Effect of lidocaine after experimental cerebral ischemia induced by air embolism

Evans, Delbert E.; Catron, Philip W.; McDermott, James J.; Thomas, Linda B.; Kobrine, Arthur I.; Flynn, ET

doi:10.3171/jns.1989.70.1.0097

Cited by 52 publications

(17 citation statements)

References 32 publications

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“…10 " 12 The first of these studies administered lidocaine before air embolism, 10 the second demonstrated improved recovery with therapeutic administration but without concurrent hyperbaric treatment, 11 and in the third lidocaine was no better than hyperbaric treatment alone. 12 Late deterioration was rare in the animals in these studies, and no indicators of recovery other than SSEP were studied.…”

Section: See Editorial Comment P 1520mentioning

confidence: 99%

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

Dutka

Mink

McDermott

et al. 1992

Stroke

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Background and Purpose: Victims of air embolism often recover rapidly on hyperbaric treatment then deteriorate again, even if hyperbaric treatment is continued. In previous animal experiments, lidocaine has been shown to improve recovery of somatosensory evoked response amplitude after air embolism. However, animals in these experiments rarely deteriorated. We have shown that the induction of air embolism and transient hypertension in canines produces deterioration despite hyperbaric treatment, and we decided to test the effect of lidocaine on somatosensory evoked potential recovery and cerebral blood flow in this model.Methods: Dogs were treated with repeated doses of lidocaine or equivalent volumes of saline during hyperbaric therapy after internal carotid air embolism and transient hypertension. The investigators were unaware of treatment group assignment during the experiments. The amplitude of the median nerve somatosensory evoked potential and cerebral blood flow measured with carbon-14-labeled iodoantipyrine autoradiography were used to assess effect of therapy.Results: Lidocaine-treated dogs recovered 60±10% (mean±95% confidence limits) of the baseline somatosensory evoked potential amplitude 220 minutes after air embolism; saline-treated dogs recovered 32±10% (a significant difference atp<0.01). Lidocaine-treated dogs also had higher cerebral blood flow values than saline-treated dogs 220 minutes after air embolism.Conclusions: Lidocaine ameliorated the delayed deterioration of evoked potential associated with air embolism and hypertension in this canine model. The improved cerebral blood flow may be a mechanism of action of lidocaine or an associated effect of improved neuronal survival. (Stroke 1992;23:1515-1521 KEY WORDS • cerebral blood flow • embolism • evoked potentials, somatosensory • lidocaine • dogs

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Section: See Editorial Comment P 1520mentioning

confidence: 99%

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

Dutka

Mink

McDermott

et al. 1992

Stroke

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“…We believe this to be caused by the random distribution of the air bubbles through the cerebral vasculature. Our strategy using titrated embolization was based on the work of other researchers who demonstrated reproducible injury by titrating embolization based on EEG or somatosensory evoked potentials (14,16,(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34).…”

Section: Discussionmentioning

confidence: 99%

Hyperbaric Oxygen Does Not Improve Cerebral Function When Started 2 or 4 Hours After Cerebral Arterial Gas Embolism in Swine*

Weenink¹,

Hollmann

Vrijdag

et al. 2013

Critical Care Medicine

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We did not observe an effect of hyperbaric oxygenation on cerebral function after a delay of 2 or 4 hours. The injury caused in our model could be too severe for a single session of hyperbaric oxygenation to be effective. Our study should not change current hyperbaric oxygenation strategies for cerebral arterial gas embolism, but further research is necessary to elucidate our results. Whether less severe injury benefits from hyperbaric oxygenation should be investigated in models using smaller amounts of air and clinical outcome measures.

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“…The host response to these cytokines may include diffuse endovascular injury, microvascular thrombosis, organ ischemia, multiorgan dysfunction, and death. Animal studies suggest that agents such as heparin [10] and lidocaine [15] attenuate the thrombo-inflammatory response of the endothelium to luminal air.…”

Section: Discussionmentioning

confidence: 99%

Untitled

Kapoor

Gutiérrez

2003

Crit Care

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Effect of lidocaine after experimental cerebral ischemia induced by air embolism

Cited by 52 publications

References 32 publications

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

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

Hyperbaric Oxygen Does Not Improve Cerebral Function When Started 2 or 4 Hours After Cerebral Arterial Gas Embolism in Swine*

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