Effect of O<sub>2</sub> and CO<sub>2</sub> Tensions Upon the Resistance of Pulmonary Blood Vessels

Stroud, Robert C.; Rahn, Hermann

doi:10.1152/ajplegacy.1952.172.1.211

Cited by 87 publications

(25 citation statements)

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“…As demonstrated by others (14-16) with arterial oxygen saturations above 55 %, pulmonary blood flow tended to remain unchanged and thus pulmonary vascular resistance increased. In spontaneously breathing dogs, the mean rise of pulmonary vascular resistance ranged from 38 to 48o (14)(15)(16), whereas in the present series of dogs that were artificially ventilated it increased 60%. In conscious trained dogs, breathing of 6 to 15%o oxygen in nitrogen mixtures increased both pulmonary vascular resistance and pulmonary blood flow at any inspired mixture (17).…”

Section: Resultscontrasting

confidence: 59%

“…In the latter, hypoxia vasoconstriction would serve as a protective mechanism to shunt blood to better ventilated parts of the lung. Regional arterial and arteriolar vasoconstriction might be a direct effect of the low oxygen tension in small airways and alveoli affecting the arteriolar or capillary vessel wall by diffusion (26) or as yet anatomically undemonstrated axon connections from the pulmonary veins to arteries (15).…”

Section: Resultsmentioning

confidence: 99%

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The site of pulmonary vasomotor activity during hypoxia or serotonin administration.

Sackner¹,

Will²,

DuBois³

1966

J. Clin. Invest.

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Pulmonary arterial pressure increases in dogs exposed to alveolar hypoxia or intravascular infusion of 5-hydroxytryptamine (serotonin). Although most investigators believe that this increase in pressure reflects a vasoconstriction in the pulmonary vascular bed, the site of vasoconstriction, whether venular, capillary, or arteriolar, is controversial. Interpretations have been based previously upon measurements of pressure and flow at various sites in the pulmonary circulation and have been handicapped by the inability to measure the volumes of the segments under study (1-3). MethodsEleven mongrel dogs weighing 12.3 to 17.7 kg were used in the experiments. They were anesthetized with sodium pentobarbital in a dosage of 26 mg per kg body weight. An 8F or 9F Cournand cardiac catheter 1 was introduced into the external jugular vein, and under fluoroscopic guidance its tip was placed within the pulmonary artery. A second catheter was placed so that its tip lay within the superior vena cava. A pediatric 7F Brockenbrough left heart catheter 1 was introduced into the femoral vein and the atrial septum punctured so that the tip of the catheter lay free in the left atrial cavity. The femoral artery was cannulated with polyethylene tubing 25 cm in length and 2 mm in diameter in such a way that its tip lay in the distal aorta. The animal was enclosed within a horizontal Plexiglas body plethysmograph (4), then paralyzed with succinylcholine and ventilated with a Starling pump. Intravascular pressures were measured by strain gauges 2 balanced to a reference pressure level 9.8 cm above the surface of the dog board. Plethysmographic pressure was measured by a differential strain gauge.3 A direct-writing instrument 4 recorded pressures from the strain gauges, the electrocardiogram, and dye concentration from a cuvette densitometer.5The plethysmograph was calibrated by injection and withdrawal of 10 ml of air with a syringe, and this produced a deflection of 20 to 30 mm on the record. The pulmonary arterial pressure was monitored while the catheter was pulled back slowly until a ventricular pressure tracing was recorded, and then the tip of the catheter was advanced to the point where a pulmonary arterial pressure tracing was again recorded from a position just beyond the pulmonic valve. A 0.5-ml volume of solution, containing 0.1 ml of ether in 0.4 ml of alcohol, was instilled into the catheter to be flushed into the animal by 5 ml of saline. In several experiments designed to determine whether C02 evolution rate was affected, 0.5 ml of a 0.5 M lactic acid solution was instilled into the catheter to be flushed into the animal by 5 ml of saline, or 5 ml of a 0.9 M sodium bicarbonate solution was placed into the catheter and connecting tubing, and this was also ad-

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Section: Resultscontrasting

confidence: 59%

Section: Resultsmentioning

confidence: 99%

The site of pulmonary vasomotor activity during hypoxia or serotonin administration.

Sackner¹,

Will²,

DuBois³

1966

J. Clin. Invest.

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“…Many investigators, using dogs or cats, have reported that the hypoxic pulmonary pressor response was reduced or abolished by pharmacological or surgical sympathectomy (3)(4)(5)(6)(7)(8)(9). However, other work may be cited in which the pulmonary vascular response to hypoxia persisted in Alpha Adrenergic Blockade and Pulmonary Vascular Response to Hypoxia dogs, cats (10)(11)(12), calves (13), and humans (26) after similar maneuvers.…”

Section: Discussionmentioning

confidence: 99%

“…Subsequent investigations have been inconclusive in either supporting or refuting this hypothesis. Several investigators have concluded that blockade of the sympathetic nervous system reduces or abolishes the pulmonary pressor response to hypoxia (3)(4)(5)(6)(7)(8)(9). There is equally strong evidence to dispute this…”

Section: Introductionmentioning

confidence: 99%

Effects of alpha adrenergic blockade and tissue catecholamine depletion on pulmonary vascular response to hypoxia

Silove¹,

Grover²

1968

J. Clin. Invest.

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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.

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“…Since then, factors modulating HPV have been identified by dissecting the mechanism of HPV using a variety of approaches including isolated organs, tissues and single cells. Modulating factors include sex, local and circulating vasoactive substances, pH, partial pressure of carbon dioxide [17,18] and red blood cells, although there was an early consensus that the mechanism itself was independent from neural [19] or humoral [20,21] triggers.…”

Section: Characteristics and Kinetics Of Hpvmentioning

confidence: 99%

Regulation of hypoxic pulmonary vasoconstriction: basic mechanisms

Sommer¹,

Dietrich²,

Schermuly³

et al. 2008

Eur Respir J

186

142

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Hypoxic pulmonary vasoconstriction (HPV), also known as the von Euler-Liljestrand mechanism, is a physiological response to alveolar hypoxia which distributes pulmonary capillary blood flow to alveolar areas of high oxygen partial pressure.Impairment of this mechanism may result in hypoxaemia. Under conditions of chronic hypoxia generalised vasoconstriction of the pulmonary vasculature in concert with hypoxia-induced vascular remodelling leads to pulmonary hypertension. Although the principle of HPV was recognised decades ago, its exact pathway still remains elusive. Neither the oxygen sensing process nor the exact pathway underlying HPV is fully deciphered yet. The effector pathway is suggested to include L-type calcium channels, nonspecific cation channels and voltagedependent potassium channels, whereas mitochondria and nicotinamide adenine dinucleotide phosphate oxidases are discussed as oxygen sensors. Reactive oxygen species, redox couples and adenosine monophosphate-activated kinases are under investigation as mediators of hypoxic pulmonary vasoconstriction. Moreover, the role of calcium sensitisation, intracellular calcium stores and direction of change of reactive oxygen species is still under debate.In this context the present article focuses on the basic mechanisms of hypoxic pulmonary vasoconstriction and also outlines differences in current concepts that have been suggested for the regulation of hypoxic pulmonary vasoconstriction.

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Effect of O₂ and CO₂ Tensions Upon the Resistance of Pulmonary Blood Vessels

Cited by 87 publications

References 0 publications

The site of pulmonary vasomotor activity during hypoxia or serotonin administration.

The site of pulmonary vasomotor activity during hypoxia or serotonin administration.

Effects of alpha adrenergic blockade and tissue catecholamine depletion on pulmonary vascular response to hypoxia

Regulation of hypoxic pulmonary vasoconstriction: basic mechanisms

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Effect of O2 and CO2 Tensions Upon the Resistance of Pulmonary Blood Vessels

Cited by 87 publications

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The site of pulmonary vasomotor activity during hypoxia or serotonin administration.

The site of pulmonary vasomotor activity during hypoxia or serotonin administration.

Effects of alpha adrenergic blockade and tissue catecholamine depletion on pulmonary vascular response to hypoxia

Regulation of hypoxic pulmonary vasoconstriction: basic mechanisms

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Effect of O₂ and CO₂ Tensions Upon the Resistance of Pulmonary Blood Vessels