique responses to hypoxia and not hypercarbia.