David J. Goode

Effect of incubation in human plasma on electrophoretic mobility of brain-type creatine phosphokinase.

1. Electrophoretic mobility of brain-type creatine phosphokinase (CPK) from rabbit, rat and human decreased after incubation in human plasma for 3 h or 17 h but did not change after incubation in isotonic saline solution. The presence of the reducing agent mercaptoethanol during incubation in human plasma tended to reduce the rate of change of electrophoretic mobility of BB-CPK. 2. The activity of brain CPK was almost completely lost after incubation for 17 h in human plasma. The addition of mercaptoethanol after incubation of brain CPK in human plasma could only partially restore the enzyme activity. 3. The decrease in electrophoretic mobility of rat brain CPK occurred after incubation in an ultra-filtrate of human plasma which contained molecules whose molecular weight did not exceed 1000. 4. Gel chromatography indicated that incubation of brain CPK in human plasma did not markedly change the molecular size of the enzyme.

Descriptive studies of H-reflex recovery curves in psychiatric patients

The rate of recovery of the H-reflex, an electrical evoked monosynaptic spinal cord reflex, was abnormally high (fast) in over 20% of unmedicated psychotic patients of all major diagnostic classes. A few patients had significantly lower H-reflex recovery curves. Chronic neuroleptic treatment produced relatively lower recovery curves, whereas fluoxetine, a specific serotonin uptake blocker, produced relatively higher curves.

The role of isometric muscle tension in the production of muscle toxicity by phencyclidine and restraint stress.

A restraint cage with a strain gauge attached to a movable roof to record the isometric force exerted by rats during restraint is described. The isometric activity score, an integral of the total upward force exerted during restraint, correlated significantly with plasma creatine phosphokinase (CPK) activity in rats following restraint. Phencyclidine 5 mg/kg administered intraperitoneally to rats 15 min prior to 1/2 hr restraint has been shown to produce muscle damage associated with large increases of plasma CPK activity. Dose-response curves for the effects of phencyclidine on isometric activity score and plasma CPK activity were essentially parallel, and isometric activity scores were linearly related to plasma CPK activity. Rats restrained and painfully stimulated on the tail developed both elevated isometric activity scores and elevations of plasma CPK activity. Slopes of the curves relating isometric activity to plasma CPK activity were identical for painfully stimulated and phencyclidine treated rats. Phencyclidine has been reported to produce large increases in locomotor activity in unrestrained rats without muscle damage or elevated plasma CPK activity. Thus, increased isometric muscle tension developed during phencyclidine plus restraint is related to the production of muscle damage and increased efflux of CPK in rats.

Cytotoxic effects of imipramine on platelets

Abstract Incubation for 30 min at 30° with 1 mM imipramine, chlorpromazine or phencyclidine produced increases in creatine phosphokinase (CPK) activity of rat platelet-rich plasma (PRP). Increases in lactic dehydrogenase (LDH) activity of human PRP were produced by imipramine at 0.5 mM. Ouabain, diphenylhydantoin, calcium chloride, EDTA and thrombin did not affect CPK activity of rat PRP. None of the dugs tested except 10 mM diphenylhydantoin affected CPK or LDH activity in platelet-poor plasma. Increases in enzyme activity of PRP produced by 1 mM imipramine were associated with a decrease in platelet count. The increases were independent of temperature of incubation from 0° to 30° and were maximal after a 5-min incubation. The release of LDH and CPK caused by the above drugs is not related to platelet aggregation or the platelet release reaction. The increases in LDH and CPK activity in PRP appear to be the result of platelet destruction or damage to the platelet plasma membrane with release of these enzymes.