In vivo diffusion-weighted magnetic resonance microscopy of rat spinal cord: effect of ischemia and intrathecal hyperbaric 5% lidocaine.

Background And Objectives: Pathophysiologic mechanisms underlying persistent neurologic deficits after continuous spinal anesthesia using hyperbaric 5% lidocaine are still not well understood. It has been suggested that high-dose intrathecal lidocaine induces irreversible conduction block and even ischemia in white matter tracts by breakdown of the blood-nerve barrier. In this study, we use diffusion-weighted magnetic resonance microscopy to characterize the effect of intrathecal hyperbaric 5% lidocaine in rat spinal cord.

Extracellular glutamate and dopamine measured by microdialysis in the rat striatum during blockade of synaptic transmission in anesthetized and awake rats.

We investigated the effect of high dose tetrodotoxin (TTX) on microdialysis measurements of extracellular striatal glutamate and dopamine in normal female rats. Both halothane-anesthetized rats with acutely implanted microdialysis probes and awake rats with microdialysis probes implanted for 24 h were tested. Glutamate levels in awake rats were 45% higher than those of anesthetized rats.

Calcitonin gene-related peptide mediates hypotension and tachycardia in endotoxic rats.

Circulating calcitonin gene-related peptide (CGRP) concentrations are elevated in experimental and clinical sepsis. CGRP causes hypotension and tachycardia, suggesting that the peptide might mediate the acute circulatory changes in sepsis. To test this hypothesis we administered Escherichia coli endotoxin (8 mg/kg iv) to Nembutal- (pentobarbital sodium; 50 mg/kg) anesthetized rats.

Microdialysis measurements of PGD2, TXB2 and 6-KETO-PGF1 alpha in rat CA1 hippocampus during transient cerebral ischemia.

We measured hippocampal CA1 concentrations of PGD2, TxB2 and 6-keto-PGF1 alpha in 18 anesthetized rats with stereotaxically implanted microdialysis probes before, during and after 20 min of global cerebral ischemia. The insertion of the microdialysis probe did not appear to cause a continuous major disturbance of arachidonic acid (AA) metabolism because stable eicosanoid concentrations were obtained prior to ischemia. During reperfusion all three eicosanoids increased significantly reaching a peak after 30-60 min and then gradually declined to baseline levels over the next 2-3 h.