Abstract:The effects of progressive anoxia on the hemodynamic changes in the pulmonary circuit were reinvestigated in anesthetized dogs. Evidence is presented that some increase in pulmonary arterial resistance takes place, but that the augmented output of the right ventricle is dominantly responsible for elevation of the pulmonary arterial pressure when anoxia affects the bodv as a whole.
“…The fact that the 02 uptake consistently decreased when 15.65 per cent 02 was breathed is not understood but has been commonly observed to occur in this laboratory under resting conditions whether ventilation is controlled (21) or uncontrolled. It seems possible that in these three experiments the low 02 produced a change in the pulmonary vascular bed (22,23) so that all the conditions necessary for the valid calculation of Do2 may not have been satisfied. (Table I) were, however, not unusually large nor were their tidal volumes during exercise.…”
It is generally accepted that the exchange of pulmonary gases between "alveolar air" and pulmonary blood takes place by simple diffusion across the "pulmonary membrane." 2 Two properties of this membrane, namely, its permeability to gases and its surface area, are of considerable interest since a decrease in either could limit the rate of gaseous diffusion. There is no known physiological method for measuring specifically the permeability as contrasted to the area of the pulmonary diffusing surface in man. In 1915, M. Krogh (1), using carbon monoxide, made the first determinations of the pulmonary "diffusion constant" in human beings. This constant was considered to be proportional to both permeability and area of the diffusing surface and was expressed in cc. of CO diffusing per mm. Hg of CO partial pressure difference on either side of the pulmonary membrane. Roughton (2) has viewed the diffusion constant of normal persons as a measure of the number and size of patent pulmonary capillaries. Several investigators (3), in considering the diffusion constant for oxygen, have recommended that it be referred to as the "diffusing capacity" because its magnitude is greater during exercise than at rest.Carbon monoxide is peculiarly suitable for studies of gas diffusion across the pulmonary membrane because of the tenacity with which it is bound by hemoglobin after it has diffused into the red cells. For this reason, CO is taken up from respired gas for considerable periods of time (4) without there being a significant change in the Pco, or "escaping tendency," in the pulmonary capillary blood. The driving force responsible for CO transport across 1 These studies were aided by a contract between the Office of Naval Research, Department of the Navy, and the Trudeau Foundation
“…The fact that the 02 uptake consistently decreased when 15.65 per cent 02 was breathed is not understood but has been commonly observed to occur in this laboratory under resting conditions whether ventilation is controlled (21) or uncontrolled. It seems possible that in these three experiments the low 02 produced a change in the pulmonary vascular bed (22,23) so that all the conditions necessary for the valid calculation of Do2 may not have been satisfied. (Table I) were, however, not unusually large nor were their tidal volumes during exercise.…”
It is generally accepted that the exchange of pulmonary gases between "alveolar air" and pulmonary blood takes place by simple diffusion across the "pulmonary membrane." 2 Two properties of this membrane, namely, its permeability to gases and its surface area, are of considerable interest since a decrease in either could limit the rate of gaseous diffusion. There is no known physiological method for measuring specifically the permeability as contrasted to the area of the pulmonary diffusing surface in man. In 1915, M. Krogh (1), using carbon monoxide, made the first determinations of the pulmonary "diffusion constant" in human beings. This constant was considered to be proportional to both permeability and area of the diffusing surface and was expressed in cc. of CO diffusing per mm. Hg of CO partial pressure difference on either side of the pulmonary membrane. Roughton (2) has viewed the diffusion constant of normal persons as a measure of the number and size of patent pulmonary capillaries. Several investigators (3), in considering the diffusion constant for oxygen, have recommended that it be referred to as the "diffusing capacity" because its magnitude is greater during exercise than at rest.Carbon monoxide is peculiarly suitable for studies of gas diffusion across the pulmonary membrane because of the tenacity with which it is bound by hemoglobin after it has diffused into the red cells. For this reason, CO is taken up from respired gas for considerable periods of time (4) without there being a significant change in the Pco, or "escaping tendency," in the pulmonary capillary blood. The driving force responsible for CO transport across 1 These studies were aided by a contract between the Office of Naval Research, Department of the Navy, and the Trudeau Foundation
“…The pulmonary pressor response to hypoxia was studied in each animal under three different circumstances: (1) with the animal awake, (2) in the anesthetized animal with intact pulmonary circulation in which changes in pulmonary vascular resistance could be calculated as in Group A, and (3) during constant flow perfusion of a portion of the pulmonary vasculature.…”
Section: Group Bmentioning
confidence: 99%
“…15 yr ago it was suggested that the catecholamines were involved in this response (1,2). Subsequent investigations have been inconclusive in either supporting or refuting this hypothesis.…”
A B S T R A C T The highly reactive pulmonary vascular bed of the neonatal calf was utilized to determine whether the hypoxic pulmonary pressor response is modified by a-adrenergic blockade with phenoxybenzamine (Group A) or by tissue catecholamine depletion with reserpine (Group B). In addition, in Group A, the effects of hypoxia on the pulmonary circulation were compared and contrasted with those of l-norepinephrine (a-receptor stimulator) and isoproterenol (,8-receptor stimulator).In Group A, changes in pulmonary vascular resistance were calculated from measurements of appropriate pressures and of pulmonary blood flow (electromagnetic flowmeter). The increase in pulmonary vascular resistance produced by hypoxia was not diminished by a-adrenergic blockade. However, blockade abolished the pulmonary vasoconstrictor effect of norepinephrine. During hypoxic pulmonary vasoconstriction, the administration of either norepinephrine or isoproterenol lowered the pulmonary vascular resistance both before and after a-blockade. 25 September 1967. sels secondary to an increased pulmonary blood flow.The pulmonary vascular response to hypoxia in the reserpinized calves (Group B) was tested under three circumstances: (1) in the awake animal, (2) in the anesthetized animal prepared in the same way as those in Group A, and (3) during constant flow perfusion of the left lower lobe pulmonary artery. From these studies it was concluded that tissue catecholamine depletion did not diminish the pulmonary vascular response to hypoxia.Thus, neither a-adrenergic blockade nor tissue catecholamine depletion prevents the hypoxic pulmonary pressor response. Furthermore, a-blockade prevents the pulmonary vasoconstrictor response to norepinephrine but not to hypoxia. Therefore it is concluded that hypoxic pulmonary vasoconstriction is not mediated through adrenergic receptor stimulation or release of endogenous catecholamines.
“…The site of action of this vasomotor response has not been definitely identified. (7), Rahn and Bahnson (20), Hiirlimann and Wiggers (21), and Stroud and Conn (22). It has also been proposed that the vasomotor activity of the alveolar capillaries could be responsible for the hemodynamic changes that follow alterations in alveolar oxygen tension (4).…”
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.