Cardiorespiratory adjustments during hypercarbia in rainbow trout Oncorhynchus mykiss are initiated by external CO2 receptors on the first gill arch

摘要

Experiments were performed to test the hypothesis that the marked ventilatory and cardiovascular responses to hypercarbia in rainbow trout Oncorhynchus mykiss arise from specific stimulation of chemoreceptors localised to the first gill arch. This was accomplished by measuring cardiorespiratory variables during acute hypercarbia (20min at P-CO2=8mmHg; 1 mmHg=0.133kPa) in fish subjected to selective bilateral extirpation of the first gill arch. The cardiovascular responses to hypercarbia in the intact fish included a significant bradycardia (from 75.0+/-1.6 to 69.0+/-2.0 beats min(-1); means S.E.M.; N=16), an increase in dorsal aortic blood pressure (from 30.8+/-1.5 to 41.9+/-2.5 mmHg; N=16) and a rise in systemic vascular resistance (from 1.1+/-0.1 to 1.4+/-0.1 mmHg ml(-1) kg(-1) min-1; N=16). Removal of the first gill arch or pre-treatment with the muscarinic receptor antagonist atropine prevented the hypercarbic bradycardia without affecting the pressure or resistance responses. Correlation analysis, however, revealed shallow but significant inverse relationships between water P-CO2 and cardiac frequency in both atropinised (r(2)=0.75) and gill-extirpated (r(2)=0.90) fish, suggesting a direct mild effect Of CO2 on cardiac function. The ventilatory response to hypercarbia in the intact fish consisted of an increase in ventilation amplitude (from 0.62+/-0.06 to 1.0+/-0.13cm; N=16) with no change in breathing frequency. Removal of the first gill arch lowered resting breathing frequency and prevented the statistically significant elevation of breathing amplitude. Gill extirpation, however, did not totally abolish the positive correlation between water P-CO2 and ventilation amplitude (r(2)=0.84), suggesting the presence of additional (although less important) chemoreceptive sites that are not confined to the first gill arch. Plasma catecholamine levels were elevated during hypercarbia, and this response was unaffected by prior gill extirpation.