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.
2006
SUMMARY 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
( P w O 2=10 mmHg) for 360 min. Respiratory frequency
( f r) and heart rate ( f h) were recorded
simultaneously with ASR. Intact (control) fish increased
f r, 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 f h 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.
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