Pre-and post-branchial blood respiratory status during acute hypercapnia or hypoxia in rainbow trout,Oncorhynchus mykiss

Abstract

Simultaneous venous (pre-branchial) and arterial (post-branchial) extracorporeal blood circulations were utilized to monitor continuously the rapid and progressive effects of acute environmental hypercapnia (water partial pressure of CO2 4.8±0.2 torr) or hypoxia (water partial pressure of O2 25±2 torr) on oxygen and carbon dioxide tensions and pH in the blood of rainbow trout (Oncorhynchus mykiss). During hypercapnia, the CO2 tension in the arterial blood increased from 1.7±0.1 to 6.2±0.2 torr within 20 min and this was associated with a decrease of arterial extracellular pH from 7.95±0.03 to 7.38±0.03; the acid-base status of the mixed venous blood changed in a similar fashion. The decrease in blood pH in vivo was greater than in blood equilibrated in vitro with a similar CO2 tension indicating a significant metabolic component to the acidosis in vivo. Under normocapnic conditions, venous blood CO2 tension was slightly higher than arterial blood CO2 tension difference was abolished or reversed during the initial 25 min of hypercapnia indicating that CO2 was absorbed from the water during this period. Arterial O2 tension remained constant during hypercapnia; however, venous blood O2 tension decreased significantly (from 22.0±2.6 to 9.0±1.0 torr) during the initial 10 min. Hypercapnia elicited the release of catecholamines (adrenaline and noradrenaline) into the blood. The adrenaline concentration increased from 6±3 to 418±141 nmol · l-1 within 25 min; noradrenaline concentration increased from 3±0.5 to 50±21 nmol · l-1 within 15 min. During hypoxia arterial blood O2 tension declined progressively from 108.4±9.9 to 12.8±1.7 torr within 30 min. Venous blood O2 tension initially was stable but then decreased abruptly as catecholamines were released into the circulation. The release of catecholamines occurred concomitantly with a sudden metabolic acidosis in both blood compartments and a rise in CO2 tension in the mixed venous blood only.