Showing papers by "Giuseppe Mancia published in 1975"

Influence of carotid baroreceptors on vascular responses to carotid chemoreceptor stimulation in the dog.

Abstract: The modification by the carotid baroreceptors of the vascular responses to chemoreceptor stimulation was studied in anesthetized, artificially ventilated, vagotomized dogs. The carotid bifurcations were vascularly isolated and perfused with blood at constant pressures of 134, 215, and 51 mm Hg to cause intermediate, maximal, and minimal inhibition, respectively, of the vasomotor center. At each pressure, stimulation of the carotid chemoreceptors was achieved by perfusion with hypoxic hypercapnic blood. With intermediate inhibition, the chemoreceptor stimulation increased the aortic pressure by 50% and decreased the hind-limb and kidney blood flow (perfusion at constant pressure) by 59% and 19%, respectively. At carotid sinus pressures of 215 and 51 mm Hg, the effects of chemoreceptor stimulation were absent or markedly attenuated. With intermediate sinus pressure, chemoreceptor stimulation decreased the perfusion pressure of the saphenous vein by 27% (perfusion at constant flow). When the sinus pressure was increased to 215 mm Hg, the tone of the vein did not change, but chemoreceptor stimulation was without effect. The present study indicates a central interaction (which may be presynaptic) between the chemoreceptor and baroreceptor inputs such that the vascular responses to chemoreceptor stimulation are inhibited when the carotid sinus activity is maximal or minimal.

Demonstration that the atria, ventricles, and lungs each are responsible for a tonic inhibition of the vasomotorcenter in the dog.

Abstract: To localize the areas of the cardiopulmonary region involved in tonic inhibition of the vasomotor center, anesthetized dogs were subjected to sinoaortic denervation and diaphragmatic vagotomy. Afferent vagal nerve traffic was interrupted in the neck by cooling. With the venous return taken from the venae cavae, oxygenated extracorporeally, and returned to the aorta, the heart was removed, leaving the ventilated lungs (condition 1), and the lungs and the ventricles were removed, leaving the beating atria (condition 3). With the venous return taken from the pulmonary arteries, oxygenated extracorporeally, and returned to the left atrium, the lungs were removed, leaving the intact working heart (condition 2), and the lungs were removed and the atria were denervated, leaving the working innervated ventricles (condition 4). Vagal cooling increased aortic pressure by 25 plus or minus 2 (SE) mm Hg in condition 1, by 36 plus or minus 2 mm Hg in condition 2, by 29 plus or minus 2 mm Hg in condition 3, and by 29 plus or minus 7 mm Hg in condition 4. Removing the atria in condition 3 or denervating the ventricles in condition 4 abolished the reflex response. Thus, afferent vagal nerves from the lungs and the heart tonically inhibit the vasomotor center. The inhibition exerted by the heart is caused by receptors in the atria and the ventricles.

Role of cardiac, pulmonary, and carotid mechanoreceptors in the control of hind-limb and renal circulation in dogs.

Abstract: Reflex control of hind-limb and renal resistance vessels by cardiac and pulmonary receptors was studied by interrupting afferent vagal nerve traffic when only the heart or only the lungs were in situ in anesthetized dogs with sinoaortic denervation. During normocapnia, interruption of cardiac and of pulmonary vagal traffic decreased hind-limb blood flow (constant-pressure perfusion) by 23% and 21%, respectively. Corresponding decreases in renal blood flow were 23% and 33%. Hypercapnia augmented the decreases in renal blood flow due to the vagal block. Thus, the inhibitions exerted by the heart and lung receptores on these two beds were similar during normocapnia but were greater on the renal vessels during hypercapnia. In closed-chest dogs with their aortic nerves sectioned and their carotid sinus pressure controlled, combined withdrawal of carotid and cardiopulmonary inhibition decreased hind-limb and renal blood flow by about 80% and 40%, respectively, during both normovolemia and hypervolemia. Interruption of cardiopulmonary inhibition was responsible for 17% and 31% of the decrease in hind-limb blood flow at normal and increased blood volumes, respectively; values for the decreases in renal blood flow were 50% and 65%. Thus, cardiopulmonary receptors oppose the vasoconstriction due to carotid hypotension more effectively in the kidney than they do in the hind limb.