The relation between carotid body chemoreceptor discharge, carotid sinus pressure and carotid body venous flow

Abstract

SUMMARY1. Activity in forty-two single chemoreceptor afferent fibres from the carotid body in thirty-nine cats was measured when the carotid body was naturally and artificially perfused. In nine of these cats, carotid body venous flow was also measured.2. When pressure within the carotid sinus segment was suddenly raised or lowered, chemoreceptor activity changed in the opposite direction within the first 5-10 sec by an amount which was significantly greater than the variation of activity in the control period. Thereafter activity stabilized at a level which was not different from control.3. Whether the carotid body was naturally or artificially perfused, carotid body chemoreceptor activity, following this initial transient change, was unaffected in eight out of twelve fibres by alterations in carotid sinus pressure within the range 60-160 mm Hg and carotid body venous flow 10-60 ,ul./min, blood gas tensions and pH being maintained constant. In the four remaining fibres, chemoreceptor activity increased slightly but significantly as pressure was lowered in this range. Chemoreceptor activity increased in all fibres tested when pressure was lowered below 50-60 mm Hg. 5. These results indicate that the carotid body chemoreceptors are relatively unaffected by sustained changes in arterial pressure or in total carotid body flow within the physiological range.

Effects of ouabain on carotid body chemoreceptor activity in the cat.

“…in our experiments. However, although we cannot entirely preclude such a vascular mechanism, we consider it unlikely because moderate alterations in carotid blood flow do not cause sustained changes in chemoreceptor discharge (Biscoe, Bradley & Purves, 1970) and, in any event, chemoexcitation induced by ouabain was still manifest after stopping the infusion, even though any vascular effects of ouabain would have terminated (Treat et al 1971).…”

Carbon dioxide and venous return and their interaction as stimuli to ventilation in the cat

“…The effect of altering the volume of venous return upon respiration was probably first documented by Krogh & Linhard (1913) and subsequently confirmed by Bouckaert & Pannier (1942), Yeomans, Porter & Swank (1943), Mills (1944 and Brown, Goei, Greenfield & Plassavas (1966). Respiration has also been shown to be affected by intravenous infusion (Harrison, Harrison & Marsh, 1932;Coleridge & Linden, 1955;Hirsch, Boyd & Katz, 1964) while more recently, Wasserman et al (1974) have shown that an increase in cardiac output induced by electrical pacing or by isoproterenol is associated with hyperpnoea and that beta-adrenergic blockade causes hypopnoea (Brown, Wasserman & Whipp, 1976 (Lipski, McAllen & Trzebski, 1976), an action which will be enhanced by activation of arterial chemoreceptors which are sensitive to small, transient changes in perfusion pressure (Lee, Mayou & Torrance, 1964;Biscoe, Bradley & Purves, 1970) and possibly potentiated centrally (Heistad, Abboud, Mark & Schmid, 1974 Fig. 7).…”

Ventilatory baroreflex sensitivity in humans is not modulated by chemoreflex activation

“…Rapidly increasing blood pressure causes decreased ventilation, whereas decreasing blood pressure causes increased ventilation. While these ventilatory effects were at one time attributed to increased or decreased perfusion of the arterial chemoreceptors (26,32), subsequent investigations in experimental preparations have shown that exclusion of the carotid body from the carotid sinus area does not alter the ventilatory response in vagotomized dogs (7) and sinoaortic denervation eliminates the pressuresensitive ventilation response in dogs (47), whereas the carotid body chemoreceptor in cats is insensitive to blood pressure change (3).…”