TY - JOUR
T1 - Control of ventilation in the hypercapnic skate Raja ocellata
T2 - I. Blood and extradural fluid
AU - Graham, M. S.
AU - Turner, J. D.
AU - Wood, C. M.
N1 - Funding Information:
Acknowledgements. The authors are grateful to Dr D.R. Idler, former Director of the Marine Sciences Research Laboratory, Memorial University of Newfoundland, and his staff for their hospitality and assistance, and particularly Dr G.L. Fletcher, who provided many resources for this study. R.S. Munger is thanked for excellent technical assistance. Dr J. N. Cameron kindly provided the modified Van Dam boxes used in this study. This research was supported by operating grants from NSERC to CMW.
PY - 1990
Y1 - 1990
N2 - In order to study the role of CO2 and acid-base status in contributing to ventilatory drive, skate were exposed to normoxic hypercapnia (PICO2 = 7.5 Torr) under conditions where the primary O2 drive a small Bohr effect. Red blood cell pHi was not preferentially regulated, and there was no evidence of RBC swelling or nucleoside triphosphate adjustment. Although there were no changes in arterial O2 levels during hypercapnia, ventilation immediately increased 2.7-fold through large changes in stroke volume and small changes in frequency, and declined only slightly through 24-48 h. PaCO2 equilibrated rapidly with PICO2, driving down arterial pHa, which was 65% corrected through HCO3- accumulation by 24 h. In contrast, the extradural fluid outside the brain equilibrated only very slowly, and was clearly not involved in the ventilatory stimulation. Increased ventilation during hypercapnia may be related to depressions in pHa.
AB - In order to study the role of CO2 and acid-base status in contributing to ventilatory drive, skate were exposed to normoxic hypercapnia (PICO2 = 7.5 Torr) under conditions where the primary O2 drive a small Bohr effect. Red blood cell pHi was not preferentially regulated, and there was no evidence of RBC swelling or nucleoside triphosphate adjustment. Although there were no changes in arterial O2 levels during hypercapnia, ventilation immediately increased 2.7-fold through large changes in stroke volume and small changes in frequency, and declined only slightly through 24-48 h. PaCO2 equilibrated rapidly with PICO2, driving down arterial pHa, which was 65% corrected through HCO3- accumulation by 24 h. In contrast, the extradural fluid outside the brain equilibrated only very slowly, and was clearly not involved in the ventilatory stimulation. Increased ventilation during hypercapnia may be related to depressions in pHa.
KW - Animal, skate
KW - Blood, O transport properties in skate
KW - Bohr effect in skate
KW - Cerebrospinal fluid, acid-base balance
KW - Control of breathing, cerebrospinal fluid in skate, response to CO
KW - Hypercapnia, ventilatory response in skate
KW - pH, intracellular
KW - Red cell, intracellular pH in skate
KW - Ventilation, sensitivity to CO in skate
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U2 - 10.1016/0034-5687(90)90088-G
DO - 10.1016/0034-5687(90)90088-G
M3 - Article
C2 - 2120753
AN - SCOPUS:0025362669
VL - 80
SP - 259
EP - 277
JO - Respiratory Physiology and Neurobiology
JF - Respiratory Physiology and Neurobiology
SN - 1569-9048
IS - 2-3
ER -