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

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

“…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.…”

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

“…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.…”

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

“…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.…”

“…[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.…”

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

“…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.…”

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

“…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.…”

“…[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.…”

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

“…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.…”

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

“…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.…”

“…[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.…”