The Effect of Intravenous or Subarachnoid Lidocaine on Glutamate Accumulation During Transient Forebrain Ischemia in Rats

Terada, Hiromichi; Ohta, Sukejuro; Nishikawa, Toshiaki; Mizunuma, Takahide; Iwasaki, Yoichi; Masaki, Yoko

doi:10.1097/00000539-199910000-00025

Cited by 10 publications

(17 citation statements)

References 13 publications

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“…These reported ionic and membrane events could be the explanation to the strong increase in the time constant for voltage decay induced by lidocaine. The fact that lidocaine did not change brain impedance under normal normoxic conditions but did so during ischemia reducing the progression of edema, detected by its most important sign, change in tissue impedance [18][19][20][21] , strongly supports the notion of the neuroprotective effect of lidocaine, which agrees with other reported brain-protective actions of lidocaine in experimental [28][29][30] , neuropathological [26,31] and clinical studies [32,33] .…”

Section: Discussionsupporting

confidence: 81%

“…This mechanism may in turn activate intracellular signaling cascades that lead to altered expression of protective genes [34] . Activation of NMDA channels, mitochondrial Na + /Ca 2+ cotransporters and synaptic glutamate liberation [4,28,29,31] are processes strongly associated with the early formation of cytotoxic edema [17,20] and when blocked or reduced by lidocaine could explain results reported in the present report.…”

Section: Discussionsupporting

confidence: 52%

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Time Course of Acute Neuroprotective Effects of Lidocaine Evaluated by Brain Impedanciometry in the Global Ischemia Model

Wix-Ramos¹,

Eblén-Zajjur²

2011

Pharmacology

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Voltage-activated sodium channels play a primary role during ischemic brain edema and thus are a pharmacological target for therapy. Lidocaine, a sodium channel blocker, was tested in male Sprague-Dawley rats anesthetized with thiobarbital (60 mg·kg^–1 i.p.) and perfused i.v. with Ringer’s solution (n = 9) or lidocaine (0.75 mg·kg^–1, n = 9, or 1.5 mg·kg^–1, n = 6). Two tungsten microelectrodes were implanted in the cerebral cortex to register changes in tissue impedance in response to the voltage fall of a square wave electric pulse (100 µA, 10 ms), before and after infusion of lidocaine or Ringer’s solution and during global cerebral ischemia due to a respiratory arrest induced by D-tubocurarine. Lidocaine infusion under normoxic conditions did not change voltage values (Mann-Whitney U = 51; p > 0.05). In animals infused with Ringer’s solution, the voltage fall induced by global cerebral ischemia was fast for ∼8 min at –8.0 ± 2.3%·min^–1 followed by a slow decay at –0.96 ± 0.17%·min^–1. The time constant of voltage decay (λ) was 215.6 s (F = 547.4; p = 0.00000). Voltage values of lidocaine-infused animals were significantly higher than those of rats infused with Ringer’s solution (U = 100; p = 0.000089). The decay rates were –4.97 ± 1.36%·min^–1 (fast phase) and –1.04 ± 0.3%·min^–1 (slow phase) with λ = 672.5 s (+211.9%; p = 0.000000). These results suggest that lidocaine significantly reduced cerebral impedance, hence exerting a strong early anti-edema effect probably by blocking voltage-activated sodium channels.

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Section: Discussionsupporting

confidence: 81%

Section: Discussionsupporting

confidence: 52%

Time Course of Acute Neuroprotective Effects of Lidocaine Evaluated by Brain Impedanciometry in the Global Ischemia Model

Wix-Ramos¹,

Eblén-Zajjur²

2011

Pharmacology

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“…Mechanisms of action of intravenous (IV) lidocaine include the suppression of autonomic reflexes, a neuronal membrane stabilizing effect and inhibition of the release of excitatory neuroamines, particularly glutamate (Terada et al. ). In humans, IV lidocaine administration prior to intubation has been shown to reduce the pressor response (Wilson et al.…”

Section: Introductionmentioning

confidence: 99%

Effects of intravenous and topical laryngeal lidocaine on heart rate, mean arterial pressure and cough response to endotracheal intubation in dogs

Thompson

Rioja

2016

Veterinary Anaesthesia and Analgesia

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“…In the penumbra, PIDs are thought to be generated by glutamate and potassium released from the ischemic core (Mies et al, 1994;Dirnagl et al, 1999). Previous studies have reported that administration of lidocaine did not suppress glutamate release at doses < 5 mg/kg (Terada et al, 1999). Since the lidocaine was infused at the rate of 2 mg/kg/h (total dose: 5 mg/kg in 150 min) in this study, glutamate release was not likely to be suppressed.…”

Section: Discussionmentioning

confidence: 63%

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

et al. 2013

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Rats were subjected to 90 min of focal ischemia by occluding the left middle cerebral and both common carotid arteries. The dynamic changes in formation of brain ischemic areas were analyzed by measuring the direct current (DC) potential and 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 amounts 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 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 the ischemia, the 4 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.

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The Effect of Intravenous or Subarachnoid Lidocaine on Glutamate Accumulation During Transient Forebrain Ischemia in Rats

Cited by 10 publications

References 13 publications

Time Course of Acute Neuroprotective Effects of Lidocaine Evaluated by Brain Impedanciometry in the Global Ischemia Model

Time Course of Acute Neuroprotective Effects of Lidocaine Evaluated by Brain Impedanciometry in the Global Ischemia Model

Effects of intravenous and topical laryngeal lidocaine on heart rate, mean arterial pressure and cough response to endotracheal intubation in dogs

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

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