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Biomedical subjects

M W Kalichman

Publications and source records attributed to M W Kalichman.

40 records · Page 3Linked to original sources
PubMedDate not supplied

Differential antiepileptic sensitivity between cortical sites in the rat.

The relative efficacies of phenobarbital (PB), phenytoin (PHT), carbamazepine (CBZ), and valproic acid (VPA) in the suppression of focal and generalized seizures produced by electrical stimulation of two different cortical sites (areas 3 and 10) were evaluated in the rat. The two cortical sites were distinguished by significantly different dose-response curve slopes for the suppression of afterdischarge duration by PHT, CBZ and VPA, which suggests more than one mechanism of action for these drugs. The dose-response curve slopes for PB, on the contrary, were not significantly different, although its potency was significantly greater in area 10. For suppression of generalized convulsions, dose-response curve slopes were not significantly different for any of the drugs. Potencies of PHT, CBZ and VPA were equivalent in the two areas, but PB was significantly more potent in the suppression of generalized convulsions triggered from area 10. It is concluded that focal seizures elicited by the stimulation of different cortical sites are differentially refractory to antiepileptic drugs.

Animals↗
PubMedDate not supplied

Physiologic mechanisms by which local anesthetics may cause injury to nerve and spinal cord.

OBJECTIVE: Review evidence for possible physiologic mechanisms by which local anesthetics cause nerve injury was reviewed. METHODS: Published clinical case reports, and both in vivo and in vitro experimental studies in animals, were reviewed. Reports with direct bearing on possible mechanisms of local anesthetic neurotoxicity were included. RESULTS: There is basic and clinical evidence that local anesthetics can cause nerve injury. Nerve injury may result from direct toxicity to the axon or Schwann cell, or may be secondary to disruption of the nerve microenvironment. Although each of these possibilities is supported by published experiments, injury to the axon is the most likely explanation for persistent neurologic deficits, such as those believed to result from clinical use of local anesthetics. Whether the injury is direct or indirect, and the precise mechanism by which it occurs, has received only limited study. CONCLUSIONS: In rare instances, the clinical use of local anesthetics is associated with neurologic morbidity. The physiologic mechanisms of toxicity for which there is the best evidence are inhibition of fast axonal transport, disruption of the axonal cytoskeleton, axonal degeneration, and ischemic nerve injury. The effects of local anesthetics on nerve blood flow may be related to inhibition of endothelium-dependent vasodilation or interruption of the synthesis of vasodilating prostaglandins. Both the prevention and the treatment of nerve injury caused by local anesthetics requires information that is not yet available about the physiologic and molecular mechanisms for direct neural toxicity of local anesthetics.

Anesthetics, Local↗