Lidocaine accelerates neuroelectrical recovery after incomplete global ischemia in rabbits.

Abstract

The use of high-dose lidocaine for cerebral protection during ischemia has produced varied results. Our study uses a new, single carotid artery preparation in the rabbit to produce incomplete global ischemia by graded carotid occlusion; specific electroencephalographic changes are used as the end point for the extent of blood flow reduction sustained during 20 minutes. We monitored arterial pressure, intracranial pressure, and internal carotid blood flow that were recorded with an electromagnetic flowmeter after surgical ligation of the opposite internal and the two vertebral arteries, and we studied the electroencephalogram and somatosensory-evoked potentials elicited by stimulation of the sciatic nerve. Low-dose lidocaine (0.2 mg/kg/min) infused throughout the experiment significantly accelerated the time course of the return of electroencephalographic and evoked-potential amplitudes toward control. Deep halothane anesthesia alone elicited the slowest recovery, suggesting that the action of lidocaine was independent of its general anesthetic effect There were very small differences among the groups in the measured arterial pressure, intracranial pressure, and cerebral blood flow, suggesting that lidocaine changed recovery rate without markedly modifying any characteristic of the postischemic cerebral perfusion. The protective effect of lidocaine may be the result of a specific blockade of Na + channels or a decrease in excitatory neurotransmitter release, either of which would cause a delay in the onset of the events that lead to neuronal damage during ischemia. (Stroke 1990;21:929-935)

Effect of lidocaine on somatosensory evoked response and cerebral blood flow after canine cerebral air embolism.

“…30 This dose is close to that causing increased metabolism in hippocampal neurons. 22 Pretreatment with 5 mg/kg lidocaine led to preservation of electrocortical activity after global ischemia in rabbits 31 and some reduction in hippocampal neuron loss after forebrain ischemia in rats. 32 It appears that lidocaine may reduce ischemic damage at the lower doses used for cardiac arrhythmias and that this beneficial effect is lost at higher doses associated with preepileptogenic or burst-suppression EEG patterns, perhaps because the increased metabolic demand of neurons generating the EEG activation decreases their resistance to ischemia.…”

Neuroprotective properties of lifarizine compared with those of other agents in a mouse model of focal cerebral ischaemia

“…More recently, Vornov et al (1994) described a protective affect of TTX against histologically-assessed damage produced by metabolic inhibition in organotypic hippocampal slice cultures. Systemically-administered lignocaine has been shown to limit infarct size in a cat middle cerebral artery occlusion model (Shokunbi et al, 1990) and to promote the recovery of electrical activity in a rabbit model of incomplete global ischaemia (Rasool et al, 1990). It is interesting to note that the non-selective sodium and calcium channel blocker, flunarizine, displays a similar profile to phenytoin in models of hypoxia in vitro (Ashton et al, 1990;Pauwels et al, 1991) and has a similar anticonvulsant profile in vivo (Binnie, 1988).…”

Brain pHi, cerebral blood flow, and NADH fluorescence during severe incomplete global ischemia in rabbits.

“…In the former we observed hypoperfusion to be established at approximately 30 [40][41][42][43] The faster the development of hypoperfusion with concomitant reduction in glucose and oxygen delivery, the greater the ischemic stress placed on the recovering brain. This postulate is supported by the increase in NADH fluorescence following the development of hypoperfusion that presumably was due to a decrease in tissue 02 availability.…”

“…There was a heterogeneous pattern of fluorescence that increased significantly following 60 minutes of reperfusion, coinciding with a postischemic hypoperfusion. The hypoperfusion was a uniform reduction in cerebral blood flow over the brain's surface, with reductions of 42.5% and 44.2% at 30 and 45 minutes, respectively.…”