Abstract

Chickens and pigeons were exposed to similar changes in arterial blood gas tensions as ducks had experienced in a previous study (Butler and Taylor, 1973), so that the resulting respiratory and cardiovascular changes could be compared between the three species. Thus in the present study hypoxia means a reduction in Pa O 2 of 33 mm Hg and hypercapnia means an increase in PaCO 2 of 9 mm Hg. Spontaneously breathing chickens were exposed to hypoxia and hypercapnia either separately or together, whereas spontaneously breathing pigeons were only subjected to hypercapnic hypoxia. In the chickens, hypocapnic hypoxia caused I to increase to 138% of control and mean arterial pressure (M.A.P.) to drop to 59% of control. Raising Pa co, reduced this hypotension, such that during hypercapnic hypoxia M.A.P. was 84% of control. Also, Vl was increased by a factor of 3.52, which is less than would be expected from the addition of the separate effects of hypoxia and hypercapnia, and there was no change in f card. In pigeons, hypercapnic hypoxia caused I to increase by a factor of 3.40, and there was a significant rise in f card. Relaxed chickens, artificially ventilated at different 'values of f resp and V t, were also exposed to hypercapnic hypoxia. When f resp and V t were at those values previously recorded in normal control animals, hypercapnic hypoxia caused f card a to fall to 81% of control. This bradycardia was not apparent when f resp and V t were increased to the values previously recorded in spontaneously breathing chickens during hypercapnic hypoxia. During 60 sec apnoea in air f card fell to 46% of control. It was concluded that in response to the present levels of hypercapnia and hypoxia, t increases less in spontaneously breathing pigeons and chickens than it does in ducks. The primary effect of hypercapnic hypoxia on heart rate of chickens is bradycardia, and this is less than that shown by ducks. This bradycardia is obscured by lung ventilation in chickens as it is in ducks.

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