Venous return as stimulus for respiration in rabbit.

The "exercise hyperpnoea" problem was studied in 44 anaesthetized rabbits by increasing the cardiac output by: a) tilting by 12 degrees the hindlimbs up; b) injecting into the right heart 15 ml of dextran; c) normocapnic or d) hypocapnic blood. In all cases there was an increase in minute ventilation, VE, independently of the presence or absence of an increase in CO2 flux to the lungs. We decreased the cardiac output by tilting up the head by 10 degrees; this elicited a decrease in VE accompanied by an increase in the fractional end-tidal CO2. For elucidating the role played by carotid body chemoreceptors in eleven rabbits the legs were tilted up before and while the animals breathed pure oxygen. The results were very similar. When the hindlimbs were tilted up after cervical bilateral vagotomy the VE response diminished about fifty per cent. We conclude that: a) hyperpnoea and hypopnoea elicited by a change in cardiac output are due to stimulation or depression of mechanoreceptors localized in the pulmonary circulation, b) carotid body chemoreceptors are not required for these responses, c) fifty per cent of the VE response depends on the integrity of the vagus nerves, d) it is probable that the increase in venous return plays an important role in the hyperpnoea at the onset of muscular exercise.

Reversal of oxygen difference between arterial blood and cerebrospinal fluid in the rabbit.

The experiments were carried out in rabbits under general anaesthesia with muscle relaxation and artificial ventilation with atmospheric air. Samples of arterial blood and cerebrospinal fluid were obtained. Of particular interest was reversal of the oxygen gradient, that is PaO2 less than PCSFO2 at arterial blood hypoxia below 65 Torr. The animals were given then acetazolamide intravenously which was followed by acidification and increased partial oxygen pressure in the arterial blood. At the same time the oxygen gradient between the arterial blood and cerebrospinal fluid (CSF) practically disappeared. Administration of a hypoxic breathing mixture reversed again the oxygen gradient. It is worth stressing that the pH of the arterial blood showed no statistically significant fall. In view of this it is postulated that Bohr's effect is not responsible for the reversal of the oxygen gradient although it has been suggested by Jankowska and Grieb [13]. We put forward the hypothesis that the rate of oxygen passage on the arterial side of the blood-brain barrier is not identical in both directions, and its passage from the blood into the CSF decreases with increasing arterial hypoxia. This mechanism of "oxygen trap" may be the cause of reversal of the oxygen gradient between the arterial blood and CSF in hypoxia.