Cardiorespiratory response to progressive hypoxia and hypercapnia in the turtle Trachemys scripta

Citation
Jk. Herman et Nj. Smatresk, Cardiorespiratory response to progressive hypoxia and hypercapnia in the turtle Trachemys scripta, J EXP BIOL, 202(22), 1999, pp. 3205-3213
Citations number
41
Categorie Soggetti
Biology,"Experimental Biology
Journal title
JOURNAL OF EXPERIMENTAL BIOLOGY
ISSN journal
00220949 → ACNP
Volume
202
Issue
22
Year of publication
1999
Pages
3205 - 3213
Database
ISI
SICI code
0022-0949(199911)202:22<3205:CRTPHA>2.0.ZU;2-8
Abstract
The ventilatory responses of chelonian reptiles to hypoxic and hypercapnic stress have been fairly well described. As turtles are capable of large car diac shunts, changes in pulmonary perfusion may be an equally viable and po tent response to these stressors, To test this hypothesis, conscious unrest rained turtles were unidirectionally ventilated while blood flow in the lef t pulmonary artery ((Q) over dot(LPA)) and left aortic arch ((Q) over dot(L Ao)) was monitored. Turtles were exposed to step changes (2.5 h step(-1)) i n O-2 tension (30, 15, 5, 2.5 or 0 % O-2; CO2 inflow maintained constant) o n day 1 followed by step changes in CO2 tension (0, 2, 4, 8 % CO2; O-2 infl ow maintained constant) on day 2. Steady-state cardiorespiratory variables were recorded for the last 30 min of each step change in gas tension. Progr essive hypoxia resulted in progressive increases in ventilation, (Q) over d ot(LPA) and (Q) over dot(LAo) and a small, but non-significant, increase in heart rate. Progressive hypercapnia resulted in a progressive increase in ventilation, white (Q) over dot(LPA) and (Q) over dot(LAo) did not change at any level o f CO2. These results suggest that information from the O-2-sensitive chemor eceptors appears to be stimulatory to both the cardiovascular and ventilato ry control systems, while CO2 chemoreception appears to affect primarily th e ventilatory control system. These results also suggest that, in animals c apable of intracardiac shunting, increasing pulmonary perfusion may be an i ntegral component of the reflex response to hypoxia.