The effects of systemic hypothermia on a murine model of thoracic aortic ischemia reperfusion

Jeanwan Kang, Hassan Albadawi, Patrick J. Casey, Thomas A. Abbruzzese, Virendra I. Patel, Hyung J. Yoo, Richard P. Cambria, Michael T. Watkins

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Introduction: Hypothermia is widely used to mediate ischemia-reperfusion injury associated with repair of the thoracoabdominal aorta. Experiments were designed in a murine model of thoracic aortic ischemia-reperfusion (TAR) to evaluate the effect of moderate systemic hypothermia on neurologic function, spinal cord morphology, and indices of inflammation in critical organs. Methods: C57BL/6 mice were subjected to TAR under hypothermic (34°C) or normothermic (38°C) conditions, followed by 24 or 48 hours of normothermic reperfusion. Neurologic functions were assessed during reperfusion. Spinal cords were examined at 24 and 48 hours after reperfusion, and the degree of injury qualified by counting the number of viable motor neurons within the anterior horns. Keratinocyte chemokine, interleukin-6, and myeloperoxidase levels were measured from lung, liver, and kidney at 24 and 48 hours. Results: Normothermic TAR resulted in a dense neurologic deficit in all mice throughout the reperfusion period. Mice subjected to TAR under hypothermic conditions had transient, mild neurologic deficit during the initial periods of reperfusion. Between 24 and 48 hours, delayed paralysis developed in half of these mice, whereas the other half remained neurologically intact. Spinal cord histology showed a graded degree of injury that correlated with neurologic function. There was no correlation between markers of inflammation in various organs and neurologic outcomes following TAR. Conclusion: Systemic moderate hypothermia was protective against immediate paralysis after TAR in all cases and was associated with delayed paralysis in 50% of mice. This study suggests that delayed-onset paralysis may be the result of a local insult, rather than a systemic inflammatory event, precipitating spinal cord injury.

Original languageEnglish (US)
Pages (from-to)435-443
Number of pages9
JournalJournal of Vascular Surgery
Volume52
Issue number2
DOIs
StatePublished - Aug 1 2010
Externally publishedYes

Fingerprint

Hypothermia
Reperfusion
Thorax
Ischemia
Paralysis
Nervous System
Spinal Cord
Neurologic Manifestations
Reperfusion Injury
Inflammation
Motor Neurons
Horns
Spinal Cord Injuries
Inbred C57BL Mouse
Keratinocytes
Chemokines
Peroxidase
Aorta
Interleukin-6
Histology

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

The effects of systemic hypothermia on a murine model of thoracic aortic ischemia reperfusion. / Kang, Jeanwan; Albadawi, Hassan; Casey, Patrick J.; Abbruzzese, Thomas A.; Patel, Virendra I.; Yoo, Hyung J.; Cambria, Richard P.; Watkins, Michael T.

In: Journal of Vascular Surgery, Vol. 52, No. 2, 01.08.2010, p. 435-443.

Research output: Contribution to journalArticle

Kang, J, Albadawi, H, Casey, PJ, Abbruzzese, TA, Patel, VI, Yoo, HJ, Cambria, RP & Watkins, MT 2010, 'The effects of systemic hypothermia on a murine model of thoracic aortic ischemia reperfusion', Journal of Vascular Surgery, vol. 52, no. 2, pp. 435-443. https://doi.org/10.1016/j.jvs.2010.03.021
Kang, Jeanwan ; Albadawi, Hassan ; Casey, Patrick J. ; Abbruzzese, Thomas A. ; Patel, Virendra I. ; Yoo, Hyung J. ; Cambria, Richard P. ; Watkins, Michael T. / The effects of systemic hypothermia on a murine model of thoracic aortic ischemia reperfusion. In: Journal of Vascular Surgery. 2010 ; Vol. 52, No. 2. pp. 435-443.
@article{482897cb4a434ccbb2151e0e2d685b4e,
title = "The effects of systemic hypothermia on a murine model of thoracic aortic ischemia reperfusion",
abstract = "Introduction: Hypothermia is widely used to mediate ischemia-reperfusion injury associated with repair of the thoracoabdominal aorta. Experiments were designed in a murine model of thoracic aortic ischemia-reperfusion (TAR) to evaluate the effect of moderate systemic hypothermia on neurologic function, spinal cord morphology, and indices of inflammation in critical organs. Methods: C57BL/6 mice were subjected to TAR under hypothermic (34°C) or normothermic (38°C) conditions, followed by 24 or 48 hours of normothermic reperfusion. Neurologic functions were assessed during reperfusion. Spinal cords were examined at 24 and 48 hours after reperfusion, and the degree of injury qualified by counting the number of viable motor neurons within the anterior horns. Keratinocyte chemokine, interleukin-6, and myeloperoxidase levels were measured from lung, liver, and kidney at 24 and 48 hours. Results: Normothermic TAR resulted in a dense neurologic deficit in all mice throughout the reperfusion period. Mice subjected to TAR under hypothermic conditions had transient, mild neurologic deficit during the initial periods of reperfusion. Between 24 and 48 hours, delayed paralysis developed in half of these mice, whereas the other half remained neurologically intact. Spinal cord histology showed a graded degree of injury that correlated with neurologic function. There was no correlation between markers of inflammation in various organs and neurologic outcomes following TAR. Conclusion: Systemic moderate hypothermia was protective against immediate paralysis after TAR in all cases and was associated with delayed paralysis in 50{\%} of mice. This study suggests that delayed-onset paralysis may be the result of a local insult, rather than a systemic inflammatory event, precipitating spinal cord injury.",
author = "Jeanwan Kang and Hassan Albadawi and Casey, {Patrick J.} and Abbruzzese, {Thomas A.} and Patel, {Virendra I.} and Yoo, {Hyung J.} and Cambria, {Richard P.} and Watkins, {Michael T.}",
year = "2010",
month = "8",
day = "1",
doi = "10.1016/j.jvs.2010.03.021",
language = "English (US)",
volume = "52",
pages = "435--443",
journal = "Journal of Vascular Surgery",
issn = "0741-5214",
publisher = "Mosby Inc.",
number = "2",

}

TY - JOUR

T1 - The effects of systemic hypothermia on a murine model of thoracic aortic ischemia reperfusion

AU - Kang, Jeanwan

AU - Albadawi, Hassan

AU - Casey, Patrick J.

AU - Abbruzzese, Thomas A.

AU - Patel, Virendra I.

AU - Yoo, Hyung J.

AU - Cambria, Richard P.

AU - Watkins, Michael T.

PY - 2010/8/1

Y1 - 2010/8/1

N2 - Introduction: Hypothermia is widely used to mediate ischemia-reperfusion injury associated with repair of the thoracoabdominal aorta. Experiments were designed in a murine model of thoracic aortic ischemia-reperfusion (TAR) to evaluate the effect of moderate systemic hypothermia on neurologic function, spinal cord morphology, and indices of inflammation in critical organs. Methods: C57BL/6 mice were subjected to TAR under hypothermic (34°C) or normothermic (38°C) conditions, followed by 24 or 48 hours of normothermic reperfusion. Neurologic functions were assessed during reperfusion. Spinal cords were examined at 24 and 48 hours after reperfusion, and the degree of injury qualified by counting the number of viable motor neurons within the anterior horns. Keratinocyte chemokine, interleukin-6, and myeloperoxidase levels were measured from lung, liver, and kidney at 24 and 48 hours. Results: Normothermic TAR resulted in a dense neurologic deficit in all mice throughout the reperfusion period. Mice subjected to TAR under hypothermic conditions had transient, mild neurologic deficit during the initial periods of reperfusion. Between 24 and 48 hours, delayed paralysis developed in half of these mice, whereas the other half remained neurologically intact. Spinal cord histology showed a graded degree of injury that correlated with neurologic function. There was no correlation between markers of inflammation in various organs and neurologic outcomes following TAR. Conclusion: Systemic moderate hypothermia was protective against immediate paralysis after TAR in all cases and was associated with delayed paralysis in 50% of mice. This study suggests that delayed-onset paralysis may be the result of a local insult, rather than a systemic inflammatory event, precipitating spinal cord injury.

AB - Introduction: Hypothermia is widely used to mediate ischemia-reperfusion injury associated with repair of the thoracoabdominal aorta. Experiments were designed in a murine model of thoracic aortic ischemia-reperfusion (TAR) to evaluate the effect of moderate systemic hypothermia on neurologic function, spinal cord morphology, and indices of inflammation in critical organs. Methods: C57BL/6 mice were subjected to TAR under hypothermic (34°C) or normothermic (38°C) conditions, followed by 24 or 48 hours of normothermic reperfusion. Neurologic functions were assessed during reperfusion. Spinal cords were examined at 24 and 48 hours after reperfusion, and the degree of injury qualified by counting the number of viable motor neurons within the anterior horns. Keratinocyte chemokine, interleukin-6, and myeloperoxidase levels were measured from lung, liver, and kidney at 24 and 48 hours. Results: Normothermic TAR resulted in a dense neurologic deficit in all mice throughout the reperfusion period. Mice subjected to TAR under hypothermic conditions had transient, mild neurologic deficit during the initial periods of reperfusion. Between 24 and 48 hours, delayed paralysis developed in half of these mice, whereas the other half remained neurologically intact. Spinal cord histology showed a graded degree of injury that correlated with neurologic function. There was no correlation between markers of inflammation in various organs and neurologic outcomes following TAR. Conclusion: Systemic moderate hypothermia was protective against immediate paralysis after TAR in all cases and was associated with delayed paralysis in 50% of mice. This study suggests that delayed-onset paralysis may be the result of a local insult, rather than a systemic inflammatory event, precipitating spinal cord injury.

UR - http://www.scopus.com/inward/record.url?scp=77955514232&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77955514232&partnerID=8YFLogxK

U2 - 10.1016/j.jvs.2010.03.021

DO - 10.1016/j.jvs.2010.03.021

M3 - Article

C2 - 20541344

AN - SCOPUS:77955514232

VL - 52

SP - 435

EP - 443

JO - Journal of Vascular Surgery

JF - Journal of Vascular Surgery

SN - 0741-5214

IS - 2

ER -