The influence of the sympathetic outflow on aortic chemoreceptors of the cat during hypoxia and hypercapnia.

Abstract

SUMMARY1. An attempt has been made to reconcile differing observations, made by different groups of investigators, on the responses of aortic chemoreceptors of cats during normoxia, hypoxia and hypercapnia.2. In cats anaesthetized with sodium pentobarbitone it was observed that during hypoxic stimulation of twelve chemoreceptors, an intravenous injection of about 20 mg sodium pentobarbitone produced hypotension which was accompanied by an initial fall in chemoreceptor activity instead of the expected increase that invariably occurred in all the receptors when hypotension was produced mechanically by distending a balloon in the right atrium (twenty-six during normoxia, eleven during hypoxia and eight during hypercapnia).3. In twelve receptors a reflex fall in blood pressure produced by injecting 8-25 ,ug veratridine (Bezold-Jarisch reflex) yielded results qualitatively similar to those following injection of sodium pentobarbitone.4. In sixteen out of twenty-five chemoreceptors it was observed that ventilating the cat with 5-6-6-7 % CO2 produced either no or little increase in activity; in nine receptors there was a clear increase in activity, which fell initially or was abolished after injecting a single dose of 20 mg sodium pentobarbitone. 5. In all seven chemoreceptors tested in seven deeply anaesthetized cats it was found that a larger dose (about 50-60 mg) of sodium pentobarbitone had no direct depressant effect on aortic chemoreceptor activity. It followed that the initial depressant effect of the much smaller doses of sodium pentobarbitone observed during hypoxic and hypercapnic stimulation (see above) must be due to reduction in the sympathetic outflow to the aortic bodies. This conclusion was supported by the results following injections of veratridine.6. By comparing the present results with those reported previously it was concluded that the variations in the responses of aortic chemoreceptors during hypoxia and hypercapnia reported by different investigators could be partly due to variations in the level of sympathetic activity prevailing under different experimental conditions.

Reflex stimulation of aortic chemoreceptors through the stellate ganglion during hypoxia and hypotension in cats.

“…It is well known that hypotension stimulates aortic chemoreceptors (Lee et al 1964;Paintal 1967;Lahiri, Nishino, Mokashi & Mulligan, 1980;Anand & Paintal, 1988). The present results show that such stimulation is reduced by about one-third after removal of the sympathetic outflow to them by stellectoiny and also by a bolus injection of sodium pentobarbitone.…”

“…It has been shown that if a bolus injection of sodium pentobarbitone is given intravenously while the aortic chemoreceptors are being stimulated by hypoxia or hypercapnia, the chemoreceptor activity falls within a few seconds despite the simultaneous fall in blood pressure. This fall in activity, which is not due to any direct depressant action of sodium pentobarbitone on chemoreceptors, was attributed by Anand & Paintal (1988) to the reduction of sympathetic outflow known to be produced by sodium pentobarbitone (Goodman & Gilman, 1955). The present investigation was undertaken to determine the peripheral mechanism responsible for this fall in chemoreceptor activity, i.e.…”

“…By this time the effect of the sodium pentobarbitone bolus had largely worn off, as shown by the rise in blood pressure during hypoxia (see Results). It should be noted that sodium pentobarbitone does not depress the transduction mechanisms of aortic chemoreceptors, as shown by their marked excitation following injection of relatively much larger (60 mg) doses of the drug (Anand & Paintal, 1988). (3) To test the effect of injecting sodium pentobarbitone on chemoreceptor activity during hypoxia before and after cutting the vagi and carotid sinus nerves.…”

“…This was typically about 28 mmHg (pH 7 3). However, since CO2 has no excitatory effect on aortic chemoreceptors (Anand & Paintal, 1988) anid since the values for Pa,co, remained at the same level before and during individual manoeuvres, the values for Pa,co2 and pH are not given in the Results. Since the chest was opened for removing the stellate ganglion, positive end-expiratory pressure of 5 cmH2( was applied.…”

“…This fall in activity, which is not due to any direct depressant action of sodium pentobarbitone on chemoreceptors, was attributed by Anand & Paintal (1988) to the reduction of sympathetic outflow known to be produced by sodium pentobarbitone (Goodman & Gilman, 1955). The present investigation was undertaken to determine the peripheral mechanism responsible for this fall in chemoreceptor activity, i.e.…”