Control of cardiorespiratory function in response to hypoxia in an air-breathing fish, the African sharptooth catfish, Clarias gariepinus

Abstract We evaluated the role of the first pair of gill arches in the control of cardiorespiratory responses to normoxia and hypoxia in the air-breathing catfish, Clarias gariepinus . An intact group (IG) and an experimental group (EG, bilateral excision of first gill arch) were submitted to graded hypoxia, with and without access to air. The first pair of gill arches ablations reduced respiratory surface area and removed innervation by cranial nerve IX. In graded hypoxia without access to air, both groups displayed bradycardia and increased ventilatory stroke volume ( V T ), and the IG showed a significant increase in breathing frequency ( f R ). The EG exhibited very high f R in normoxia that did not increase further in hypoxia, this was linked to reduced O 2 extraction from the ventilatory current ( E O 2 ) and a significantly higher critical O 2 tension ( P cO 2 ) than the IG. In hypoxia with access to air, only the IG showed increased air-breathing, indicating that the first pair of gill arches excision severely attenuated air-breathing responses. Both groups exhibited bradycardia before and tachycardia after air-breaths. The f H and gill ventilation amplitude ( V AMP ) in the EG were overall higher than the IG. External and internal NaCN injections revealed that O 2 chemoreceptors mediating ventilatory hypoxic responses ( f R and V T ) are internally oriented. The NaCN injections indicated that f R responses were mediated by receptors predominantly in the first pair of gill arches but V T responses by receptors on all gill arches. Receptors eliciting cardiac responses were both internally and externally oriented and distributed on all gill arches or extra-branchially. Air-breathing responses were predominantly mediated by receptors in the first pair of gill arches. In conclusion, the role of the first pair of gill arches is related to: (a) an elevated E O 2 providing an adequate O 2 uptake to maintain the aerobic metabolism during normoxia; (b) a significant bradycardia and increased f AB elicited by externally oriented O 2 chemoreceptors; (c) increase in the ventilatory variables ( f R and V AMP ) stimulated by internally oriented O 2 chemoreceptors.