Hypothermic modulation of cerebral ischemic injury during cardiopulmonary bypass in pigs

Brendan P. Conry, Cheng Y. Lin, Larry W. Jenkins, Douglas Dewitt, Mark H. Zornow, Tatsuo Uchida, William E. Johnston

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Background: The aim of this study was to determine whether progressive levels of hypothermia (37, 34, 31, or 28°C) during cardiopulmonary bypass (CPB) in pigs reduce the physiologic and metabolic consequences of global cerebral ischemia. Methods: Sagittal sinus and cortical microdialysis catheters were inserted into anesthetized pigs. Animals were placed on CPB and randomly assigned to 37°C (n = 10), 34°C (n = 10), 31°C (n = 11), or 28°C (n = 10) management. Next 20 min of global cerebral ischemia was produced by temporarily ligating the innominate and left subclavian arteries, followed by reperfusion, rewarming, and termination of CPB. Cerebral oxygen metabolism (CMRO2) was calculated by cerebral blood flow (radioactive microspheres) and arteriovenous oxygen content gradient. Cortical excitatory amino acids (EAA) by microdialysis were measured using high-performance liquid chromatography. Electroencephalographic (EEG) signals were graded by observers blinded to the protocol. After CPB, cerebrospinal fluid was sampled to test for S-100 protein and the cerebral cortex was biopsied. Results: Cerebral oxygen metabolism increased after rewarming from 28°C, 31°C, and 34°C CPB but not in the 37°animals; CMRO2 remained lower with 370C (1.8 ± 0.2 ml · min-1 · 100 g-1) than with 28°C (3.1 ± 0.1 ml · min-1 · 100 g-1; p < 0.05). The EEG scores after CPB were depressed in all groups and remained significantly lower in the 37°C animals. With 28°C and 31°C CPB, EAA concentrations did not change. In contrast, glutamate increased by sixfold during ischemia at 37°C and remained significantly greater during reperfusion in the 34°C and 37°C groups. Cortical biopsy specimens showed no intergroup differences in energy metabolites except two to three times greater brain lactate in the 37°C animals. S-100 protein in cerebrospinal fluid was greater in the 37°C (6 ± 0.9 μg/l) and 34°C (3.5 ± 0.5 μg/l) groups than the 31°C (1.9 ± 0.1 μg/l) and 28°C (1.7 ± 0.2 μg/l) animals. Conclusions: Hypothermia to 28°C and 31°C provides significant cerebral recovery from 20 min of global ischemia during CPB in terms of EAA release, EEG and cerebral metabolic recovery, and S-100 protein release without greater advantage from cooling to 28°C compared with 31°C. In contrast, ischemia during 34°C and particularly 37°C CPB showed greater FAA release and evidence of neurologic morbidity. Cooling to 31°C was necessary to improve acute recovery during global cerebral ischemia on CPB.

Original languageEnglish (US)
Pages (from-to)390-402
Number of pages13
JournalAnesthesiology
Volume88
Issue number2
DOIs
StatePublished - 1998
Externally publishedYes

Fingerprint

Cardiopulmonary Bypass
Swine
Wounds and Injuries
Excitatory Amino Acids
S100 Proteins
Brain Ischemia
Rewarming
Ischemia
Microdialysis
Oxygen
Hypothermia
Reperfusion
Cerebrospinal Fluid
Cerebrovascular Circulation
Subclavian Artery
Microspheres
Cerebral Cortex
Nervous System
Glutamic Acid
Lactic Acid

Keywords

  • Cerebral blood flow
  • Cerebral oxygen metabolism
  • Excitatory neurotransmitters

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Conry, B. P., Lin, C. Y., Jenkins, L. W., Dewitt, D., Zornow, M. H., Uchida, T., & Johnston, W. E. (1998). Hypothermic modulation of cerebral ischemic injury during cardiopulmonary bypass in pigs. Anesthesiology, 88(2), 390-402. https://doi.org/10.1097/00000542-199802000-00018

Hypothermic modulation of cerebral ischemic injury during cardiopulmonary bypass in pigs. / Conry, Brendan P.; Lin, Cheng Y.; Jenkins, Larry W.; Dewitt, Douglas; Zornow, Mark H.; Uchida, Tatsuo; Johnston, William E.

In: Anesthesiology, Vol. 88, No. 2, 1998, p. 390-402.

Research output: Contribution to journalArticle

Conry, BP, Lin, CY, Jenkins, LW, Dewitt, D, Zornow, MH, Uchida, T & Johnston, WE 1998, 'Hypothermic modulation of cerebral ischemic injury during cardiopulmonary bypass in pigs', Anesthesiology, vol. 88, no. 2, pp. 390-402. https://doi.org/10.1097/00000542-199802000-00018
Conry, Brendan P. ; Lin, Cheng Y. ; Jenkins, Larry W. ; Dewitt, Douglas ; Zornow, Mark H. ; Uchida, Tatsuo ; Johnston, William E. / Hypothermic modulation of cerebral ischemic injury during cardiopulmonary bypass in pigs. In: Anesthesiology. 1998 ; Vol. 88, No. 2. pp. 390-402.
@article{d0973cb7ee524b95a47df787ff75e053,
title = "Hypothermic modulation of cerebral ischemic injury during cardiopulmonary bypass in pigs",
abstract = "Background: The aim of this study was to determine whether progressive levels of hypothermia (37, 34, 31, or 28°C) during cardiopulmonary bypass (CPB) in pigs reduce the physiologic and metabolic consequences of global cerebral ischemia. Methods: Sagittal sinus and cortical microdialysis catheters were inserted into anesthetized pigs. Animals were placed on CPB and randomly assigned to 37°C (n = 10), 34°C (n = 10), 31°C (n = 11), or 28°C (n = 10) management. Next 20 min of global cerebral ischemia was produced by temporarily ligating the innominate and left subclavian arteries, followed by reperfusion, rewarming, and termination of CPB. Cerebral oxygen metabolism (CMRO2) was calculated by cerebral blood flow (radioactive microspheres) and arteriovenous oxygen content gradient. Cortical excitatory amino acids (EAA) by microdialysis were measured using high-performance liquid chromatography. Electroencephalographic (EEG) signals were graded by observers blinded to the protocol. After CPB, cerebrospinal fluid was sampled to test for S-100 protein and the cerebral cortex was biopsied. Results: Cerebral oxygen metabolism increased after rewarming from 28°C, 31°C, and 34°C CPB but not in the 37°animals; CMRO2 remained lower with 370C (1.8 ± 0.2 ml · min-1 · 100 g-1) than with 28°C (3.1 ± 0.1 ml · min-1 · 100 g-1; p < 0.05). The EEG scores after CPB were depressed in all groups and remained significantly lower in the 37°C animals. With 28°C and 31°C CPB, EAA concentrations did not change. In contrast, glutamate increased by sixfold during ischemia at 37°C and remained significantly greater during reperfusion in the 34°C and 37°C groups. Cortical biopsy specimens showed no intergroup differences in energy metabolites except two to three times greater brain lactate in the 37°C animals. S-100 protein in cerebrospinal fluid was greater in the 37°C (6 ± 0.9 μg/l) and 34°C (3.5 ± 0.5 μg/l) groups than the 31°C (1.9 ± 0.1 μg/l) and 28°C (1.7 ± 0.2 μg/l) animals. Conclusions: Hypothermia to 28°C and 31°C provides significant cerebral recovery from 20 min of global ischemia during CPB in terms of EAA release, EEG and cerebral metabolic recovery, and S-100 protein release without greater advantage from cooling to 28°C compared with 31°C. In contrast, ischemia during 34°C and particularly 37°C CPB showed greater FAA release and evidence of neurologic morbidity. Cooling to 31°C was necessary to improve acute recovery during global cerebral ischemia on CPB.",
keywords = "Cerebral blood flow, Cerebral oxygen metabolism, Excitatory neurotransmitters",
author = "Conry, {Brendan P.} and Lin, {Cheng Y.} and Jenkins, {Larry W.} and Douglas Dewitt and Zornow, {Mark H.} and Tatsuo Uchida and Johnston, {William E.}",
year = "1998",
doi = "10.1097/00000542-199802000-00018",
language = "English (US)",
volume = "88",
pages = "390--402",
journal = "Anesthesiology",
issn = "0003-3022",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

TY - JOUR

T1 - Hypothermic modulation of cerebral ischemic injury during cardiopulmonary bypass in pigs

AU - Conry, Brendan P.

AU - Lin, Cheng Y.

AU - Jenkins, Larry W.

AU - Dewitt, Douglas

AU - Zornow, Mark H.

AU - Uchida, Tatsuo

AU - Johnston, William E.

PY - 1998

Y1 - 1998

N2 - Background: The aim of this study was to determine whether progressive levels of hypothermia (37, 34, 31, or 28°C) during cardiopulmonary bypass (CPB) in pigs reduce the physiologic and metabolic consequences of global cerebral ischemia. Methods: Sagittal sinus and cortical microdialysis catheters were inserted into anesthetized pigs. Animals were placed on CPB and randomly assigned to 37°C (n = 10), 34°C (n = 10), 31°C (n = 11), or 28°C (n = 10) management. Next 20 min of global cerebral ischemia was produced by temporarily ligating the innominate and left subclavian arteries, followed by reperfusion, rewarming, and termination of CPB. Cerebral oxygen metabolism (CMRO2) was calculated by cerebral blood flow (radioactive microspheres) and arteriovenous oxygen content gradient. Cortical excitatory amino acids (EAA) by microdialysis were measured using high-performance liquid chromatography. Electroencephalographic (EEG) signals were graded by observers blinded to the protocol. After CPB, cerebrospinal fluid was sampled to test for S-100 protein and the cerebral cortex was biopsied. Results: Cerebral oxygen metabolism increased after rewarming from 28°C, 31°C, and 34°C CPB but not in the 37°animals; CMRO2 remained lower with 370C (1.8 ± 0.2 ml · min-1 · 100 g-1) than with 28°C (3.1 ± 0.1 ml · min-1 · 100 g-1; p < 0.05). The EEG scores after CPB were depressed in all groups and remained significantly lower in the 37°C animals. With 28°C and 31°C CPB, EAA concentrations did not change. In contrast, glutamate increased by sixfold during ischemia at 37°C and remained significantly greater during reperfusion in the 34°C and 37°C groups. Cortical biopsy specimens showed no intergroup differences in energy metabolites except two to three times greater brain lactate in the 37°C animals. S-100 protein in cerebrospinal fluid was greater in the 37°C (6 ± 0.9 μg/l) and 34°C (3.5 ± 0.5 μg/l) groups than the 31°C (1.9 ± 0.1 μg/l) and 28°C (1.7 ± 0.2 μg/l) animals. Conclusions: Hypothermia to 28°C and 31°C provides significant cerebral recovery from 20 min of global ischemia during CPB in terms of EAA release, EEG and cerebral metabolic recovery, and S-100 protein release without greater advantage from cooling to 28°C compared with 31°C. In contrast, ischemia during 34°C and particularly 37°C CPB showed greater FAA release and evidence of neurologic morbidity. Cooling to 31°C was necessary to improve acute recovery during global cerebral ischemia on CPB.

AB - Background: The aim of this study was to determine whether progressive levels of hypothermia (37, 34, 31, or 28°C) during cardiopulmonary bypass (CPB) in pigs reduce the physiologic and metabolic consequences of global cerebral ischemia. Methods: Sagittal sinus and cortical microdialysis catheters were inserted into anesthetized pigs. Animals were placed on CPB and randomly assigned to 37°C (n = 10), 34°C (n = 10), 31°C (n = 11), or 28°C (n = 10) management. Next 20 min of global cerebral ischemia was produced by temporarily ligating the innominate and left subclavian arteries, followed by reperfusion, rewarming, and termination of CPB. Cerebral oxygen metabolism (CMRO2) was calculated by cerebral blood flow (radioactive microspheres) and arteriovenous oxygen content gradient. Cortical excitatory amino acids (EAA) by microdialysis were measured using high-performance liquid chromatography. Electroencephalographic (EEG) signals were graded by observers blinded to the protocol. After CPB, cerebrospinal fluid was sampled to test for S-100 protein and the cerebral cortex was biopsied. Results: Cerebral oxygen metabolism increased after rewarming from 28°C, 31°C, and 34°C CPB but not in the 37°animals; CMRO2 remained lower with 370C (1.8 ± 0.2 ml · min-1 · 100 g-1) than with 28°C (3.1 ± 0.1 ml · min-1 · 100 g-1; p < 0.05). The EEG scores after CPB were depressed in all groups and remained significantly lower in the 37°C animals. With 28°C and 31°C CPB, EAA concentrations did not change. In contrast, glutamate increased by sixfold during ischemia at 37°C and remained significantly greater during reperfusion in the 34°C and 37°C groups. Cortical biopsy specimens showed no intergroup differences in energy metabolites except two to three times greater brain lactate in the 37°C animals. S-100 protein in cerebrospinal fluid was greater in the 37°C (6 ± 0.9 μg/l) and 34°C (3.5 ± 0.5 μg/l) groups than the 31°C (1.9 ± 0.1 μg/l) and 28°C (1.7 ± 0.2 μg/l) animals. Conclusions: Hypothermia to 28°C and 31°C provides significant cerebral recovery from 20 min of global ischemia during CPB in terms of EAA release, EEG and cerebral metabolic recovery, and S-100 protein release without greater advantage from cooling to 28°C compared with 31°C. In contrast, ischemia during 34°C and particularly 37°C CPB showed greater FAA release and evidence of neurologic morbidity. Cooling to 31°C was necessary to improve acute recovery during global cerebral ischemia on CPB.

KW - Cerebral blood flow

KW - Cerebral oxygen metabolism

KW - Excitatory neurotransmitters

UR - http://www.scopus.com/inward/record.url?scp=0031939842&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031939842&partnerID=8YFLogxK

U2 - 10.1097/00000542-199802000-00018

DO - 10.1097/00000542-199802000-00018

M3 - Article

VL - 88

SP - 390

EP - 402

JO - Anesthesiology

JF - Anesthesiology

SN - 0003-3022

IS - 2

ER -