Isoflurane Impairs Motor Function Recovery by Increasing Neuroapoptosis and Degeneration during Spinal Ischemia-Reperfusion Injury in Rats

Shi-Yuan Fang, Jung-Shun Lee, Jun-Neng Roan, Yu-Chuan Tsai, Chen Fuh Lam

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

BACKGROUND: Spinal cord ischemia (SCI) leads to variable degrees of neurologic deficit in patients undergoing major cardiovascular surgery. The effect of intraoperative neuroprotection against SCI and the subsequent ischemia-reperfusion injury is still limited. Because isoflurane is a commonly used anesthetic agent during major operation, and its neuroprotective and neurotoxicity effects have both been discussed, this study aimed to investigate the effect of isoflurane on the spinal cord's functional recovery in a rat model of cord ischemia. METHODS: Rats were randomly anesthetized by parenteral anesthetic (Zoletil®) and isoflurane (0% and 1.5% v/v in oxygen). Cord ischemia was induced by cross-clamping of thoracic aorta at the level of T5, and cord perfusion was resumed after 25 minutes. The motor function was assessed independently up to 48 hours after reperfusion. Spinal cords were harvested and analyzed for molecular and histologic changes. RESULTS: The locomotor rating scale was significantly reduced in rats that received isoflurane treatment during SCI at 12 to 48 hours after reperfusion. Isoflurane enhanced the expression of heme oxygenase-1, glial fibrillary acidic protein, cleaved caspase-3, and Iba-1 in the spinal cord. Increased apoptotic cells and the presence of axonal damage were also observed in the histologic sections. CONCLUSION: Our results demonstrate that the administration of inhaled isoflurane in spinal cord ischemia-reperfusion injury impairs the recovery of motor function. This response is associated with the neuronal apoptosis and degeneration. This study highlights the potential adverse effect of isoflurane on the functional recovery of ischemic spinal cord during major aortic surgery.

Original languageEnglish
Pages (from-to)254-261
Number of pages8
JournalAnesthesia and analgesia
Volume124
Issue number1
DOIs
Publication statusPublished - 2017 Jan 1

Fingerprint

Isoflurane
Recovery of Function
Reperfusion Injury
Spinal Cord Ischemia
Spinal Cord
Reperfusion
Anesthetics
Ischemia
Heme Oxygenase-1
Glial Fibrillary Acidic Protein
Neuroprotective Agents
Neurologic Manifestations
Thoracic Aorta
Constriction
Caspase 3
Perfusion
Apoptosis
Oxygen

All Science Journal Classification (ASJC) codes

  • Anesthesiology and Pain Medicine

Cite this

@article{51cd8fc622414de9b93424700b8f72fc,
title = "Isoflurane Impairs Motor Function Recovery by Increasing Neuroapoptosis and Degeneration during Spinal Ischemia-Reperfusion Injury in Rats",
abstract = "BACKGROUND: Spinal cord ischemia (SCI) leads to variable degrees of neurologic deficit in patients undergoing major cardiovascular surgery. The effect of intraoperative neuroprotection against SCI and the subsequent ischemia-reperfusion injury is still limited. Because isoflurane is a commonly used anesthetic agent during major operation, and its neuroprotective and neurotoxicity effects have both been discussed, this study aimed to investigate the effect of isoflurane on the spinal cord's functional recovery in a rat model of cord ischemia. METHODS: Rats were randomly anesthetized by parenteral anesthetic (Zoletil{\circledR}) and isoflurane (0{\%} and 1.5{\%} v/v in oxygen). Cord ischemia was induced by cross-clamping of thoracic aorta at the level of T5, and cord perfusion was resumed after 25 minutes. The motor function was assessed independently up to 48 hours after reperfusion. Spinal cords were harvested and analyzed for molecular and histologic changes. RESULTS: The locomotor rating scale was significantly reduced in rats that received isoflurane treatment during SCI at 12 to 48 hours after reperfusion. Isoflurane enhanced the expression of heme oxygenase-1, glial fibrillary acidic protein, cleaved caspase-3, and Iba-1 in the spinal cord. Increased apoptotic cells and the presence of axonal damage were also observed in the histologic sections. CONCLUSION: Our results demonstrate that the administration of inhaled isoflurane in spinal cord ischemia-reperfusion injury impairs the recovery of motor function. This response is associated with the neuronal apoptosis and degeneration. This study highlights the potential adverse effect of isoflurane on the functional recovery of ischemic spinal cord during major aortic surgery.",
author = "Shi-Yuan Fang and Jung-Shun Lee and Jun-Neng Roan and Yu-Chuan Tsai and Lam, {Chen Fuh}",
year = "2017",
month = "1",
day = "1",
doi = "10.1213/ANE.0000000000001704",
language = "English",
volume = "124",
pages = "254--261",
journal = "Anesthesia and Analgesia",
issn = "0003-2999",
publisher = "Lippincott Williams and Wilkins",
number = "1",

}

TY - JOUR

T1 - Isoflurane Impairs Motor Function Recovery by Increasing Neuroapoptosis and Degeneration during Spinal Ischemia-Reperfusion Injury in Rats

AU - Fang, Shi-Yuan

AU - Lee, Jung-Shun

AU - Roan, Jun-Neng

AU - Tsai, Yu-Chuan

AU - Lam, Chen Fuh

PY - 2017/1/1

Y1 - 2017/1/1

N2 - BACKGROUND: Spinal cord ischemia (SCI) leads to variable degrees of neurologic deficit in patients undergoing major cardiovascular surgery. The effect of intraoperative neuroprotection against SCI and the subsequent ischemia-reperfusion injury is still limited. Because isoflurane is a commonly used anesthetic agent during major operation, and its neuroprotective and neurotoxicity effects have both been discussed, this study aimed to investigate the effect of isoflurane on the spinal cord's functional recovery in a rat model of cord ischemia. METHODS: Rats were randomly anesthetized by parenteral anesthetic (Zoletil®) and isoflurane (0% and 1.5% v/v in oxygen). Cord ischemia was induced by cross-clamping of thoracic aorta at the level of T5, and cord perfusion was resumed after 25 minutes. The motor function was assessed independently up to 48 hours after reperfusion. Spinal cords were harvested and analyzed for molecular and histologic changes. RESULTS: The locomotor rating scale was significantly reduced in rats that received isoflurane treatment during SCI at 12 to 48 hours after reperfusion. Isoflurane enhanced the expression of heme oxygenase-1, glial fibrillary acidic protein, cleaved caspase-3, and Iba-1 in the spinal cord. Increased apoptotic cells and the presence of axonal damage were also observed in the histologic sections. CONCLUSION: Our results demonstrate that the administration of inhaled isoflurane in spinal cord ischemia-reperfusion injury impairs the recovery of motor function. This response is associated with the neuronal apoptosis and degeneration. This study highlights the potential adverse effect of isoflurane on the functional recovery of ischemic spinal cord during major aortic surgery.

AB - BACKGROUND: Spinal cord ischemia (SCI) leads to variable degrees of neurologic deficit in patients undergoing major cardiovascular surgery. The effect of intraoperative neuroprotection against SCI and the subsequent ischemia-reperfusion injury is still limited. Because isoflurane is a commonly used anesthetic agent during major operation, and its neuroprotective and neurotoxicity effects have both been discussed, this study aimed to investigate the effect of isoflurane on the spinal cord's functional recovery in a rat model of cord ischemia. METHODS: Rats were randomly anesthetized by parenteral anesthetic (Zoletil®) and isoflurane (0% and 1.5% v/v in oxygen). Cord ischemia was induced by cross-clamping of thoracic aorta at the level of T5, and cord perfusion was resumed after 25 minutes. The motor function was assessed independently up to 48 hours after reperfusion. Spinal cords were harvested and analyzed for molecular and histologic changes. RESULTS: The locomotor rating scale was significantly reduced in rats that received isoflurane treatment during SCI at 12 to 48 hours after reperfusion. Isoflurane enhanced the expression of heme oxygenase-1, glial fibrillary acidic protein, cleaved caspase-3, and Iba-1 in the spinal cord. Increased apoptotic cells and the presence of axonal damage were also observed in the histologic sections. CONCLUSION: Our results demonstrate that the administration of inhaled isoflurane in spinal cord ischemia-reperfusion injury impairs the recovery of motor function. This response is associated with the neuronal apoptosis and degeneration. This study highlights the potential adverse effect of isoflurane on the functional recovery of ischemic spinal cord during major aortic surgery.

UR - http://www.scopus.com/inward/record.url?scp=85001966889&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85001966889&partnerID=8YFLogxK

U2 - 10.1213/ANE.0000000000001704

DO - 10.1213/ANE.0000000000001704

M3 - Article

C2 - 27918332

AN - SCOPUS:85001966889

VL - 124

SP - 254

EP - 261

JO - Anesthesia and Analgesia

JF - Anesthesia and Analgesia

SN - 0003-2999

IS - 1

ER -