Effect of lidocaine on dynamic changes in cortical reduced nicotinamide adenine dinucleotide fluorescence during transient focal cerebral ischemia in rats

Hiromichi Naito, Yoshimasa Takeda, T. Danura, I. S. Kass, K. Morita

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Abstract

Rats were subjected to 90. min of focal ischemia by occluding the left middle cerebral and both common carotid arteries. The dynamic changes in the formation of brain ischemic areas were analyzed by measuring the direct current (DC) potential and reduced nicotinamide adenine dinucleotide (NADH) fluorescence with ultraviolet irradiation. In the lidocaine group (n= 10), 30. min before ischemia, an intravenous bolus (1.5. mg/kg) of lidocaine was administered, followed by a continuous infusion (2. mg/kg/h) for 150. min. In the control group (n= 10), an equivalent amount of saline was administered. Following the initiation of ischemia, an area of high-intensity NADH fluorescence rapidly developed in the middle cerebral artery territory in both groups and the DC potential in this area showed ischemic depolarization. An increase in NADH fluorescence closely correlated with the DC depolarization. The blood flow in the marginal zone of both groups showed a similar decrease. Five minutes after the onset of ischemia, the area of high-intensity NADH fluorescence was significantly smaller in the lidocaine group (67% of the control; P= 0.01). This was likely due to the suppression of ischemic depolarization by blockage of voltage-dependent sodium channels with lidocaine. Although lidocaine administration did not attenuate the number of peri-infarct depolarizations during ischemia, the high-intensity area and infarct volume were significantly smaller in the lidocaine group both at the end of ischemia (78% of the control; P= 0.046) and 24. h later (P= 0.02). A logistic regression analysis demonstrated a relationship between the duration of ischemic depolarization and histologic damage and revealed that lidocaine administration did not attenuate neuronal damage when the duration of depolarization was identical. These findings indicate that the mechanism by which lidocaine decreases infarct volume is primarily through a reduction of the brain area undergoing NADH fluorescence increases which closely correlates with depolarization.

Original languageEnglish
Pages (from-to)59-69
Number of pages11
JournalNeuroscience
Volume235
DOIs
Publication statusPublished - Apr 3 2013

Fingerprint

Transient Ischemic Attack
Lidocaine
NAD
Fluorescence
Ischemia
Control Groups
Sodium Channels
Common Carotid Artery
Middle Cerebral Artery
Brain
Logistic Models
Regression Analysis

Keywords

  • DC potential
  • Depolarization
  • Hypoxia
  • Infarction
  • Lidocaine
  • NADH fluorescence

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

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title = "Effect of lidocaine on dynamic changes in cortical reduced nicotinamide adenine dinucleotide fluorescence during transient focal cerebral ischemia in rats",
abstract = "Rats were subjected to 90. min of focal ischemia by occluding the left middle cerebral and both common carotid arteries. The dynamic changes in the formation of brain ischemic areas were analyzed by measuring the direct current (DC) potential and reduced nicotinamide adenine dinucleotide (NADH) fluorescence with ultraviolet irradiation. In the lidocaine group (n= 10), 30. min before ischemia, an intravenous bolus (1.5. mg/kg) of lidocaine was administered, followed by a continuous infusion (2. mg/kg/h) for 150. min. In the control group (n= 10), an equivalent amount of saline was administered. Following the initiation of ischemia, an area of high-intensity NADH fluorescence rapidly developed in the middle cerebral artery territory in both groups and the DC potential in this area showed ischemic depolarization. An increase in NADH fluorescence closely correlated with the DC depolarization. The blood flow in the marginal zone of both groups showed a similar decrease. Five minutes after the onset of ischemia, the area of high-intensity NADH fluorescence was significantly smaller in the lidocaine group (67{\%} of the control; P= 0.01). This was likely due to the suppression of ischemic depolarization by blockage of voltage-dependent sodium channels with lidocaine. Although lidocaine administration did not attenuate the number of peri-infarct depolarizations during ischemia, the high-intensity area and infarct volume were significantly smaller in the lidocaine group both at the end of ischemia (78{\%} of the control; P= 0.046) and 24. h later (P= 0.02). A logistic regression analysis demonstrated a relationship between the duration of ischemic depolarization and histologic damage and revealed that lidocaine administration did not attenuate neuronal damage when the duration of depolarization was identical. These findings indicate that the mechanism by which lidocaine decreases infarct volume is primarily through a reduction of the brain area undergoing NADH fluorescence increases which closely correlates with depolarization.",
keywords = "DC potential, Depolarization, Hypoxia, Infarction, Lidocaine, NADH fluorescence",
author = "Hiromichi Naito and Yoshimasa Takeda and T. Danura and Kass, {I. S.} and K. Morita",
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T1 - Effect of lidocaine on dynamic changes in cortical reduced nicotinamide adenine dinucleotide fluorescence during transient focal cerebral ischemia in rats

AU - Naito, Hiromichi

AU - Takeda, Yoshimasa

AU - Danura, T.

AU - Kass, I. S.

AU - Morita, K.

PY - 2013/4/3

Y1 - 2013/4/3

N2 - Rats were subjected to 90. min of focal ischemia by occluding the left middle cerebral and both common carotid arteries. The dynamic changes in the formation of brain ischemic areas were analyzed by measuring the direct current (DC) potential and reduced nicotinamide adenine dinucleotide (NADH) fluorescence with ultraviolet irradiation. In the lidocaine group (n= 10), 30. min before ischemia, an intravenous bolus (1.5. mg/kg) of lidocaine was administered, followed by a continuous infusion (2. mg/kg/h) for 150. min. In the control group (n= 10), an equivalent amount of saline was administered. Following the initiation of ischemia, an area of high-intensity NADH fluorescence rapidly developed in the middle cerebral artery territory in both groups and the DC potential in this area showed ischemic depolarization. An increase in NADH fluorescence closely correlated with the DC depolarization. The blood flow in the marginal zone of both groups showed a similar decrease. Five minutes after the onset of ischemia, the area of high-intensity NADH fluorescence was significantly smaller in the lidocaine group (67% of the control; P= 0.01). This was likely due to the suppression of ischemic depolarization by blockage of voltage-dependent sodium channels with lidocaine. Although lidocaine administration did not attenuate the number of peri-infarct depolarizations during ischemia, the high-intensity area and infarct volume were significantly smaller in the lidocaine group both at the end of ischemia (78% of the control; P= 0.046) and 24. h later (P= 0.02). A logistic regression analysis demonstrated a relationship between the duration of ischemic depolarization and histologic damage and revealed that lidocaine administration did not attenuate neuronal damage when the duration of depolarization was identical. These findings indicate that the mechanism by which lidocaine decreases infarct volume is primarily through a reduction of the brain area undergoing NADH fluorescence increases which closely correlates with depolarization.

AB - Rats were subjected to 90. min of focal ischemia by occluding the left middle cerebral and both common carotid arteries. The dynamic changes in the formation of brain ischemic areas were analyzed by measuring the direct current (DC) potential and reduced nicotinamide adenine dinucleotide (NADH) fluorescence with ultraviolet irradiation. In the lidocaine group (n= 10), 30. min before ischemia, an intravenous bolus (1.5. mg/kg) of lidocaine was administered, followed by a continuous infusion (2. mg/kg/h) for 150. min. In the control group (n= 10), an equivalent amount of saline was administered. Following the initiation of ischemia, an area of high-intensity NADH fluorescence rapidly developed in the middle cerebral artery territory in both groups and the DC potential in this area showed ischemic depolarization. An increase in NADH fluorescence closely correlated with the DC depolarization. The blood flow in the marginal zone of both groups showed a similar decrease. Five minutes after the onset of ischemia, the area of high-intensity NADH fluorescence was significantly smaller in the lidocaine group (67% of the control; P= 0.01). This was likely due to the suppression of ischemic depolarization by blockage of voltage-dependent sodium channels with lidocaine. Although lidocaine administration did not attenuate the number of peri-infarct depolarizations during ischemia, the high-intensity area and infarct volume were significantly smaller in the lidocaine group both at the end of ischemia (78% of the control; P= 0.046) and 24. h later (P= 0.02). A logistic regression analysis demonstrated a relationship between the duration of ischemic depolarization and histologic damage and revealed that lidocaine administration did not attenuate neuronal damage when the duration of depolarization was identical. These findings indicate that the mechanism by which lidocaine decreases infarct volume is primarily through a reduction of the brain area undergoing NADH fluorescence increases which closely correlates with depolarization.

KW - DC potential

KW - Depolarization

KW - Hypoxia

KW - Infarction

KW - Lidocaine

KW - NADH fluorescence

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