Abstract

Purpose: The response in arterial oxygen tensions to one lung ventilation (OLV) during thoracotomy is not predictable in humans. The major response of the human lung to OLV is hypoxic pulmonary vasoconstriction (HPV), which increases pulmonary vascular resistance and subsequent right ventricular (RV) afterload. RV afterload may cause right heart dilation, which is a potent stimulus for atrial naturetic peptide (ANP) release. Since ANP is known to be a potent pulmonary vasodilator, right heart ANP release may inhibit HPV, increasing intrapulmonaiy shunt (QS/QT) fraction and result in systemic reduction in arterial oxygen tension. We investigated the relationship of ANP release with Qs/Qt prior to and after the institution of OLV in humans. Methods: After IRB approval and patient consent, 10 patients scheduled for thoracotomy requiring OLV had catheters placed in a radial artery and the right atrium (RA). Blood for ANP determination (RIA technique, Peninsula Labs, Belmont, CA) was drawn simultaneously from the RA catheters and by direct puncture from the left atrium LA at 1) during both lung ventilation (BLV), 2) after 20 min of OLV. Blood for blood gas tensions were drawn simultaneously (simultaneously with ANP) from the arterial line and RA. Qs/Qt was calculated by standard equation. FIO2 was 1.0, end tidal isoflurane concentrations were always under 1.0%, and in all patients tidal volume and respiratory rate were decreased and increased, respectively, by 20% with onset of OLV. The Spearman correlation coefficient (C.C.) for small data sets was used to determine significance. Results: Qs/Qt: BLV 20.6±8% OLV 36.4±11% ANP concentrations (pg·ml-1) BLV OLV C.C. RA 134±31 163±96.8 r=55 LA 155.4±41 185.1±72.6 r=49 Conclusions: These results demonstrate ANP release is not consistently found during OLV. Clinical Implications: RV dilation and ANP release do not impact on arterial oxygenation during OLV.

Original languageEnglish (US)
JournalChest
Volume110
Issue number4 SUPPL.
StatePublished - Oct 1 1996

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One-Lung Ventilation
Heart Atria
Lung
Thoracotomy
Vasoconstriction
Dilatation
Arterial Pressure
Catheters
antiarrhythmic peptide
Oxygen
Vascular Access Devices
Radial Artery
Research Ethics Committees
Isoflurane
Tidal Volume
Respiratory Rate
Vasodilator Agents
Punctures
Vascular Resistance
Ventilation

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Effect of one lung ventilation on atrial naturetic peptide release. / Lackner, Rudy P; Sisson, Joseph Harold; Roy, Shyamal K; Hill, G. E.

In: Chest, Vol. 110, No. 4 SUPPL., 01.10.1996.

Research output: Contribution to journalArticle

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title = "Effect of one lung ventilation on atrial naturetic peptide release",
abstract = "Purpose: The response in arterial oxygen tensions to one lung ventilation (OLV) during thoracotomy is not predictable in humans. The major response of the human lung to OLV is hypoxic pulmonary vasoconstriction (HPV), which increases pulmonary vascular resistance and subsequent right ventricular (RV) afterload. RV afterload may cause right heart dilation, which is a potent stimulus for atrial naturetic peptide (ANP) release. Since ANP is known to be a potent pulmonary vasodilator, right heart ANP release may inhibit HPV, increasing intrapulmonaiy shunt (QS/QT) fraction and result in systemic reduction in arterial oxygen tension. We investigated the relationship of ANP release with Qs/Qt prior to and after the institution of OLV in humans. Methods: After IRB approval and patient consent, 10 patients scheduled for thoracotomy requiring OLV had catheters placed in a radial artery and the right atrium (RA). Blood for ANP determination (RIA technique, Peninsula Labs, Belmont, CA) was drawn simultaneously from the RA catheters and by direct puncture from the left atrium LA at 1) during both lung ventilation (BLV), 2) after 20 min of OLV. Blood for blood gas tensions were drawn simultaneously (simultaneously with ANP) from the arterial line and RA. Qs/Qt was calculated by standard equation. FIO2 was 1.0, end tidal isoflurane concentrations were always under 1.0{\%}, and in all patients tidal volume and respiratory rate were decreased and increased, respectively, by 20{\%} with onset of OLV. The Spearman correlation coefficient (C.C.) for small data sets was used to determine significance. Results: Qs/Qt: BLV 20.6±8{\%} OLV 36.4±11{\%} ANP concentrations (pg·ml-1) BLV OLV C.C. RA 134±31 163±96.8 r=55 LA 155.4±41 185.1±72.6 r=49 Conclusions: These results demonstrate ANP release is not consistently found during OLV. Clinical Implications: RV dilation and ANP release do not impact on arterial oxygenation during OLV.",
author = "Lackner, {Rudy P} and Sisson, {Joseph Harold} and Roy, {Shyamal K} and Hill, {G. E.}",
year = "1996",
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T1 - Effect of one lung ventilation on atrial naturetic peptide release

AU - Lackner, Rudy P

AU - Sisson, Joseph Harold

AU - Roy, Shyamal K

AU - Hill, G. E.

PY - 1996/10/1

Y1 - 1996/10/1

N2 - Purpose: The response in arterial oxygen tensions to one lung ventilation (OLV) during thoracotomy is not predictable in humans. The major response of the human lung to OLV is hypoxic pulmonary vasoconstriction (HPV), which increases pulmonary vascular resistance and subsequent right ventricular (RV) afterload. RV afterload may cause right heart dilation, which is a potent stimulus for atrial naturetic peptide (ANP) release. Since ANP is known to be a potent pulmonary vasodilator, right heart ANP release may inhibit HPV, increasing intrapulmonaiy shunt (QS/QT) fraction and result in systemic reduction in arterial oxygen tension. We investigated the relationship of ANP release with Qs/Qt prior to and after the institution of OLV in humans. Methods: After IRB approval and patient consent, 10 patients scheduled for thoracotomy requiring OLV had catheters placed in a radial artery and the right atrium (RA). Blood for ANP determination (RIA technique, Peninsula Labs, Belmont, CA) was drawn simultaneously from the RA catheters and by direct puncture from the left atrium LA at 1) during both lung ventilation (BLV), 2) after 20 min of OLV. Blood for blood gas tensions were drawn simultaneously (simultaneously with ANP) from the arterial line and RA. Qs/Qt was calculated by standard equation. FIO2 was 1.0, end tidal isoflurane concentrations were always under 1.0%, and in all patients tidal volume and respiratory rate were decreased and increased, respectively, by 20% with onset of OLV. The Spearman correlation coefficient (C.C.) for small data sets was used to determine significance. Results: Qs/Qt: BLV 20.6±8% OLV 36.4±11% ANP concentrations (pg·ml-1) BLV OLV C.C. RA 134±31 163±96.8 r=55 LA 155.4±41 185.1±72.6 r=49 Conclusions: These results demonstrate ANP release is not consistently found during OLV. Clinical Implications: RV dilation and ANP release do not impact on arterial oxygenation during OLV.

AB - Purpose: The response in arterial oxygen tensions to one lung ventilation (OLV) during thoracotomy is not predictable in humans. The major response of the human lung to OLV is hypoxic pulmonary vasoconstriction (HPV), which increases pulmonary vascular resistance and subsequent right ventricular (RV) afterload. RV afterload may cause right heart dilation, which is a potent stimulus for atrial naturetic peptide (ANP) release. Since ANP is known to be a potent pulmonary vasodilator, right heart ANP release may inhibit HPV, increasing intrapulmonaiy shunt (QS/QT) fraction and result in systemic reduction in arterial oxygen tension. We investigated the relationship of ANP release with Qs/Qt prior to and after the institution of OLV in humans. Methods: After IRB approval and patient consent, 10 patients scheduled for thoracotomy requiring OLV had catheters placed in a radial artery and the right atrium (RA). Blood for ANP determination (RIA technique, Peninsula Labs, Belmont, CA) was drawn simultaneously from the RA catheters and by direct puncture from the left atrium LA at 1) during both lung ventilation (BLV), 2) after 20 min of OLV. Blood for blood gas tensions were drawn simultaneously (simultaneously with ANP) from the arterial line and RA. Qs/Qt was calculated by standard equation. FIO2 was 1.0, end tidal isoflurane concentrations were always under 1.0%, and in all patients tidal volume and respiratory rate were decreased and increased, respectively, by 20% with onset of OLV. The Spearman correlation coefficient (C.C.) for small data sets was used to determine significance. Results: Qs/Qt: BLV 20.6±8% OLV 36.4±11% ANP concentrations (pg·ml-1) BLV OLV C.C. RA 134±31 163±96.8 r=55 LA 155.4±41 185.1±72.6 r=49 Conclusions: These results demonstrate ANP release is not consistently found during OLV. Clinical Implications: RV dilation and ANP release do not impact on arterial oxygenation during OLV.

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