Cardiovascular Effects of Hypercarbia in Rainbow Trout (Oncorhynchus Mykiss): A Role for Externally Oriented Chemoreceptors

In situ and in vivo experiments were performed on rainbow trout (Oncorhynchus mykiss) to examine (i) the direct effect of CO₂ on the systemic vasculature and (ii) the influence of internal versus external hypercapnic acidosis on cardiovascular variables including blood pressure, cardiac output and systemic vascular resistance. Results from in situ saline-perfused trunk preparations indicated that CO₂ (0.6, 1.0 or 2.0 % CO₂) elicited a significant vasodilation, but only in the presence of pre-existing humoral adrenergic tone. In the absence of pre-existing vascular tone, CO₂ was without effect on systemic resistance. In contrast, hypercarbia in vivo triggered a statistically significant increase in systemic resistance (approximately 70 %) that was associated with elevated ventral aortic (approximately 42 %) and dorsal aortic (approximately 43 %) blood pressures and with a significant bradycardia (approximately 12 %); cardiac output was not significantly affected.

To determine the potential roles of internal versus external chemoreceptors in mediating the cardiovascular responses to hypercarbia, experiments were performed to elevate the endogenous arterial partial pressure of CO₂ without an accompanying increase in external ⁠. In one series, trout were given a bolus injection of the carbonic anhydrase inhibitor acetazolamide (30 mg kg⁻¹) to inhibit CO₂ excretion, and thus raise ⁠, 5–7 h prior to being exposed to an acute increase in (maximum =6.3±0.4mmHg; 1mmHg=0.133 kPa). Despite a marked increase in (approximately 7 mmHg) after injection of acetazolamide, there was no increase in dorsal aortic blood pressure (P_DA) or systemic resistance (R_S). The ensuing exposure to hypercarbia, however, significantly increased P_DA (by approximately 20 %) and R_S (by approximately 35 %). A second series of experiments used a 5–7 h period of exposure to hyperoxia to establish a new, elevated baseline (7.8±1.1 mmHg) without any change in ⁠. Despite a steadily increasing during the 5–7 h of hyperoxia, there was no associated increase in P_DA or R_S. Ensuing exposure to hypercarbia, however, significantly increased P_DA (by approximately 20 %) and R_S (by approximately 150 %). Plasma adrenaline levels were increased significantly during exposure to hypercarbia and, therefore, probably contributed to the accompanying cardiovascular effects.

These findings demonstrate that the cardiovascular effects associated with hypercarbia in rainbow trout are unrelated to any direct constrictory effects of CO₂ on the systemic vasculature and are unlikely to be triggered by activation of internally oriented receptors. Instead, the data suggest that the cardiovascular responses associated with hypercarbia are mediated exclusively by externally oriented chemoreceptors.