Lidocaine reduces the hypoxia-induced release of an excitatory amino acid analog from rat striatal slices in superfusion

Díaz, L L María; Gómez, Ariel; Bustos, Gonzalo

doi:10.1016/0278-5846(95)00122-c

Cited by 7 publications

(3 citation statements)

References 47 publications

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“…23 With more conventional dosing of lidocaine (0.2 mg/kg/min) administered to rabbits undergoing global ischemia, anoxic depolarization was again delayed. 24 As a consequence, secondary neurotoxic events such as intracellular edema, 25 cytosolic calcium accumulation, 26 and glutamate 27 and aspartate 28 release are attenuated.…”

Section: Discussionmentioning

confidence: 99%

Randomized, Double-Blinded, Placebo Controlled Study of Neuroprotection With Lidocaine in Cardiac Surgery

Mathew

Mackensen

Phillips-Bute

et al. 2009

Stroke

141

128

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Background and Purpose Cognitive decline after cardiac surgery remains common and diminishes patients’ quality of life. Based on experimental and clinical evidence, this study assessed the potential of intravenously administered lidocaine to reduce postoperative cognitive dysfunction following cardiac surgery employing cardiopulmonary bypass. Methods Following IRB approval, 277 patients undergoing cardiac surgery were enrolled into this prospective, randomized, double-blinded placebo controlled clinical trial. Subjects were randomized to receive: 1) Lidocaine as a 1 mg/kg bolus followed by a continuous infusion through 48 hours postoperatively or 2) Placebo bolus and infusion. Cognitive function was assessed preoperatively and again at 6 weeks and 1 year postoperatively. The effect of lidocaine on postoperative cognition was tested using multivariable regression modeling; p <0.05 was considered significant. Results Among the 241 allocated subjects (Lidocaine: N=114; Placebo: N=127), the incidence of cognitive deficit in the lidocaine group was 45.5% versus 45.7% in the placebo group (p=0.97). Multivariable analysis revealed a significant interaction between treatment group and diabetes, such that diabetic subjects receiving lidocaine were more likely to suffer cognitive decline (p=0.004). Secondary analysis identified total lidocaine dose (mg/kg) as a significant predictor of cognitive decline and also revealed a protective effect of lower dose lidocaine in nondiabetic subjects. Conclusions Lidocaine administered during and after cardiac surgery does not reduce the high rate of postoperative cognitive dysfunction. Higher doses of lidocaine and diabetic status were independent predictors of cognitive decline. Protective effects of lower dose lidocaine in nondiabetic subjects need to be further evaluated.

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Section: Discussionmentioning

confidence: 99%

Randomized, Double-Blinded, Placebo Controlled Study of Neuroprotection With Lidocaine in Cardiac Surgery

Mathew

Mackensen

Phillips-Bute

et al. 2009

Stroke

141

128

View full text Add to dashboard Cite

show abstract

“…Neuroprotective mechanisms of lidocaine have been postulated to include one or more of the following pharmacologic effects of this drug: (1) deceleration of ischemic transmembrane ion shifts and inhibition of anoxic depolarization, 3,20 (2) reduction in cerebral metabolic rate, 21 (3) reduction in the release of excitatory amino acids, [22][23][24] (4) modulation of leukocyte activity, 25 (5) increase in cerebral blood flow, 15,16 (6) scavenging of oxygen free radicals, 26 or (7) reduction in the intracranial pressure. 27 However, the exact mechanism for the neuroprotective effect of lidocaine, especially low- dose lidocaine, is not known.…”

Section: Discussionmentioning

confidence: 99%

“…[32][33][34][35] It is possible that low-dose lidocaine may increase the tolerance of cells in the ischemic penumbra to repetitive depolarizations by attenuating ATP depletion. 3 In addition, lidocaine may also reduce periinfarct depolarizations by blocking Na influx 3 or inhibiting the release of glutamate [22][23][24] ; this may limit the expansion of the infarction.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effect of Low-dose Lidocaine in a Rat Model of Transient Focal Cerebral Ischemia

Lei¹,

Cottrell²,

Kass³

2001

Anesthesiology

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Regionally infused lidocaine can dose-dependently protect the ischemic spinal cord in rabbits and may be associated with the EAA changes

Liu

Zhou

et al. 2020

Neuroscience Letters

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Lidocaine reduces the hypoxia-induced release of an excitatory amino acid analog from rat striatal slices in superfusion

Cited by 7 publications

References 47 publications

Randomized, Double-Blinded, Placebo Controlled Study of Neuroprotection With Lidocaine in Cardiac Surgery

Randomized, Double-Blinded, Placebo Controlled Study of Neuroprotection With Lidocaine in Cardiac Surgery

Neuroprotective Effect of Low-dose Lidocaine in a Rat Model of Transient Focal Cerebral Ischemia

Regionally infused lidocaine can dose-dependently protect the ischemic spinal cord in rabbits and may be associated with the EAA changes

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