Effect of severe smoke inhalation injury on systemic microvascular blood flow in sheep

Paul J. Schenarts, Hans G. Bone, Lillian D. Traber, Daniel L. Traber

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

Multiple nonpulmonary organ dysfunction is frequently associated with acute lung injury; however, the mechanisms underlying the pathogenesis of this process are not completely understood. Decreased oxygen delivery to distant organs due to maldistribution of blood flow may be a contributing factor. We examined the effects of acute lung injury induced by smoke inhalation on microvascular blood flow to various organs in sheep. Seven sheep were prepared with arterial, venous, pulmonary artery, and left atrial catheters. After a 5 day recovery period, a tracheostomy was performed, followed by insufflation with 48 breaths of cool cotton smoke. Determination of microvascular blood flow using colored microspheres, standard hemodynamic measures, and blood gas analysis were performed before and at 12 h intervals after smoke inhalation. Animals were resuscitated to maintain left atrial pressure at ±2 mmHg of the baseline value and FiO2 was adjusted to maintain Sao2 at >90%. After 48 h, sheep were killed and an autopsy was performed. Samples of trachea, left ventricle, ileum, colon, spleen, pancreas, and cortex from both kidneys were obtained for determination of microvascular blood flow. Blood flow to the trachea was substantially increased, while blood flow to the kidneys was preserved near baseline levels. Left ventricular blood flow decreased slightly; however, this decline was not statistically significant. Blood flow to ileum, colon, spleen, and pancreas was significantly decreased, particularly at 36 and 48 h after injury. These decreases were independent of changes in cardiac output or systemic oxygen delivery. It is likely that alteration in microvascular blood flow may contribute to the development of nonpulmonary organ dysfunction after acute lung injury.

Original languageEnglish (US)
Pages (from-to)201-205
Number of pages5
JournalShock
Volume6
Issue number3
DOIs
StatePublished - Sep 1996

Fingerprint

Smoke Inhalation Injury
Sheep
Acute Lung Injury
Smoke
Trachea
Ileum
Inhalation
Pancreas
Colon
Spleen
Oxygen
Kidney Cortex
Insufflation
Blood Gas Analysis
Atrial Pressure
Tracheostomy
Microspheres
Cardiac Output
Pulmonary Artery
Heart Ventricles

ASJC Scopus subject areas

  • Emergency Medicine
  • Critical Care and Intensive Care Medicine

Cite this

Effect of severe smoke inhalation injury on systemic microvascular blood flow in sheep. / Schenarts, Paul J.; Bone, Hans G.; Traber, Lillian D.; Traber, Daniel L.

In: Shock, Vol. 6, No. 3, 09.1996, p. 201-205.

Research output: Contribution to journalArticle

Schenarts, Paul J. ; Bone, Hans G. ; Traber, Lillian D. ; Traber, Daniel L. / Effect of severe smoke inhalation injury on systemic microvascular blood flow in sheep. In: Shock. 1996 ; Vol. 6, No. 3. pp. 201-205.
@article{7e65bf06e48847f886f1be57d32addfa,
title = "Effect of severe smoke inhalation injury on systemic microvascular blood flow in sheep",
abstract = "Multiple nonpulmonary organ dysfunction is frequently associated with acute lung injury; however, the mechanisms underlying the pathogenesis of this process are not completely understood. Decreased oxygen delivery to distant organs due to maldistribution of blood flow may be a contributing factor. We examined the effects of acute lung injury induced by smoke inhalation on microvascular blood flow to various organs in sheep. Seven sheep were prepared with arterial, venous, pulmonary artery, and left atrial catheters. After a 5 day recovery period, a tracheostomy was performed, followed by insufflation with 48 breaths of cool cotton smoke. Determination of microvascular blood flow using colored microspheres, standard hemodynamic measures, and blood gas analysis were performed before and at 12 h intervals after smoke inhalation. Animals were resuscitated to maintain left atrial pressure at ±2 mmHg of the baseline value and FiO2 was adjusted to maintain Sao2 at >90{\%}. After 48 h, sheep were killed and an autopsy was performed. Samples of trachea, left ventricle, ileum, colon, spleen, pancreas, and cortex from both kidneys were obtained for determination of microvascular blood flow. Blood flow to the trachea was substantially increased, while blood flow to the kidneys was preserved near baseline levels. Left ventricular blood flow decreased slightly; however, this decline was not statistically significant. Blood flow to ileum, colon, spleen, and pancreas was significantly decreased, particularly at 36 and 48 h after injury. These decreases were independent of changes in cardiac output or systemic oxygen delivery. It is likely that alteration in microvascular blood flow may contribute to the development of nonpulmonary organ dysfunction after acute lung injury.",
author = "Schenarts, {Paul J.} and Bone, {Hans G.} and Traber, {Lillian D.} and Traber, {Daniel L.}",
year = "1996",
month = "9",
doi = "10.1097/00024382-199609000-00008",
language = "English (US)",
volume = "6",
pages = "201--205",
journal = "Shock (Augusta, Ga.)",
issn = "1073-2322",
publisher = "Lippincott Williams and Wilkins",
number = "3",

}

TY - JOUR

T1 - Effect of severe smoke inhalation injury on systemic microvascular blood flow in sheep

AU - Schenarts, Paul J.

AU - Bone, Hans G.

AU - Traber, Lillian D.

AU - Traber, Daniel L.

PY - 1996/9

Y1 - 1996/9

N2 - Multiple nonpulmonary organ dysfunction is frequently associated with acute lung injury; however, the mechanisms underlying the pathogenesis of this process are not completely understood. Decreased oxygen delivery to distant organs due to maldistribution of blood flow may be a contributing factor. We examined the effects of acute lung injury induced by smoke inhalation on microvascular blood flow to various organs in sheep. Seven sheep were prepared with arterial, venous, pulmonary artery, and left atrial catheters. After a 5 day recovery period, a tracheostomy was performed, followed by insufflation with 48 breaths of cool cotton smoke. Determination of microvascular blood flow using colored microspheres, standard hemodynamic measures, and blood gas analysis were performed before and at 12 h intervals after smoke inhalation. Animals were resuscitated to maintain left atrial pressure at ±2 mmHg of the baseline value and FiO2 was adjusted to maintain Sao2 at >90%. After 48 h, sheep were killed and an autopsy was performed. Samples of trachea, left ventricle, ileum, colon, spleen, pancreas, and cortex from both kidneys were obtained for determination of microvascular blood flow. Blood flow to the trachea was substantially increased, while blood flow to the kidneys was preserved near baseline levels. Left ventricular blood flow decreased slightly; however, this decline was not statistically significant. Blood flow to ileum, colon, spleen, and pancreas was significantly decreased, particularly at 36 and 48 h after injury. These decreases were independent of changes in cardiac output or systemic oxygen delivery. It is likely that alteration in microvascular blood flow may contribute to the development of nonpulmonary organ dysfunction after acute lung injury.

AB - Multiple nonpulmonary organ dysfunction is frequently associated with acute lung injury; however, the mechanisms underlying the pathogenesis of this process are not completely understood. Decreased oxygen delivery to distant organs due to maldistribution of blood flow may be a contributing factor. We examined the effects of acute lung injury induced by smoke inhalation on microvascular blood flow to various organs in sheep. Seven sheep were prepared with arterial, venous, pulmonary artery, and left atrial catheters. After a 5 day recovery period, a tracheostomy was performed, followed by insufflation with 48 breaths of cool cotton smoke. Determination of microvascular blood flow using colored microspheres, standard hemodynamic measures, and blood gas analysis were performed before and at 12 h intervals after smoke inhalation. Animals were resuscitated to maintain left atrial pressure at ±2 mmHg of the baseline value and FiO2 was adjusted to maintain Sao2 at >90%. After 48 h, sheep were killed and an autopsy was performed. Samples of trachea, left ventricle, ileum, colon, spleen, pancreas, and cortex from both kidneys were obtained for determination of microvascular blood flow. Blood flow to the trachea was substantially increased, while blood flow to the kidneys was preserved near baseline levels. Left ventricular blood flow decreased slightly; however, this decline was not statistically significant. Blood flow to ileum, colon, spleen, and pancreas was significantly decreased, particularly at 36 and 48 h after injury. These decreases were independent of changes in cardiac output or systemic oxygen delivery. It is likely that alteration in microvascular blood flow may contribute to the development of nonpulmonary organ dysfunction after acute lung injury.

UR - http://www.scopus.com/inward/record.url?scp=0030227465&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030227465&partnerID=8YFLogxK

U2 - 10.1097/00024382-199609000-00008

DO - 10.1097/00024382-199609000-00008

M3 - Article

C2 - 8885086

AN - SCOPUS:0030227465

VL - 6

SP - 201

EP - 205

JO - Shock (Augusta, Ga.)

JF - Shock (Augusta, Ga.)

SN - 1073-2322

IS - 3

ER -