Hypoxia-induced oxygen tolerance: Maintenance of endothelial metabolic function

Robert Jackson, Hyung Soo Ann, Suzanne Oparil

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Hypoxia (10%12% O2) preadaptation for 4-7 days effectively protects rats from oxygen toxicity. The present study was designed to investigate the hypothesis that the lung's microvascular endothelium shares in development of oxygen tolerance and therefore that endothelial metabolic function would he protected from oxygen toxicity by prior adaptation to hypoxia. Since pulmonary oxygen toxicity decreases lung capillary angiotensin converting enzyme (ACE) activity, we assayed converting enzyme active sites in an isolated perfused rat lung preparation as a marker for the development of oxygen toxicity and tolerance. Rats were exposed to air, hypoxia (10% O2 for 4 days), hyperoxia (95% O2 for 2 days) alone, or hypoxia followed immediately by hyperoxia. Lung vascular ACE content was quantitated by measuring the single pass binding of an iodinated-converting enzyme inhibitor, 125I-MK351A, a derivative of lisinopril. Hypoxia adaptation per se had no effect on ACE content reflected in normal 125I-MK351A binding, whereas hyperoxia exposure caused a significant decrease in lung vascular ACE. Hyperoxia-induced decreases in ACE content were prevented partially by hypoxia adaptation, indicating that A CE content on luminal endothelial surfaces was protected from oxygen toxicity. In isolated perfused lungs 125I-MK351A binding reflects development of oxygen tolerance after hypoxia preadaptation and suggests that lung endothelial metabolic function is protected from oxygen toxicity.

Original languageEnglish
Pages (from-to)887-896
Number of pages10
JournalExperimental Lung Research
Volume14
Issue numberS1
DOIs
StatePublished - Jan 1 1988
Externally publishedYes

Fingerprint

Maintenance
Oxygen
Peptidyl-Dipeptidase A
Toxicity
Lung
Hyperoxia
Rats
Blood Vessels
Lisinopril
Hypoxia
Enzyme activity
Enzyme Inhibitors
Endothelium
Catalytic Domain
Air
Derivatives
Enzymes
N2-((1S)-1-carboxy-3-phenylpropyl)-N6-((4-hydroxyphenyl)iminomethyl)-L-lysyl-l-proline

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Molecular Biology
  • Clinical Biochemistry

Cite this

Hypoxia-induced oxygen tolerance : Maintenance of endothelial metabolic function. / Jackson, Robert; Ann, Hyung Soo; Oparil, Suzanne.

In: Experimental Lung Research, Vol. 14, No. S1, 01.01.1988, p. 887-896.

Research output: Contribution to journalArticle

Jackson, Robert ; Ann, Hyung Soo ; Oparil, Suzanne. / Hypoxia-induced oxygen tolerance : Maintenance of endothelial metabolic function. In: Experimental Lung Research. 1988 ; Vol. 14, No. S1. pp. 887-896.
@article{2e8f054f5c854be2924dab57026a1c7d,
title = "Hypoxia-induced oxygen tolerance: Maintenance of endothelial metabolic function",
abstract = "Hypoxia (10{\%}12{\%} O2) preadaptation for 4-7 days effectively protects rats from oxygen toxicity. The present study was designed to investigate the hypothesis that the lung's microvascular endothelium shares in development of oxygen tolerance and therefore that endothelial metabolic function would he protected from oxygen toxicity by prior adaptation to hypoxia. Since pulmonary oxygen toxicity decreases lung capillary angiotensin converting enzyme (ACE) activity, we assayed converting enzyme active sites in an isolated perfused rat lung preparation as a marker for the development of oxygen toxicity and tolerance. Rats were exposed to air, hypoxia (10{\%} O2 for 4 days), hyperoxia (95{\%} O2 for 2 days) alone, or hypoxia followed immediately by hyperoxia. Lung vascular ACE content was quantitated by measuring the single pass binding of an iodinated-converting enzyme inhibitor, 125I-MK351A, a derivative of lisinopril. Hypoxia adaptation per se had no effect on ACE content reflected in normal 125I-MK351A binding, whereas hyperoxia exposure caused a significant decrease in lung vascular ACE. Hyperoxia-induced decreases in ACE content were prevented partially by hypoxia adaptation, indicating that A CE content on luminal endothelial surfaces was protected from oxygen toxicity. In isolated perfused lungs 125I-MK351A binding reflects development of oxygen tolerance after hypoxia preadaptation and suggests that lung endothelial metabolic function is protected from oxygen toxicity.",
author = "Robert Jackson and Ann, {Hyung Soo} and Suzanne Oparil",
year = "1988",
month = "1",
day = "1",
doi = "10.3109/01902148809064181",
language = "English",
volume = "14",
pages = "887--896",
journal = "Experimental Lung Research",
issn = "0190-2148",
publisher = "Informa Healthcare",
number = "S1",

}

TY - JOUR

T1 - Hypoxia-induced oxygen tolerance

T2 - Maintenance of endothelial metabolic function

AU - Jackson, Robert

AU - Ann, Hyung Soo

AU - Oparil, Suzanne

PY - 1988/1/1

Y1 - 1988/1/1

N2 - Hypoxia (10%12% O2) preadaptation for 4-7 days effectively protects rats from oxygen toxicity. The present study was designed to investigate the hypothesis that the lung's microvascular endothelium shares in development of oxygen tolerance and therefore that endothelial metabolic function would he protected from oxygen toxicity by prior adaptation to hypoxia. Since pulmonary oxygen toxicity decreases lung capillary angiotensin converting enzyme (ACE) activity, we assayed converting enzyme active sites in an isolated perfused rat lung preparation as a marker for the development of oxygen toxicity and tolerance. Rats were exposed to air, hypoxia (10% O2 for 4 days), hyperoxia (95% O2 for 2 days) alone, or hypoxia followed immediately by hyperoxia. Lung vascular ACE content was quantitated by measuring the single pass binding of an iodinated-converting enzyme inhibitor, 125I-MK351A, a derivative of lisinopril. Hypoxia adaptation per se had no effect on ACE content reflected in normal 125I-MK351A binding, whereas hyperoxia exposure caused a significant decrease in lung vascular ACE. Hyperoxia-induced decreases in ACE content were prevented partially by hypoxia adaptation, indicating that A CE content on luminal endothelial surfaces was protected from oxygen toxicity. In isolated perfused lungs 125I-MK351A binding reflects development of oxygen tolerance after hypoxia preadaptation and suggests that lung endothelial metabolic function is protected from oxygen toxicity.

AB - Hypoxia (10%12% O2) preadaptation for 4-7 days effectively protects rats from oxygen toxicity. The present study was designed to investigate the hypothesis that the lung's microvascular endothelium shares in development of oxygen tolerance and therefore that endothelial metabolic function would he protected from oxygen toxicity by prior adaptation to hypoxia. Since pulmonary oxygen toxicity decreases lung capillary angiotensin converting enzyme (ACE) activity, we assayed converting enzyme active sites in an isolated perfused rat lung preparation as a marker for the development of oxygen toxicity and tolerance. Rats were exposed to air, hypoxia (10% O2 for 4 days), hyperoxia (95% O2 for 2 days) alone, or hypoxia followed immediately by hyperoxia. Lung vascular ACE content was quantitated by measuring the single pass binding of an iodinated-converting enzyme inhibitor, 125I-MK351A, a derivative of lisinopril. Hypoxia adaptation per se had no effect on ACE content reflected in normal 125I-MK351A binding, whereas hyperoxia exposure caused a significant decrease in lung vascular ACE. Hyperoxia-induced decreases in ACE content were prevented partially by hypoxia adaptation, indicating that A CE content on luminal endothelial surfaces was protected from oxygen toxicity. In isolated perfused lungs 125I-MK351A binding reflects development of oxygen tolerance after hypoxia preadaptation and suggests that lung endothelial metabolic function is protected from oxygen toxicity.

UR - http://www.scopus.com/inward/record.url?scp=0024203043&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024203043&partnerID=8YFLogxK

U2 - 10.3109/01902148809064181

DO - 10.3109/01902148809064181

M3 - Article

C2 - 3208727

AN - SCOPUS:0024203043

VL - 14

SP - 887

EP - 896

JO - Experimental Lung Research

JF - Experimental Lung Research

SN - 0190-2148

IS - S1

ER -