Differential activation of coronary and pulmonary endothelial cells by thermal injury

Joseph T. Murphy, Steven Duffy, Gary F. Purdue, John L. Hunt

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Remote organ dysfunction during resuscitation of severe thermal injury is characterized by early, transient pulmonary insufficiency and cardiac contractile dysfunction. Thermal injury is typified by profound systemic alterations of endothelial immunological, vasoactive, and barrier functions. The unique location of this ubiquitous, fragile monolayer makes it vulnerable to circulating serum factors created at remote cutaneous wounds. We examined endothelial "activation" in 2 distinct cell types, human coronary and pulmonary endothelial cells (EC), after severe thermal injury. By using human serum isolated at specific times after thermal injury ("early" [2 h post-burn] or "late" [26 h post-burn]), the endothelial release of vasoactive mediators, ICAM-1 expression, and monolayer permeability were assessed in vitro. Early burn serum enhanced coronary EC vasoconstrictor (ET-1) release and ICAM expression, inhibited vasodilator (PGI2) release, but had no effect on permeability. Conversely, under similar conditions, pulmonary EC PGI2 release and permeability were enhanced, ET-1 release was diminished, but ICAM was unaffected. Late burn serum enhanced vasodilator (NO) release and permeability to albumin in both coronary and pulmonary EC, whereas ET-1 release was inhibited. Under these conditions, only pulmonary ICAM expression was significantly enhanced. These data suggest that human endothelium isolated from divergent vascular beds are activated by burn injury in a unique manner for time post-burn and vascular site of cell origin.

Original languageEnglish (US)
Pages (from-to)227-231
Number of pages5
JournalShock
Volume16
Issue number3
StatePublished - Sep 2001

Fingerprint

Endothelial Cells
Hot Temperature
Lung
Permeability
Wounds and Injuries
Burns
Epoprostenol
Intercellular Adhesion Molecule-1
Serum
Vasodilator Agents
Blood Vessels
Vasoconstrictor Agents
Resuscitation
Endothelium
Albumins
Skin

Keywords

  • Capillary leak
  • ICAM expression
  • Organ-specific endothelium
  • Permeability
  • Vasoactive mediators

ASJC Scopus subject areas

  • Physiology
  • Critical Care and Intensive Care Medicine

Cite this

Murphy, J. T., Duffy, S., Purdue, G. F., & Hunt, J. L. (2001). Differential activation of coronary and pulmonary endothelial cells by thermal injury. Shock, 16(3), 227-231.

Differential activation of coronary and pulmonary endothelial cells by thermal injury. / Murphy, Joseph T.; Duffy, Steven; Purdue, Gary F.; Hunt, John L.

In: Shock, Vol. 16, No. 3, 09.2001, p. 227-231.

Research output: Contribution to journalArticle

Murphy, JT, Duffy, S, Purdue, GF & Hunt, JL 2001, 'Differential activation of coronary and pulmonary endothelial cells by thermal injury', Shock, vol. 16, no. 3, pp. 227-231.
Murphy, Joseph T. ; Duffy, Steven ; Purdue, Gary F. ; Hunt, John L. / Differential activation of coronary and pulmonary endothelial cells by thermal injury. In: Shock. 2001 ; Vol. 16, No. 3. pp. 227-231.
@article{87bedad4610a48e19f3b1412f081b0d9,
title = "Differential activation of coronary and pulmonary endothelial cells by thermal injury",
abstract = "Remote organ dysfunction during resuscitation of severe thermal injury is characterized by early, transient pulmonary insufficiency and cardiac contractile dysfunction. Thermal injury is typified by profound systemic alterations of endothelial immunological, vasoactive, and barrier functions. The unique location of this ubiquitous, fragile monolayer makes it vulnerable to circulating serum factors created at remote cutaneous wounds. We examined endothelial {"}activation{"} in 2 distinct cell types, human coronary and pulmonary endothelial cells (EC), after severe thermal injury. By using human serum isolated at specific times after thermal injury ({"}early{"} [2 h post-burn] or {"}late{"} [26 h post-burn]), the endothelial release of vasoactive mediators, ICAM-1 expression, and monolayer permeability were assessed in vitro. Early burn serum enhanced coronary EC vasoconstrictor (ET-1) release and ICAM expression, inhibited vasodilator (PGI2) release, but had no effect on permeability. Conversely, under similar conditions, pulmonary EC PGI2 release and permeability were enhanced, ET-1 release was diminished, but ICAM was unaffected. Late burn serum enhanced vasodilator (NO) release and permeability to albumin in both coronary and pulmonary EC, whereas ET-1 release was inhibited. Under these conditions, only pulmonary ICAM expression was significantly enhanced. These data suggest that human endothelium isolated from divergent vascular beds are activated by burn injury in a unique manner for time post-burn and vascular site of cell origin.",
keywords = "Capillary leak, ICAM expression, Organ-specific endothelium, Permeability, Vasoactive mediators",
author = "Murphy, {Joseph T.} and Steven Duffy and Purdue, {Gary F.} and Hunt, {John L.}",
year = "2001",
month = "9",
language = "English (US)",
volume = "16",
pages = "227--231",
journal = "Shock",
issn = "1073-2322",
publisher = "Lippincott Williams and Wilkins",
number = "3",

}

TY - JOUR

T1 - Differential activation of coronary and pulmonary endothelial cells by thermal injury

AU - Murphy, Joseph T.

AU - Duffy, Steven

AU - Purdue, Gary F.

AU - Hunt, John L.

PY - 2001/9

Y1 - 2001/9

N2 - Remote organ dysfunction during resuscitation of severe thermal injury is characterized by early, transient pulmonary insufficiency and cardiac contractile dysfunction. Thermal injury is typified by profound systemic alterations of endothelial immunological, vasoactive, and barrier functions. The unique location of this ubiquitous, fragile monolayer makes it vulnerable to circulating serum factors created at remote cutaneous wounds. We examined endothelial "activation" in 2 distinct cell types, human coronary and pulmonary endothelial cells (EC), after severe thermal injury. By using human serum isolated at specific times after thermal injury ("early" [2 h post-burn] or "late" [26 h post-burn]), the endothelial release of vasoactive mediators, ICAM-1 expression, and monolayer permeability were assessed in vitro. Early burn serum enhanced coronary EC vasoconstrictor (ET-1) release and ICAM expression, inhibited vasodilator (PGI2) release, but had no effect on permeability. Conversely, under similar conditions, pulmonary EC PGI2 release and permeability were enhanced, ET-1 release was diminished, but ICAM was unaffected. Late burn serum enhanced vasodilator (NO) release and permeability to albumin in both coronary and pulmonary EC, whereas ET-1 release was inhibited. Under these conditions, only pulmonary ICAM expression was significantly enhanced. These data suggest that human endothelium isolated from divergent vascular beds are activated by burn injury in a unique manner for time post-burn and vascular site of cell origin.

AB - Remote organ dysfunction during resuscitation of severe thermal injury is characterized by early, transient pulmonary insufficiency and cardiac contractile dysfunction. Thermal injury is typified by profound systemic alterations of endothelial immunological, vasoactive, and barrier functions. The unique location of this ubiquitous, fragile monolayer makes it vulnerable to circulating serum factors created at remote cutaneous wounds. We examined endothelial "activation" in 2 distinct cell types, human coronary and pulmonary endothelial cells (EC), after severe thermal injury. By using human serum isolated at specific times after thermal injury ("early" [2 h post-burn] or "late" [26 h post-burn]), the endothelial release of vasoactive mediators, ICAM-1 expression, and monolayer permeability were assessed in vitro. Early burn serum enhanced coronary EC vasoconstrictor (ET-1) release and ICAM expression, inhibited vasodilator (PGI2) release, but had no effect on permeability. Conversely, under similar conditions, pulmonary EC PGI2 release and permeability were enhanced, ET-1 release was diminished, but ICAM was unaffected. Late burn serum enhanced vasodilator (NO) release and permeability to albumin in both coronary and pulmonary EC, whereas ET-1 release was inhibited. Under these conditions, only pulmonary ICAM expression was significantly enhanced. These data suggest that human endothelium isolated from divergent vascular beds are activated by burn injury in a unique manner for time post-burn and vascular site of cell origin.

KW - Capillary leak

KW - ICAM expression

KW - Organ-specific endothelium

KW - Permeability

KW - Vasoactive mediators

UR - http://www.scopus.com/inward/record.url?scp=0035461051&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035461051&partnerID=8YFLogxK

M3 - Article

C2 - 11531026

AN - SCOPUS:0035461051

VL - 16

SP - 227

EP - 231

JO - Shock

JF - Shock

SN - 1073-2322

IS - 3

ER -