Pulmonary Arteriovenous Shunting Due to Epinephrine

Berk, John L.; Hagen, Joan F.; Koo, R; Nomoto, Shinnosuke; Rupright, M

doi:10.1055/s-0028-1099376

Cited by 5 publications

(2 citation statements)

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“…This finding was demonstrated to be eliminated in dogs ventilated with 100% O 2 (Berk et al . ) demonstrating that 100% O 2 prevented blood flow through IPAVAs as we have suggested occurs in humans (Lovering et al . ; Elliott et al .…”

Section: Discussionsupporting

confidence: 72%

Increased cardiac output, not pulmonary artery systolic pressure, increases intrapulmonary shunt in healthy humans breathing room air and 40% O₂

Elliott

Duke

Hawn

et al. 2014

The Journal of Physiology

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Key pointsr The contribution of blood flow through intrapulmonary arteriovenous anastomoses (IPAVAs) to pulmonary gas exchange efficiency remains unknown and controversial.r Intravenous infusion of adrenaline (epinephrine) increases blood flow through IPAVAs detected by the transpulmonary passage of saline contrast and breathing 40% O 2 minimizes potential contributions from ventilation-to-perfusion inequality and diffusion limitation. r Pulmonary gas exchange efficiency was impaired to the same degree, and the transpulmonary passage of saline contrast was not different, in humans at rest during the intravenous infusion of adrenaline before and after atropine when breathing room air and 40% O 2 .r Cardiac output increased to the same degree during intravenous infusion of adrenaline before and after atropine, but pulmonary artery systolic pressure only increased significantly before atropine.r These data demonstrate that blood flow through IPAVAs contributes to pulmonary gas exchange efficiency and that blood flow through IPAVAs is predominantly mediated by increases in cardiac output rather than increases in pulmonary artery systolic pressure.Abstract Blood flow through intrapulmonary arteriovenous anastomoses (IPAVAs) has been demonstrated to increase in healthy humans during a variety of conditions; however, whether or not this blood flow represents a source of venous admixture (Q VA /Q T ) that impairs pulmonary gas exchange efficiency (i.e. increases the alveolar-to-arterial P O 2 difference (A-aDO 2 )) remains controversial and unknown. We hypothesized that blood flow through IPAVAs does provide a source ofQ VA /Q T . To test this, blood flow through IPAVAs was increased in healthy humans at rest breathing room air and 40% O 2 : (1) during intravenous adrenaline (epinephrine) infusion at 320 ng kg −1 min −1 (320 ADR), and (2) with vagal blockade (2 mg atropine), before and during intravenous adrenaline infusion at 80 ng kg −1 min −1 (ATR + 80 ADR). When breathing room air the A-aDO 2 increased by 6 ± 2 mmHg during 320 ADR and by 5 ± 2 mmHg during ATR + 80 ADR, and the change in calculatedQ VA /Q T was +2% in both conditions. When breathing 40% O 2 , which minimizes contributions from diffusion limitation and alveolar ventilation-to-perfusion inequality, the A-aDO 2 increased by 12 ± 7 mmHg during 320 ADR, and by 9 ± 6 mmHg during ATR + 80 ADR, and the change in calculatedQ VA /Q T was +2% in both conditions. During 320 ADR cardiac output (Q T ) and pulmonary artery systolic pressure (PASP) were significantly increased; however, during ATR + 80 ADR onlyQ T was significantly increased, yet blood flow through IPAVAs as detected with saline contrast echocardiography was not different between conditions. Accordingly, we suggest that blood flow through IPAVAs provides a source of intrapulmonary shunt, and is mediated primarily by increases inQ T rather than PASP. Abbreviations A-aDO 2 , alveolar-to-arterial difference in P O2 ; ADR, adrenaline (epinephrine); ATR, atropine; C aO2 , arterial oxygen content; C vO...

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Section: Discussionsupporting

confidence: 72%

Increased cardiac output, not pulmonary artery systolic pressure, increases intrapulmonary shunt in healthy humans breathing room air and 40% O₂

Elliott

Duke

Hawn

et al. 2014

The Journal of Physiology

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“…Indeed, using 15-to 30-m radioactive albumin microspheres, Nomoto et al (40) demonstrated that IPAVA open in dogs infused with EPI. Additionally, Berk and colleagues also suggested a direct effect of EPI increasing venous admixture in anesthetized dogs based on an immediate fall in arterial partial pressure of oxygen (PO 2 ) during EPI infusion (2)(3)(4), while Huckauf et al (22) suggested a similar effect in patients with left heart failure receiving DA infusion. Thus these catecholamines could potentially be opening IPAVA; however, their role and mechanism of action in opening IPAVA in healthy humans is unknown.…”

mentioning

confidence: 99%

Catecholamine-induced opening of intrapulmonary arteriovenous anastomoses in healthy humans at rest

Laurie

Elliott

Goodman

et al. 2012

Journal of Applied Physiology

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The mechanism or mechanisms that cause intrapulmonary arteriovenous anastomoses (IPAVA) to either open during exercise in subjects breathing room air and at rest when breathing hypoxic gas mixtures, or to close during exercise while breathing 100% oxygen, remain unknown. During conditions when IPAVA are open, plasma epinephrine (EPI) and dopamine (DA) concentrations both increase, potentially representing a common mechanism. The purpose of this study was to determine whether EPI or DA infusions open IPAVA in resting subjects breathing room air and, subsequently, 100% oxygen. We hypothesized that these catecholamine infusions would open IPAVA. We performed saline-contrast echocardiography in nine subjects without a patent foramen ovale before and during serial EPI and DA infusions while breathing room air and then while breathing 100% oxygen. Bubble scores (0-5) were assigned based on the number and spatial distribution of bubbles in the left ventricle. Pulmonary artery systolic pressure (PASP) was estimated using Doppler ultrasound, while cardiac output (Q(C)) was measured using echocardiography. Bubble scores were significantly greater during EPI infusions of 80-320 ng·kg(-1)·min(-1) compared with baseline when subjects breathed room air; however, bubble scores did not increase when they breathed 100% oxygen. At comparable Q(C) and PASP, intravenous DA (16 μg·kg(-1)·min(-1)) and EPI (40 ng·kg(-1)·min(-1)) resulted in identical bubble scores. Subsequent studies revealed that β-blockade did not prevent hypoxia-induced opening of IPAVA. We suggest that increases in Q(C) or PASP (or both) secondary to EPI or DA infusions open IPAVA in normoxia. The closing mechanism associated with breathing 100% oxygen is independent from the opening mechanisms.

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Pulmonary Anatomic Arteriovenous Shunting Caused by Epinephrine

Nomoto¹,

Berk²,

Hagen³

et al. 1974

Arch Surg

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Pulmonary Arteriovenous Shunting Due to Epinephrine

Cited by 5 publications

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Increased cardiac output, not pulmonary artery systolic pressure, increases intrapulmonary shunt in healthy humans breathing room air and 40% O₂

Increased cardiac output, not pulmonary artery systolic pressure, increases intrapulmonary shunt in healthy humans breathing room air and 40% O₂

Catecholamine-induced opening of intrapulmonary arteriovenous anastomoses in healthy humans at rest

Pulmonary Anatomic Arteriovenous Shunting Caused by Epinephrine

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Pulmonary Arteriovenous Shunting Due to Epinephrine

Cited by 5 publications

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Increased cardiac output, not pulmonary artery systolic pressure, increases intrapulmonary shunt in healthy humans breathing room air and 40% O2

Increased cardiac output, not pulmonary artery systolic pressure, increases intrapulmonary shunt in healthy humans breathing room air and 40% O2

Catecholamine-induced opening of intrapulmonary arteriovenous anastomoses in healthy humans at rest

Pulmonary Anatomic Arteriovenous Shunting Caused by Epinephrine

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Increased cardiac output, not pulmonary artery systolic pressure, increases intrapulmonary shunt in healthy humans breathing room air and 40% O₂

Increased cardiac output, not pulmonary artery systolic pressure, increases intrapulmonary shunt in healthy humans breathing room air and 40% O₂