Effects of hypoxia and hyperoxia on lung prostaglandin E1 metabolism

Jorge B. Pisarello, Daniel Flores, Robert Jackson

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Exposure to hypoxia (10% O2 for 5 to 7 days) results in increased survival and decreased pulmonary toxicity of adult rats subsequently exposed to hyperoxia (>97% 02)These experiments tested whether hypoxia preexposure minimized the decrease in lung metabolism of prostaglandin E1 (PGE1), a vasoactive and antiinflammatory prostaglandin, caused by hyperoxia. Transpulmonary PGE1 clearance was measured as fractional metabolism of PGE1 (2 μM to 30 μM) infused during a 45-second period in an isolated, buffer- perfused rat lung preparation after exposure of rats to one of the following conditions: (1) hyperoxia (>97% O2 for 48 hours), (2) hypoxia (10% 02 for 120 hours), or (3) hypoxia followed by hyperoxia. Hyperoxia exposure decreased both lung PGE1 metabolism and lung prostaglandin dehydrogenase activity (PGDH). Hypoxia also decreased lung PGE1 metabolism but, in contrast, increased lung PGDH activity. Hypoxia preexposure did not prevent the depression of PGE1 metabolism or PGDH activity caused by hyperoxia, which indicates that survival in hyperoxia did not depend on lung PGE1 metabolism. Hypoxia itself impaired transpulmonary metabolism of PGE1 despite increasing PGDH activity, which suggests possible interference with substrate delivery.

Original languageEnglish
Pages (from-to)147-152
Number of pages6
JournalAmerican Journal of the Medical Sciences
Volume313
Issue number3
DOIs
StatePublished - Jan 1 1997
Externally publishedYes

Fingerprint

Hyperoxia
Alprostadil
Lung
Prostaglandins
Oxidoreductases
Hypoxia
Buffers
Anti-Inflammatory Agents

Keywords

  • Hypoxia adaptation
  • Isolated perfused lungs
  • Oxygen toxicity
  • Prostaglandin dehydrogenase
  • Prostaglandin E

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Effects of hypoxia and hyperoxia on lung prostaglandin E1 metabolism. / Pisarello, Jorge B.; Flores, Daniel; Jackson, Robert.

In: American Journal of the Medical Sciences, Vol. 313, No. 3, 01.01.1997, p. 147-152.

Research output: Contribution to journalArticle

Pisarello, Jorge B. ; Flores, Daniel ; Jackson, Robert. / Effects of hypoxia and hyperoxia on lung prostaglandin E1 metabolism. In: American Journal of the Medical Sciences. 1997 ; Vol. 313, No. 3. pp. 147-152.
@article{6378f374708344ba9ba5b281b68f23d8,
title = "Effects of hypoxia and hyperoxia on lung prostaglandin E1 metabolism",
abstract = "Exposure to hypoxia (10{\%} O2 for 5 to 7 days) results in increased survival and decreased pulmonary toxicity of adult rats subsequently exposed to hyperoxia (>97{\%} 02)These experiments tested whether hypoxia preexposure minimized the decrease in lung metabolism of prostaglandin E1 (PGE1), a vasoactive and antiinflammatory prostaglandin, caused by hyperoxia. Transpulmonary PGE1 clearance was measured as fractional metabolism of PGE1 (2 μM to 30 μM) infused during a 45-second period in an isolated, buffer- perfused rat lung preparation after exposure of rats to one of the following conditions: (1) hyperoxia (>97{\%} O2 for 48 hours), (2) hypoxia (10{\%} 02 for 120 hours), or (3) hypoxia followed by hyperoxia. Hyperoxia exposure decreased both lung PGE1 metabolism and lung prostaglandin dehydrogenase activity (PGDH). Hypoxia also decreased lung PGE1 metabolism but, in contrast, increased lung PGDH activity. Hypoxia preexposure did not prevent the depression of PGE1 metabolism or PGDH activity caused by hyperoxia, which indicates that survival in hyperoxia did not depend on lung PGE1 metabolism. Hypoxia itself impaired transpulmonary metabolism of PGE1 despite increasing PGDH activity, which suggests possible interference with substrate delivery.",
keywords = "Hypoxia adaptation, Isolated perfused lungs, Oxygen toxicity, Prostaglandin dehydrogenase, Prostaglandin E",
author = "Pisarello, {Jorge B.} and Daniel Flores and Robert Jackson",
year = "1997",
month = "1",
day = "1",
doi = "10.1097/00000441-199703000-00004",
language = "English",
volume = "313",
pages = "147--152",
journal = "American Journal of the Medical Sciences",
issn = "0002-9629",
publisher = "Lippincott Williams and Wilkins",
number = "3",

}

TY - JOUR

T1 - Effects of hypoxia and hyperoxia on lung prostaglandin E1 metabolism

AU - Pisarello, Jorge B.

AU - Flores, Daniel

AU - Jackson, Robert

PY - 1997/1/1

Y1 - 1997/1/1

N2 - Exposure to hypoxia (10% O2 for 5 to 7 days) results in increased survival and decreased pulmonary toxicity of adult rats subsequently exposed to hyperoxia (>97% 02)These experiments tested whether hypoxia preexposure minimized the decrease in lung metabolism of prostaglandin E1 (PGE1), a vasoactive and antiinflammatory prostaglandin, caused by hyperoxia. Transpulmonary PGE1 clearance was measured as fractional metabolism of PGE1 (2 μM to 30 μM) infused during a 45-second period in an isolated, buffer- perfused rat lung preparation after exposure of rats to one of the following conditions: (1) hyperoxia (>97% O2 for 48 hours), (2) hypoxia (10% 02 for 120 hours), or (3) hypoxia followed by hyperoxia. Hyperoxia exposure decreased both lung PGE1 metabolism and lung prostaglandin dehydrogenase activity (PGDH). Hypoxia also decreased lung PGE1 metabolism but, in contrast, increased lung PGDH activity. Hypoxia preexposure did not prevent the depression of PGE1 metabolism or PGDH activity caused by hyperoxia, which indicates that survival in hyperoxia did not depend on lung PGE1 metabolism. Hypoxia itself impaired transpulmonary metabolism of PGE1 despite increasing PGDH activity, which suggests possible interference with substrate delivery.

AB - Exposure to hypoxia (10% O2 for 5 to 7 days) results in increased survival and decreased pulmonary toxicity of adult rats subsequently exposed to hyperoxia (>97% 02)These experiments tested whether hypoxia preexposure minimized the decrease in lung metabolism of prostaglandin E1 (PGE1), a vasoactive and antiinflammatory prostaglandin, caused by hyperoxia. Transpulmonary PGE1 clearance was measured as fractional metabolism of PGE1 (2 μM to 30 μM) infused during a 45-second period in an isolated, buffer- perfused rat lung preparation after exposure of rats to one of the following conditions: (1) hyperoxia (>97% O2 for 48 hours), (2) hypoxia (10% 02 for 120 hours), or (3) hypoxia followed by hyperoxia. Hyperoxia exposure decreased both lung PGE1 metabolism and lung prostaglandin dehydrogenase activity (PGDH). Hypoxia also decreased lung PGE1 metabolism but, in contrast, increased lung PGDH activity. Hypoxia preexposure did not prevent the depression of PGE1 metabolism or PGDH activity caused by hyperoxia, which indicates that survival in hyperoxia did not depend on lung PGE1 metabolism. Hypoxia itself impaired transpulmonary metabolism of PGE1 despite increasing PGDH activity, which suggests possible interference with substrate delivery.

KW - Hypoxia adaptation

KW - Isolated perfused lungs

KW - Oxygen toxicity

KW - Prostaglandin dehydrogenase

KW - Prostaglandin E

UR - http://www.scopus.com/inward/record.url?scp=0030893459&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030893459&partnerID=8YFLogxK

U2 - 10.1097/00000441-199703000-00004

DO - 10.1097/00000441-199703000-00004

M3 - Article

VL - 313

SP - 147

EP - 152

JO - American Journal of the Medical Sciences

JF - American Journal of the Medical Sciences

SN - 0002-9629

IS - 3

ER -