THE EFFECTS OF EXPERIMENTAL ANEMIA ON CO2 EXCRETION IN-VITRO IN RAINBOW-TROUT, ONCORHYNCHUS-MYKISS

Citation
Km. Gilmour et Sf. Perry, THE EFFECTS OF EXPERIMENTAL ANEMIA ON CO2 EXCRETION IN-VITRO IN RAINBOW-TROUT, ONCORHYNCHUS-MYKISS, Fish physiology and biochemistry, 15(1), 1996, pp. 83-94
Citations number
37
Categorie Soggetti
Biology,Fisheries
ISSN journal
09201742
Volume
15
Issue
1
Year of publication
1996
Pages
83 - 94
Database
ISI
SICI code
0920-1742(1996)15:1<83:TEOEAO>2.0.ZU;2-2
Abstract
The effects of severe experimental anaemia on red blood cell HCO3- deh ydration in vitro were examined in rainbow trout, Oncorhynchus mykiss. After 5 days of anaemia (haematocrit = 4.9 +/- 1.1%) induced by intra peritoneal injection of phenylhydrazine hydrochloride, fish displayed elevated arterial CO2 tensions (anaemic PaCO2 = 3.19 +/- 0.42 torr vs. control PaCO2 = 1.35 +/- 0.17 torr) and a significant acidosis (anaem ic pHa = 7.73 +/- 0.04 vs. control pHa = 7.99 +/- 0.04). However, afte r 15-20 days of anaemia (hct = 6.6 +/- 0.8%) induced by blood withdraw al, the arterial CO2 tension was significantly lower than the control value, suggesting that physiological adjustments occurred within this time period to compensate for the lowered haematocrit. Compensation pr obably did not involve alterations in ventilation, which was unaffecte d by 5 days of anaemia (anaemic Vw = 786 +/- 187 ml min(-1) kg(-1) vs. control Vw = 945 +/- 175 min(-1) kg(-1)), based on indirect Fick prin ciple measurements. Potential adaptations to longer term anaemia at th e level of the red blood cells were investigated using a radioisotopic HCO3- dehydration assay. Owing to the difference in haematocrits, the HCO3- dehydration rate for blood from anaemic fish was significantly lower than that for control fish following equilibration at the same C O2 tension. This difference was eliminated when HCO3- dehydration rate s were measured on blood samples adjusted to the same haematocrit, a r esult which implies that the intrinsic rate of CO2 excretion at the le vel of the red blood cell was not 'up-regulated' during anaemia. The d ifference was also eliminated by equilibrating the blood samples with CO2 tensions appropriate for the group from which the sample was obtai ned, i.e., PCO2 = 1.4 torr for control samples and PCO2 = 3.2 torr for anaemic samples; each at the appropriate haematocrit. It is concluded that the elevated PaCO2 helps to reset CO2 excretion to the control l evel, but that some additional physiological adjustment occurs to lowe r the PaCO2 after 15-20 days of anaemia.