Respiratory, circulatory and acid-base adjustments to hypercapnia in a strictly aquatic and predominantly skin-breathing urodele, Cryptobranchus alleganiensis.

Upon initial exposure to increased ambient CO2, Cryptobranchus is titrated along an in vivo buffer line whose slope is considerably reduced from that observed when whole blood samples are equilibrated in vitro. During this time, there is no apparent reduction in the PCO2 difference between arterial blood and inspired media (PaCO2 -PICO2), despite an increase in auxiliary respiratory activities (lung and buccopharyngeal ventilation). The development of this non-compensated respiratory acidosis in the skin-breathing salamander is reminiscent of the situation seen in gill-breathing fish where the control of the acid-base balance is achieved by means other than ventilation. The increased ventilatory activities in Cryptobranchus can be interpreted as a response to the effect that the acidotic conditions have on arterial oxygenation (i.e.: CO2 Bohr effect); as a result, PaO2 increases and appears to counteract the arterial hypoxaemia which would otherwise result. More prolonged hypercapnia leads to compensatory phase of acid-base adjustment whereby plasma bicarbonate increases along a gently rising PaCO2 line to a new steady state equilibrium. This compensatory stage is slow acting and offers little by way of restoring the arterial blood pH, at least over the 36-h CO2 exposure period studied. The recovery period in air-saturated conditions is very gradual with PaCO2 levels exhibiting an exponential pattern of decline. This, together with the PaCO2 -PICO2 observations above, lends support to an accumulating body of evidence which suggests that respiratory CO2 losses across the amphibian skin are passive or at best only poorly controlled.