The isolation of edema fluid from cats with cold-induced cerebral edema allowed the study of changes of Na+ and K+ content, lactate dehydrogenase and creatine phosphokinase activity, colloid osmotic pressure and the level of intravenously administered 99mTc-albumin in the edema fluid during a period of hypoxia. The changes consisted of an increase of all mentioned parameters, except Na+; and could be interpreted as a concentration of solutes (but for Na+) in the extracellular edema fluid, concomitant to a reduction of the extracellular space, as the oxygen deficiency caused improper functioning of the cellular Na+-K+ pump, with a resulting shift of fluid (including Na+) into the cellular elements.
SynopsisA slow, continuous infusion of 1000μg TRH (thyrotropin releasing hormone) over a period of 4 h had a very faint and diffuse short-lasting beneficial effect on a group of 10 depressive patients. This was assessed in a double blind cross-over trial with placebo. The effect was of no therapeutic value. No difference was found between the depressive patients and a control group of normal subjects in TSH response, T3resin uptake, T4or free thyroxine index values as a consequence of the TRH infusion.
The net contribution of vasogenic brain edema to cerebrospinal fluid (CSF) formation was studied by ventriculocisternal perfusion. Individual cats were perfused both before and 2 1/2 hours after a severe cold-induced injury to the cerebral cortex, and the results were compared. Although the edema had occupied the larger part of the hemispheric white matter and bordered the lateral ventricle, a decrease rather than an increase in CSF formation rate was observed. This decrease was related to a decrease in the cerebral perfusion pressure by a regression equation that was not affected by the cold injury.
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