The reflex effects of alterations in lung volume on systemic vascular resistance in the dog

Abstract

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

Reflex Cardiovascular Depression Produced by Stimulation of Pulmonary Stretch Receptors in the Dog

“…5, and it shows that the effects on the cardiovascular system produced by inflation of the lungs were markedly lessened by interruption of the vagus nerves. DISCUSSION Partly in confirmation of previous findings (6,7) the results of the present investigation clearly indicate that pulmonary stretch receptors do affect cardiovascular function, and that their activation results in reflex inhibition of sympathetic tone with consequent decreases in myocardial performance, heart rate, and peripheral vascular resistance. That these observed depressor responses are indeed reflex in nature rather than the result of mechanical effects produced by inflation of the lungs is indicated by the fact that they were observed in animals on right heart bypass, which means that they were not merely the result of induced changes in venous return, since blood flow into the pulmonary artery was kept constant.…”

“…Thus, the baroreceptors were undoubtedly stimulated by the intervention and the sympathetic nervous activity that was measured was probably the resultant effect of the balance between the -baroreceptor reflex and the pulmonary stretch reflex. That such a balance does indeed exist is substantiated by the findings of Daly and coworkers who observed that the magnitude of vasodepression produced by inflation of the lungs was related to the pressures within the baroreceptor areas located within the carotid sinus and aortic arch regions (7). In the study reported here, since openchest dogs were used in all except two experiments, changes in arterial pressure resulting from changes in intrathoracic pressure were avoided.…”

“…This latter view has been supported by Salisbury, Galletti, Lewin, and Rieben (6) and by Daly, Hazzledine, and Ungar (7), who noted that systemic arterial pressure fell when the lungs were expanded. The interpretation of the data that has been accumulated by these investigators has been complicated by the fact that in some of the studies the experimental animals breathed spontaneously (1,5), in some they were artificially ventilated (3)(4)(5)(6)(7), and in some studies gas exchange was produced by diffusion respiration (2). To try to resolve the question of whether or not pul-monary stretch receptors exert control over the cardiovascular system, experiments were designed that would allow separate assessment of the possible reflex effects of positive pressure inflation of the lungs on cardiac function and on the resistance of an isolated vascular bed, together with a reinvestigation of the effects produced by inflation of the lungs on the total peripheral vascular resistance.…”

Stimulus—cardiorespiratory Effector Response Profile During Arterial Hypoxia in the Unanaesthetized Rabbit

“…Previous analysis has shown tliut lung inflation plays ati important part in modifying the cardiovascular response of the rahhit and of other species during strong clu-moreceptor stimulation. Thus, Daly et al (1967), Daly and Rohinson (1968) and Angel! James and Daly (1969) have shown in the dog that lung inflation inhibits the primary circulatory effects of strong ehemoreeeptor stimulation (i.e.…”

Cardiovascular responses to diving in the turtle, Pseudemys scripta

“…In addition, it is possible that whereas the respira tory reflex response is inhibited by facial receptors, the cardiac ren rx "is ér!nrtrî(":hcl n i " triril i Î wnrr -i n-r "i a -r n r-2 t : c cc 'r\\r na 1 /Hal \/ a w/n Scott; 1958; and vasodilation in the splanchnic vascular bed, skin, and muscle by reducing the activity of adrenergic sympathetic fibers (Daly et al, 1967). The receptors responsible for initiating these changes are the pulmonary stretch receptors (Daly and Robinson, 1968;Hainsworth et al.…”