The effects of estrogen on pulmonary artery vasoreactivity and hypoxic pulmonary vasoconstriction: Potential new clinical implications for an old hormone

Tim Lahm, Paul R. Crisostomo, Troy A. Markel, Meijing Wang, Brent R. Weil, Nathan M. Novotny, Daniel R. Meldrum

Research output: Contribution to journalArticle

49 Citations (Scopus)

Abstract

BACKGROUND AND OBJECTIVES: Recent research recognizes gender as a major factor determining the outcomes in trauma, ischemia/reperfusion, shock, and sepsis. In particular, estrogen has been demonstrated to exert protective effects in these settings. The effects of estrogens on the pulmonary vasculature are potent and complex yet not fully understood. A better mechanistic understanding may allow for future therapeutic interventions in pulmonary hypertensive crises after cardiac surgery and during acute lung injury as well as in patients with pulmonary arterial hypertension. DATA SOURCES AND STUDY SELECTION: We searched PubMed for articles in the English language by using the search words pulmonary hypertension, hypoxic pulmonary vasoconstriction, estrogen, estradiol, inflammation, acute injury, ischemia reperfusion, sepsis, trauma, and burns. These were used in various combinations. We read the abstracts of the relevant titles to confirm their relevance, and the full articles were then extracted. References from extracted articles were checked for any additional relevant articles. DATA EXTRACTION AND SYNTHESIS: Estrogen plays a critical role in the improved outcomes in the settings of trauma, shock, sepsis, myocardial ischemia/reperfusion, and acute lung injury. Several new mechanisms of action have been identified. In the pulmonary vasculature, estrogen causes vasodilation and attenuates the vasoconstrictor response to various stimuli, including hypoxia. This is mediated by increased levels of prostacyclin and nitric oxide as well as decreased levels of endothelin-1. In addition, effects on intracellular signaling pathways and several kinases as well as anti-inflammatory mechanisms may contribute as well. Recent studies suggest the importance of acute, nongenomic effects. CONCLUSION: Estrogen exerts a variety of nongenomic actions, which may allow for future therapeutic interventions in pulmonary vascular disease.

Original languageEnglish
Pages (from-to)2174-2183
Number of pages10
JournalCritical Care Medicine
Volume36
Issue number7
DOIs
StatePublished - Jul 2008

Fingerprint

Vasoconstriction
Pulmonary Artery
Estrogens
Hormones
Lung
Sepsis
Acute Lung Injury
Pulmonary Hypertension
Shock
Wounds and Injuries
Myocardial Reperfusion
Information Storage and Retrieval
Vasoconstrictor Agents
Endothelin-1
Epoprostenol
Reperfusion Injury
Burns
Vascular Diseases
PubMed
Vasodilation

Keywords

  • Estradiol
  • Lung injury
  • Nongenomic effects
  • Pulmonary hypertension
  • Sex hormones
  • Shock

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

The effects of estrogen on pulmonary artery vasoreactivity and hypoxic pulmonary vasoconstriction : Potential new clinical implications for an old hormone. / Lahm, Tim; Crisostomo, Paul R.; Markel, Troy A.; Wang, Meijing; Weil, Brent R.; Novotny, Nathan M.; Meldrum, Daniel R.

In: Critical Care Medicine, Vol. 36, No. 7, 07.2008, p. 2174-2183.

Research output: Contribution to journalArticle

Lahm, Tim ; Crisostomo, Paul R. ; Markel, Troy A. ; Wang, Meijing ; Weil, Brent R. ; Novotny, Nathan M. ; Meldrum, Daniel R. / The effects of estrogen on pulmonary artery vasoreactivity and hypoxic pulmonary vasoconstriction : Potential new clinical implications for an old hormone. In: Critical Care Medicine. 2008 ; Vol. 36, No. 7. pp. 2174-2183.
@article{ac8a85a2208e450babb3b7d0ca902cae,
title = "The effects of estrogen on pulmonary artery vasoreactivity and hypoxic pulmonary vasoconstriction: Potential new clinical implications for an old hormone",
abstract = "BACKGROUND AND OBJECTIVES: Recent research recognizes gender as a major factor determining the outcomes in trauma, ischemia/reperfusion, shock, and sepsis. In particular, estrogen has been demonstrated to exert protective effects in these settings. The effects of estrogens on the pulmonary vasculature are potent and complex yet not fully understood. A better mechanistic understanding may allow for future therapeutic interventions in pulmonary hypertensive crises after cardiac surgery and during acute lung injury as well as in patients with pulmonary arterial hypertension. DATA SOURCES AND STUDY SELECTION: We searched PubMed for articles in the English language by using the search words pulmonary hypertension, hypoxic pulmonary vasoconstriction, estrogen, estradiol, inflammation, acute injury, ischemia reperfusion, sepsis, trauma, and burns. These were used in various combinations. We read the abstracts of the relevant titles to confirm their relevance, and the full articles were then extracted. References from extracted articles were checked for any additional relevant articles. DATA EXTRACTION AND SYNTHESIS: Estrogen plays a critical role in the improved outcomes in the settings of trauma, shock, sepsis, myocardial ischemia/reperfusion, and acute lung injury. Several new mechanisms of action have been identified. In the pulmonary vasculature, estrogen causes vasodilation and attenuates the vasoconstrictor response to various stimuli, including hypoxia. This is mediated by increased levels of prostacyclin and nitric oxide as well as decreased levels of endothelin-1. In addition, effects on intracellular signaling pathways and several kinases as well as anti-inflammatory mechanisms may contribute as well. Recent studies suggest the importance of acute, nongenomic effects. CONCLUSION: Estrogen exerts a variety of nongenomic actions, which may allow for future therapeutic interventions in pulmonary vascular disease.",
keywords = "Estradiol, Lung injury, Nongenomic effects, Pulmonary hypertension, Sex hormones, Shock",
author = "Tim Lahm and Crisostomo, {Paul R.} and Markel, {Troy A.} and Meijing Wang and Weil, {Brent R.} and Novotny, {Nathan M.} and Meldrum, {Daniel R.}",
year = "2008",
month = "7",
doi = "10.1097/CCM.0b013e31817d1a92",
language = "English",
volume = "36",
pages = "2174--2183",
journal = "Critical Care Medicine",
issn = "0090-3493",
publisher = "Lippincott Williams and Wilkins",
number = "7",

}

TY - JOUR

T1 - The effects of estrogen on pulmonary artery vasoreactivity and hypoxic pulmonary vasoconstriction

T2 - Potential new clinical implications for an old hormone

AU - Lahm, Tim

AU - Crisostomo, Paul R.

AU - Markel, Troy A.

AU - Wang, Meijing

AU - Weil, Brent R.

AU - Novotny, Nathan M.

AU - Meldrum, Daniel R.

PY - 2008/7

Y1 - 2008/7

N2 - BACKGROUND AND OBJECTIVES: Recent research recognizes gender as a major factor determining the outcomes in trauma, ischemia/reperfusion, shock, and sepsis. In particular, estrogen has been demonstrated to exert protective effects in these settings. The effects of estrogens on the pulmonary vasculature are potent and complex yet not fully understood. A better mechanistic understanding may allow for future therapeutic interventions in pulmonary hypertensive crises after cardiac surgery and during acute lung injury as well as in patients with pulmonary arterial hypertension. DATA SOURCES AND STUDY SELECTION: We searched PubMed for articles in the English language by using the search words pulmonary hypertension, hypoxic pulmonary vasoconstriction, estrogen, estradiol, inflammation, acute injury, ischemia reperfusion, sepsis, trauma, and burns. These were used in various combinations. We read the abstracts of the relevant titles to confirm their relevance, and the full articles were then extracted. References from extracted articles were checked for any additional relevant articles. DATA EXTRACTION AND SYNTHESIS: Estrogen plays a critical role in the improved outcomes in the settings of trauma, shock, sepsis, myocardial ischemia/reperfusion, and acute lung injury. Several new mechanisms of action have been identified. In the pulmonary vasculature, estrogen causes vasodilation and attenuates the vasoconstrictor response to various stimuli, including hypoxia. This is mediated by increased levels of prostacyclin and nitric oxide as well as decreased levels of endothelin-1. In addition, effects on intracellular signaling pathways and several kinases as well as anti-inflammatory mechanisms may contribute as well. Recent studies suggest the importance of acute, nongenomic effects. CONCLUSION: Estrogen exerts a variety of nongenomic actions, which may allow for future therapeutic interventions in pulmonary vascular disease.

AB - BACKGROUND AND OBJECTIVES: Recent research recognizes gender as a major factor determining the outcomes in trauma, ischemia/reperfusion, shock, and sepsis. In particular, estrogen has been demonstrated to exert protective effects in these settings. The effects of estrogens on the pulmonary vasculature are potent and complex yet not fully understood. A better mechanistic understanding may allow for future therapeutic interventions in pulmonary hypertensive crises after cardiac surgery and during acute lung injury as well as in patients with pulmonary arterial hypertension. DATA SOURCES AND STUDY SELECTION: We searched PubMed for articles in the English language by using the search words pulmonary hypertension, hypoxic pulmonary vasoconstriction, estrogen, estradiol, inflammation, acute injury, ischemia reperfusion, sepsis, trauma, and burns. These were used in various combinations. We read the abstracts of the relevant titles to confirm their relevance, and the full articles were then extracted. References from extracted articles were checked for any additional relevant articles. DATA EXTRACTION AND SYNTHESIS: Estrogen plays a critical role in the improved outcomes in the settings of trauma, shock, sepsis, myocardial ischemia/reperfusion, and acute lung injury. Several new mechanisms of action have been identified. In the pulmonary vasculature, estrogen causes vasodilation and attenuates the vasoconstrictor response to various stimuli, including hypoxia. This is mediated by increased levels of prostacyclin and nitric oxide as well as decreased levels of endothelin-1. In addition, effects on intracellular signaling pathways and several kinases as well as anti-inflammatory mechanisms may contribute as well. Recent studies suggest the importance of acute, nongenomic effects. CONCLUSION: Estrogen exerts a variety of nongenomic actions, which may allow for future therapeutic interventions in pulmonary vascular disease.

KW - Estradiol

KW - Lung injury

KW - Nongenomic effects

KW - Pulmonary hypertension

KW - Sex hormones

KW - Shock

UR - http://www.scopus.com/inward/record.url?scp=47249115325&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=47249115325&partnerID=8YFLogxK

U2 - 10.1097/CCM.0b013e31817d1a92

DO - 10.1097/CCM.0b013e31817d1a92

M3 - Article

C2 - 18552699

AN - SCOPUS:47249115325

VL - 36

SP - 2174

EP - 2183

JO - Critical Care Medicine

JF - Critical Care Medicine

SN - 0090-3493

IS - 7

ER -