Summary.
A slight modification of the Hardy‐Wolff‐Goodell method for measuring pain threshold on man is described.
Eserine raises the pain threshold.
Prostigmine raises the pain threshold.
Prostigmine greatly potentiates and prolongs the analgetic action of morphine.
An experimental procedure has been elaborated to facilitate selective effects exerted by agents applied within the cerebral vessels on EEG and blood‐brain barrier phenomena. In rabbits short‐term (less than 1 minute) perfusion of one hemisphere is performed via the ipsilateral internal carotid artery with a pressure adjusted so as to obtain displacement of the blood. This displacement is controlled by inspection of the pial vessels through a trephine opening. The technique implies control of the active concentration in loco of the applied agents and of the application time, hence graded influences near the threshold levels can be obtained.
Structural and metabolic considerations make it conceivable that low grade damage of the blood‐brain barrier may be produced with no significant effect on the neuronal activity as reflected in EEG (except for the brief influence from the blood deprivation). After such damage intravenous administration of suitable substances, unable to pass the intact barrier, may give rise to unilateral EEG changes and thus reveal the defective barrier function. Two model experiments are reported. The first one shows that unilateral blood deprivation per se (for about 2 min) exerts a marked but reversible effect on the EEG without damage to the blood‐brain barrier as tested by intravenously injected trypan blue. The second experiment illustrates an attempt to induce barrier damage without significant changes in the EEG.
FLODMARK, S. and 0. STEINM'XLL. Rewrsible blood-brain barrier alteration induced by certain organic acids and indicated by means of EEG and dq'e tests. Acta physiol. scand. 1963. 58. 368-375. -With an earlier described method for studies of the interrelation between EEG and blood-brain barrier functions, alteration of the barrier was induced by intracarotidal application of certain types of organic acids (represented by penicillin G and Urokon). In long-term experiments it could be established that this type of barrier alteration was reversible as judged by intravital dye tests and further by EEG-activating tests, applied in the early and late phases of the experiments. The EEG changes evoked by the invasion of normally barred organic acids into the barrier-damaged hemisphere were of an excitatory type and sometimes caused a convulsion pattern lasting for hours. Even aftcr such a heavy stress on the neurons, however, there was areversal in thc EEG, sometimes to full normalization. 'The EEG course after this reversible barrier alteration is different from that seen after the prrsistcnt barrier dysfunction induced by mercuric ions as reported in a previous paper. The reversible action of the organic acids on the barrier is discussed as being compatible with the hypothesis, previously proposed by Steinwall, that brain-blood dirccted transport mechanisms participate in the barring of this group of acid compounds.As p a r t of a study on the relationship between blood-brain barrier functions and IiEG we recently investigated the influences on the EEG after a persistent harrier injury induced by a heavy metal (mercuric dichloride), lvhich was applied within the vessels of one hemisphere under careful dosage control (FLOD-
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