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

Dutka, A. J.; Mink, Richard; McDermott, James J.; Clark, JM; Hallenbeck, John M.

doi:10.1161/01.str.23.10.1515

Cited by 40 publications

(17 citation statements)

References 38 publications

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“…Lidocaine was shown to enhance CBF when compared to the baseline information. The degree (24%) of increase in CBF at around 2 min after lidocaine administration agrees with known information [11].…”

Section: Discussionsupporting

confidence: 86%

Influence of intravenously administered lidocaine on cerebral blood flow in a baboon model standardized under controlled general anaesthesia using single-photon emission tomography and technetium-99m hexamethylpropylene amine oxime

et al. 1993

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The baboon under general anaesthesia as a model to assess drug-induced cerebral blood flow changes (delta CBF) using single-photon emission tomography (SPET) offers great in vivo possibilities but has to comply with demands on control of anaesthesia-related influencing factors, such as PaCO2 changes. The model sought in this study and described here allows control of PaCO2, in the baboon under thiopentone anaesthesia by ventilation, and was evaluated for the functional dependence of delta CBF vs delta PaCO2, using SPET technetium-99m hexamethylpropylene amine oxime (HMPAO) and the split-dose method together with controlled ventilation. During the experiment the model was validated for normal reactivity to PaCO2 changes, and subsequently applied to investigate the mechanisms (still uncertain) of CBF increase known to follow administration of the local anaesthetic lidocaine. Six baboons received 6 mg/kg lidocaine intravenously. CBF was measured between two consecutive SPET acquisitions (split-dose method) respectively relating to HM-PAO distributions in the brain before and after the injection of lidocaine. Meanwhile the animals were maintained at constant respiratory rate and volume. The results indicate that the correlation between delta CBF and the ensuing fall in PaCO2 deviated from the baseline pattern from the model and confirmed a cerebrovascular contribution to the lidocaine-induced CBF increase. This agreed well with mean and systolic blood pressure changes and heart rate.

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Section: Discussionsupporting

confidence: 86%

Influence of intravenously administered lidocaine on cerebral blood flow in a baboon model standardized under controlled general anaesthesia using single-photon emission tomography and technetium-99m hexamethylpropylene amine oxime

et al. 1993

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“…However, the weight of clinical evidence and more than 70 years of experience support the treatment of arterial air embolism with combined pressure and oxygen. An interesting study by Dutka et al [35] in an animal model of cerebral gas embolism indicates that lidocaine may improve cerebral blood flow after an embolic insult. Combined hyperbaric oxygen therapy and intravenous lidocaine provided a greater improvement of cortical evoked response and cerebral blood flow than did saline in the control group.…”

Section: Pulmonary Barotrauma and Air Embolismmentioning

confidence: 99%

Medical Disorders Related to Diving

Bové

2002

J Intensive Care Med

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Exposure to the underwater environment is associated with several unique disorders that may require recompression in a hyperbaric chamber. Increasing pressure during descent reduces the volume of the paranasal sinuses and middle ear, which, if not properly equalized, will sustain injury due to barotrauma. Barotrauma of the inner ear results in vertigo, tinnitus, and often permanent hearing loss. During ascent, expanding gas can produce lung injury accompanied by pneumothorax, mediastinal and subcutaneous emphysema, injection of air into the pulmonary veins, and arterial air embolism to the brain. Divers with pulmonary barotrauma often present with unconsciousness, seizures, or other evidence of cerebral dysfunction. Rapid treatment with recompression often reverses the cerebral deficits. Air embolism lesions are usually diffuse, in contradistinction to a stroke which usually follows the distribution of a single cerebral artery. Decompression sickness is a disorder caused by evolution of supersaturated dissolved gas in tissues and blood following exposure to increased pressure. Protocols for avoiding excess supersaturation during ascent from depth have been available for more than 100 years, and diving is considered safe when established decompression schedules are followed. Decompression sickness causes pain in the joints of the upper and lower extremities, and can injure the spinal cord. Paralysis, paresthesias, sensory loss, and bowel and bladder paralysis accompany spinal cord injury. Treatment involves recompression and oxygen. Platelet inhibitors and other anti-inflammatory drugs are also useful. A diving disorder must be considered in any patient with a neurologic syndrome, vertigo, hearing loss, or joint pain following diving.

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“…24 In cerebral air embolism animal models, prophylactic administration of lidocaine reduced depressant effects of gas embolism on somatosensory evoked potentials and attenuated the increase in intracranial pressure. 25 In conclusion, symptomatic VAE is a rare complication of pars-plana vitrectomy and air-fluid exchange, although the exact incidence of air entrainment is not known. Nevertheless, it should be considered in the differential diagnosis of a patient who experiences an abrupt decrease of EtCO 2 , arterial desaturation, arrhythmias or hemodynamic instability.…”

mentioning

confidence: 90%