1. In dogs under chloralose and urethane anaesthesia, the carotid and aortic bodies were isolated from the circulation and separately perfused with blood, the composition of which could be controlled at will. The remainder of the systemic circulation was perfused at constant blood flow, thereby enabling the reflex vascular responses to be determined. The systemic venous blood was oxygenated in the isolated perfused lungs of a second dog and the P(O2) and P(CO2) of the systemic arterial blood was maintained constant.2. Using hypoxic hypercapnic blood to stimulate the arterial chemoreceptors, carotid body excitation in spontaneously breathing animals caused an increase in respiratory minute volume approximately seven times larger than that evoked by stimulation of the aortic bodies. Whereas the hyperpnoea of carotid body origin is due to an increase in rate and depth of breathing, that from the aortic bodies is due predominantly to an increase in respiratory frequency.3. Stimulation of the carotid bodies in spontaneously breathing animals caused small variable changes in systemic vascular resistance, whereas stimulation of the aortic bodies invariably increased the vascular resistance.4. When pulmonary ventilation was maintained constant, the vascular response to stimulation of the carotid bodies was considerably modified in that constriction invariably occurred; that from the aortic bodies, however, was little affected. There was now no significant difference in the size of responses from the two groups of chemoreceptors. These constrictor responses represent the primary vascular effects.5. A similar modification of the carotid body vascular response occurred in the spontaneously breathing animal after denervation of the lungs, and is due to abolition of a lung-inflation vasodilator reflex.6. The size of the primary vasoconstrictor responses from the carotid and aortic bodies is reduced by lowering the arterial blood P(CO2).7. The results indicate that there is a fundamental difference in the functions of the carotid and aortic bodies. They exert a quantitatively similar primary control of the ;vasomotor centre' which is in striking contrast to the relatively more powerful influence on respiration by the carotid bodies. In the spontaneously breathing animal, however, the primary vasoconstrictor response from the carotid bodies is offset to a varying degree by the lung-inflation vasodilator reflex initiated by the concomitant hyperpnoea. This is not evident with the aortic bodies because of the relatively weaker respiratory response they evoke.
SUMMARY1. The reflex effects of alterations in lung volume on systemic vascular resistance have been studied in anaesthetized dogs under conditions in which the systemic circulation was perfused at constant blood flow. The pressures in the isolated perfused carotid sinuses and aortic arch, and the arterial blood Po2 and Pco2 were maintained constant.2. A maintained inflation of the lungs produced by injection of air into the trachea caused a fall in systemic arterial perfusion pressure, indicating vasodilatation. The size of the systemic vasodilator response varied directly with the pressure and volume of gas used to inflate the lungs. A similar effect was observed when the tidal volume of lungs ventilated by an intermittent positive pressure was increased.3. Collapse of the lungs by creating a pneumothorax in closed-chest spontaneously breathing animals evoked a systemic vasoconstrictor response which was reversed when the lungs were re-expanded.4. These vasodilator responses were abolished by dividing the pulmonary branches of the thoracic vagosympathetic nerves. Evidence is presented that the afferent fibres run in the cervical vagosympathetic nerves and through the stellate ganglia.5. The responses were unaffected by atropine, but were abolished by hexamethonium, guanethidine and by bretylium tosylate, indicating that they are mediated via the sympathetic nervous system. 6. Evidence is presented that the lungs are a constant course of afferent impulses inhibiting the 'vasomotor centre', and that the lung inflationsystemic vasodilator reflex is a potential mechanism operating in eupnoeic breathing. M. DE BURGH DALY AND OTHERS
SUMMARY1. We have studied the release of noradrenaline and adrenaline from the adrenal glands of dogs and cats in response to the lowering of carotid sinus pressure (baroreceptor tests) and to the perfusion of the vascularly isolated carotid bifurcations with hypoxic blood (chemoreceptor tests).2. In cats, the resting output of catecholamines had a ratio of noradrenaline to adrenaline of 1:1. The ratio in the incremental release during baroreceptor tests rose to 3: 1, and during chemoreceptor tests it fell to 1: 6. 3. In dogs, the ratio of noradrenaline to adrenaline at rest was 1:4. The ratio did not change over a wide range of outputs during baroreceptor tests, chemoreceptor tests and splanchnic nerve stimulation.4. The release of catecholamines in response to baroreceptor tests in the cat was abolished by hexamethomium bromide at doses that did not diminish the response to chemoreceptor tests.
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