Pulmonary hemodynamics during acute acid-base changes in the intact dog

Shapiro, BJ; Simmons, D H; Lm, Linde

doi:10.1152/ajplegacy.1966.210.5.1026

Cited by 30 publications

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“…Therefore, we conclude that the constrictive pattern to metabolic acidosis is similar to those earlier findings. In previous studies, it was reported that cardiac output was unchanged significantly in response to metabolic acidosis (BERGOFSKY et al, 1962;SHAPIRO et al, 1966). Our results also indicated that, with metabolic acidosis, the volume flow in the main arterial branches remained constant.…”

supporting

confidence: 82%

“…In previous studies, by measuring the pressure-flow relationship in the pulmonary vascular bed, it was suggested that metabolic acidosis, produced by infusing lactic acid (BERGOFSKY et al, 1962;BARER et al, 1967;VILES and SHEPHERD, 1968a, b), as well as respiratory acidosis (BERGOFSKY et al, 1962;SHAPIRO et al, 1966;VILES and SHEPHERD, 1968a, b) increased pulmonary vascular resistance. For better understanding of the effect of metabolic and respiratory acidosis on pulmonary microcirculation, it was important to measure directly the changes in internal diameter (ID), flow velocity, and volume flow in small pulmonary vessels.…”

mentioning

confidence: 99%

“…From the pressure-flow relationship, it was suggested that metabolic acidosis, produced by infusing lactic acid or hydrochloric acid, increased pulmonary vascular resistance (BERGOFSKY et al, 1962;SHAPIRO et al, 1966;BARER et al, 1967;VILES and SHEPHERD, 1968a, b). In our study, the nonuniform vasoconstrictton in small pulmonary arteries during metabolic acidosis was demonstrated directly.…”

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confidence: 99%

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Effect of metabolic acidosis on pulmonary microcirculation in the cat.

Sada¹,

Shirai²,

Ninomiya³

1987

Jpn.J.Physiol

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confidence: 99%

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confidence: 99%

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Effect of metabolic acidosis on pulmonary microcirculation in the cat.

Sada¹,

Shirai²,

Ninomiya³

1987

Jpn.J.Physiol

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“…Increased hydrogen ion concentration in the perfusate has also been shown to cause constriction in the pulmonary vascular bed of various animals (3)(4)(5). Recent workers (6,7) have suggested that the vasoconstrictor effect of hypercapnia is due to the acidosis produced.…”

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confidence: 99%

Evidence for a Dilator Action of Carbon Dioxide on the Pulmonary Vessels of the Cat

Viles

Shepherd

1968

Circulation Research

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Isolated cat lungs perfused at constant flow (75 ml/min per kg total body weight) were ventilated with gases of varying CO 2 content (0 to 10%), 20% O 2 , and the balance N 2 . Tidal volume was constant, and airway pressure did not change. Left atrial pressure was held constant, and changes in pulmonary artery pressure (PPA) were taken to reflect changes in pulmonary vascular resistance. Progressive hypercapnia (Pco 2 =0 to 60 mm Hg) resulted in an increase in PPA as pH decreased. Equivalent degrees of acidosis, produced by the infusion of 0.3 N lactic acid, resulted in a higher PPA. Changes in PPA produced by lactic acid were reversible with 0.89 M sodium bicarbonate. With Pco 2 constant, and pH changed by lactic acid or sodium bicarbonate infusion, PPA was higher in lungs ventilated with room air (Pco 2 = 0) than in those ventilated with 5 or 10% CO 2 (Pco, = 30 or 60 mm Hg) at the same hydrogen ion concentration of the perfusate. These findings can be explained by two opposing actions of CO 2 on pulmonary vessels: a dilator action due to the direct effect of CO 2 and a constrictor action caused by the increase in hydrogen ion concentration.ADDITIONAL KEY WORDS respiratory acidosis metabolic acidosis pulmonary vascular resistance isolated perfused lungs pulmonary vasomotor activity• Ventilation of the isolated perfused lungs of cats with high concentrations of carbon dioxide causes the pulmonary vessels to constrict (1, 2). Increased hydrogen ion concentration in the perfusate has also been shown to cause constriction in the pulmonary vascular bed of various animals (3-5). Recent workers (6, 7) have suggested that the vasoconstrictor effect of hypercapnia is due to the acidosis produced.The present paper presents evidence that there are two opposing actions of carbon dioxide on the pulmonary vessels: a dilator From the Mayo Clinic and Mayo Foundation, Section of Physiology, and Mayo Graduate School of Medicine, University of Minnesota, Rochester, Minnesota 55901.This investigation was supported in part by U. S. Public Health Service Research Grants HE-5883 and HE-5515 from the National Heart Institute.Dr. Viles is now Resident in Pediatric Cardiology, Mayo Clinic, and he is also recipient of a Special Fellowship from the National Institute of Child Health and Human Development, Public Health Service.Accepted for publication January 10, 1968. action due to the direct effect of the carbon dioxide molecule, and a constrictor action due to the increase in hydrogen ion concentration caused by the hypercapnia. MethodsThe isolated perfused lung preparation described by Donald (8) was adapted for cats. Adult cats weighing 1.8 to 2.6 kg were anesthetized with intravenous chloralose (80 mg/kg) or pentobarbital (30 mg/kg), and the trachea was cannulated. After heparinization, and exsanguination from the carotid artery, the trachea was clamped and the chest was opened bilaterally in the fifth intercostal space. A cannula 4 or 5 mm in diameter was secured in the main pulmonary artery. A cannula 7 or 8 mm in diamete...

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“…Respiratory alkalosis rather than lung stretch reduces thromboxane-induced and hypoxia-induced pulmonary vasoconstriction by equal proportions. (Pediatr Res 24: 558-562, 1988) Abbreviations CO, cardiac output HPV, hypoxic pulmonary vasoconstriction Acute HPV in both adult and young animals is attenuated by respiratory and metabolic alkalosis (1)(2)(3)(4). Although alveolar hypoxia is not necessarily the cause of idiopathic PPHN, clinicians hyperventilate infants with PPHN to produce respiratory alkalosis in an attempt to selectively reduce PVR, increase pulmonary blood flow, and improve arterial oxygenation by reducing rightto-left shunting of venous blood through the ductus arteriosus and foramen ovale (5, 6).…”

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Effects of Respiratory Alkalosis on Thromboxane-Induced Pulmonary Hypertension in Piglets

et al. 1988

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ABSTRACT. Acute hypoxic pulmonary vasoconstriction PVR, pulmonary vascular resistance is attenuated by respiratory alkalosis. It is unknown if SVR, systemic vascular resistance alkalosis similarly reduces pulmonary vasoconstriction HR, heart rate produced by thromboxane A2. Respiratory alkalosis does Paw, peak proximal airway pressure not always attenuate persistent pulmonary hypertension in Pvoz, mixed venous oxygen tension newborns, some of whom have elevated serum thromboxane B2 levels. We hypothesized that alkalosis attenuates thromboxane-induced ~ulmonary vasoconstriction less than it does hypoxic vasoconstriction in infants. Hemodynamic responses to respiratory alkalosis during pulmonary vasoconstriction produced in random order by breathing 12% inspired oxygen and by infusing 0.1 j.~g/kg/ min of the thromboxane-mimetic U46,619 were compared in eight 2-wk-old piglets. Hypoxia increased mean pulmonary artery pressure from 12 f 3 to 29 f 2 mm Hg and pulmonary vascular resistance (PVR) from 11 f 4 to 25 f 8 mmHg/L/min; U46,619 increased pulmonary artery pressure from 16 +. 5 to 37 f 6 mm Hg and PVR from 14 f 5 to 51 f 17 mm Hg/liter/min. U46,619 also decreased cardiac output accounting in part for the greater increase in PVR compared to hypoxia-induced vasoconstriction. Respiratory alkalosis decreased PVR to 14 f 6 mm Hg/ literlmin during exposure to hypoxia and to 28 f 9 mm Hg/liter/min during infusion of U46,619. In six additional piglets with U46,619-induced pulmonary vasoconstriction, the effects of lung stretch and hypocapnic alkalosis were separated by doubling tidal volume and then adding inspired COz to return PaC02 to prehyperventilation levels. Respiratory alkalosis decreased PVR from 52 f 36 to 35 2 21 mm Hg/liter/min. Despite the increased tidal volume, PVR increased to 53 f 35 Hg/liter/min when PaCOz returned to 44 f 5 mm Hg. Respiratory alkalosis rather than lung stretch reduces thromboxane-induced and hypoxia-induced pulmonary vasoconstriction by equal proportions. (Pediatr Res 24: 558-562, 1988) Abbreviations CO, cardiac output HPV, hypoxic pulmonary vasoconstriction Acute HPV in both adult and young animals is attenuated by respiratory and metabolic alkalosis (1-4). Although alveolar hypoxia is not necessarily the cause of idiopathic PPHN, clinicians hyperventilate infants with PPHN to produce respiratory alkalosis in an attempt to selectively reduce PVR, increase pulmonary blood flow, and improve arterial oxygenation by reducing rightto-left shunting of venous blood through the ductus arteriosus and foramen ovale (5, 6). Despite ventilation with 1.0 F I O~ and hyperventilation, pulmonary hypertension does not fall below systemic levels in some of these infants, leading to a mortality of 17% or more (7)(8)(9). This experience has prompted a search for endogenous vasoactive substances which increase PVR in the absence of alveolar hypoxia, any of which may play a pathogenic role in some infants with PPHN. Hammerman, et al. (10) have reported increased serum levels of thromboxane B2, the stab...

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Pulmonary hemodynamics during acute acid-base changes in the intact dog

Cited by 30 publications

References 0 publications

Effect of metabolic acidosis on pulmonary microcirculation in the cat.

Effect of metabolic acidosis on pulmonary microcirculation in the cat.

Evidence for a Dilator Action of Carbon Dioxide on the Pulmonary Vessels of the Cat

Effects of Respiratory Alkalosis on Thromboxane-Induced Pulmonary Hypertension in Piglets

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