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Circulatory limits to oxygen supply during an acute temperature increase in the Chinook salmon (Oncorhynchus tshawytscha)

Journal article
Authors T.D. Clark
Erik Sandblom
G.K. Cox
S.G. Hinch
A. P. Farrell
Published in American Journal of Physiology: Regulatory, Integrative and Comparative Physiology
Volume 295
Pages R1631-R1639
ISSN 0363-6119
Publication year 2008
Published at Department of Zoology
Pages R1631-R1639
Language en
Links dx.doi.org/10.1152/ajpregu.90461.20...
Keywords blood pressure; blood respiratory properties; cardiac output; hematocrit; hemoglobin; heart rate; blood plasma; rate of oxygen consumption; oxygen equilibrium curves; Pacific salmon; stroke volume; vascular resistance
Subject categories Animal physiology

Abstract

This study was undertaken to provide a comprehensive set of data relevant to disclosing the physiological effects and possible oxygen transport limitations in the Chinook salmon (Oncorhynchus tshawytscha) during an acute temperature change. Fish were instrumented with a blood flow probe around the ventral aorta and catheters in the dorsal aorta and sinus venosus. Water temperature was progressively increased from 13°C in steps of 4°C up to 25°C. Cardiac output increased from 29 to 56 ml·min–1·kg–1 between 13 and 25°C through an increase in heart rate (58 to 105 beats/min). Systemic vascular resistance was reduced, causing a stable dorsal aortic blood pressure, yet central venous blood pressure increased significantly at 25°C. Oxygen consumption rate increased from 3.4 to 8.7 mg·min–1·kg–1 during the temperature increase, although there were signs of anaerobic respiration at 25°C in the form of increased blood lactate and decreased pH. Arterial oxygen partial pressure was maintained during the heat stress, although venous oxygen partial pressure (PvO2) and venous oxygen content were significantly reduced. Cardiac arrhythmias were prominent in three of the largest fish (>4 kg) at 25°C. Given the switch to anaerobic metabolism and the observation of cardiac arrhythmias at 25°C, we propose that the cascade of venous oxygen depletion results in a threshold value for PvO2 of around 1 kPa. At this point, the oxygen supply to systemic and cardiac tissues is compromised, such that the oxygen-deprived and acidotic myocardium becomes arrhythmic, and blood perfusion through the gills and to the tissues becomes compromised.

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