PubMed · 4075218
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B A Britt. 1985. Malignant hyperthermia.. https://doi.org/10.1007/bf03011418
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A method for in vivo evaluation of lipid peroxidation in the extracellular space of anaesthetized rat brain cortex was developed. This method involved the use of microdialysis perfusion and high-performance liquid chromatography. The microdialysates, eluted from implanted probes, were reacted with thiobarbituric acid (TBA) prior to analysis by an HPLC system equipped with a fluorescence detector (excitation and emission wavelengths were 515 and 550 nm, respectively). Lipid peroxidation in the extracellular space was evaluated as the concentration of malondialdehyde, a lipid peroxidation end product which reacts with TBA to form a fluorescent conjugate. Significantly increased production of malondialdehyde following hydrogen peroxide perfusion (0.03%, 0.3% at a flow-rate of 1 microl/min) was observed in the brain cortex of anaesthetized rats.
To test the hypothesis that during augmented breaths the prolonged expiratory time is correlated with the activity of medullary post-inspiratory neurons, changes in diaphragm electromyogram and post-inspiratory neuronal activities were examined in pentobarbital anesthetized rats. During augmented breaths, the mean total expiratory time significantly increased (from 0.57 +/- 0.02 to 1.20 +/- 0.07 s, P < 0.01), but the mean duration of post-inspiratory inspiratory activity (PIIA) was significantly decreased (from 0.08 +/- 0.01 to 0.02 +/- 0.003 s, P < 0.01) compared to control breaths. The mean time which the diaphragm was electrically silent was observed to be significantly prolonged during augmented breaths (from 0.48 +/- 0.02 to 1.19 +/- 0.07 s, P < 0.01). During significant prolongations of expiratory time in augmented breaths, most of the recorded neurons (9/10) in the medulla showed sustained discharges. The mean duration of discharges was longer than that of PIIA (0.02 +/- 0.003 vs. 0.50 +/- 0.10 s, P < 0.01). The mean firing frequency/breath significantly increased compared to control breaths (9.45 +/- 1.69 vs. 37.6 +/- 7.13 imp/breath, P < 0.01). These results suggested that during augmented breaths, the prolonged expiratory period may not be mediated by persisting post-inspiratory neuronal activity in the medulla.
2-Aroyl-4-(omega-aminoacyl)- (4) and 4-aroyl-2-(omega-aminoacyl)pyrroles (9) represent a new, structurally novel class of anticonvulsant agents. Compounds of type 4 were prepared by Friedel-Crafts acylation of a 2-aroylpyrrole with an omega-chloroacyl chloride followed by displacement of the chloro group by a primary or secondary amine. Compounds of type 9 were prepared by Friedel-Crafts aroylation of a 2-(omega-chloroacyl)pyrrole followed by displacement by an amine. These compounds were active in the mouse and rat maximal electroshock tests but not in the mouse metrazole test. The lead compound, RWJ-37868, 2-(4-chlorobenzoyl)-4-(1-piperidinyl-acetyl)-1,3,5-trimethylpyrrole++ + (4d), showed potency and therapeutic index comparable to those of phenytoin and carbamazepine and greater than those of sodium valproate. This compound blocked bicuculline induced seizures, did not elevate seizure threshold following iv infusion of metrazole, and blocked influx of Ca2+ ions into cerebellar granule cells induced by K+ or veratridine.