In cats the vagal bradycardia of the pulmonary chemoreflex is unusual in that it is not modulated by central respiration or lung inflation (Daly, 1991). It was proposed that mechanisms acting within the brainstem (preganglionic level) and/or at the cardiac ganglia (postganglionic level) may account for this phenomenon (Jones, 2001). To sample a large number of cardiac vagal preganglionic neurones during the pulmonary chemoreflex we used a suction microelectrode technique to record activity in vagal axons in rats and cats.

Fourteen adult male Wistar rats, weighing 233-371 g, were anaesthetised with urethane (1.5 g kg^-1 I.P.). Conduction velocity of the spontaneously active units recorded from the cardiac branch was calculated using spike triggered averaging (STA) of electrical activity in the whole ipsilateral vagus. Of the 225 units recorded and averaged, only 33 discernible averages evolved. Seventeen of these STA latencies corresponded to units in the C-fibre range (conduction velocity < 2 m s^-1) and 16 units in the B-fibre range (conduction velocity 3-15 m s^-1). Phenylbiguanide (PBG, 20 mg kg^-1) was injected into the right superior vena cava to elicit a pulmonary chemoreflex. Increased activity (< 2 s latency) was recorded in 37/192 unclassified fibres, 5/16 B-fibres and 3/17 C-fibres. Of the units responding to PBG, three B-fibres and three C-fibres had central respiratory and/or lung inflation-related activity, but this only became obvious when post-stimulus histograms (PSTHs) were constructed. Since the duration of the reflex response was shorter than the time required to acquire the PSTH data, the rat is an unsuitable model to test our hypothesis. We therefore returned to the cat, the species used by Daly (1991).

Two cats (1.8-2.5 kg) were anaesthetized with chloralose (80 mg kg^-1; I.V.). The preparation of the cats was similar to that of the rats except recordings were obtained from the cervical vagus. We recorded and tested only units that exhibited expiratory discharge patterns (n = 10). In no case was the respiratory rhythm lost during the pulmonary chemoreflex.

In conclusion, the technical approach of axonal recording developed in the rat, also works very successfully in the cat. Further experiments concentrating on the cardiac vagal branch of the cat will provide an excellent test of the hypothesis that the pulmonary chemoreflex loses respiratory modulation during the final integrative action of cardiac vagal ganglia.

This work was supported by The Wellcome Trust, UK.