Effects of exogenous and endogenous carbon monoxide on dorsal aorta pressure and cardiac output in the rainbow trout

Abstract

Carbon monoxide (CO) is an important regulator of vasomotor tone in mammals. Its endogenous effects in non‐mammals, however, are unknown. Therefore, surgeries were performed on rainbow trout (Oncorhynchus mykiss), during which the dorsal aorta and nares were canulated and a flow probe was placed around the ventral aorta. Dorsal aorta pressure, stroke volume, heart rate, and respiration rate were compared on a resting trout, trout treated with inhibitors of the endogenous CO production, and trout treated with exogenous CO (delivered via a soluble ruthenium compound, CORM‐3). Zinc protoporphyrin‐IX, and inhibitor of heme‐oxygenase, elicited a dose‐dependent (at 5, 10, and 20 μmol/kg) increase in dorsal aorta pressure (approximately 20, 40, and 50% respectively). QC‐10, a non‐specific HO inhibitor, and QC‐15, a specific inhibitor of the HO‐1 isoform, both elicited a 25% increase in dorsal aorta pressure at 3 mg/kg. QC‐15 elicited a maximal response in approximately 5 minutes, while QC‐10 responses did not reach maximum until 1 hour. Both QC‐10 and QC‐15 caused small but significant increases in cardiac output. Unexpectedly, 30 μmol/kg CORM‐3 caused dorsal aorta pressure to approximately double in minutes. The results of the inhibitors suggest that CO is constitutively produced in trout to modulate vascular resistance. The surprising result with exogenous CO delivered via CORM‐3 requires further study.