Increase in cutaneous temperature induced by hypnotic suggestion of pain.

Eight patients with atopic eczema and six healthy subjects were given hypnotic suggestion to feel pain in the upper part of the back and in one case on the palm. An average local increase in skin temperature of 0.6 degrees C (detected by thermovision) occurred under this condition. For some patients cutaneous pain threshold was increased before the experiment by means of repetitive hypnotic suggestion of analgesia. These subjects reported feeling no pain subjectively, but the local change in skin temperature was equal in both cases. The results suggest a central mechanism induced by measuring changes in pain threshold in the skin, which changes are independent of local changes in blood flow.

[Characterization of vertebrogenic pain using the short form of the McGill Pain Questionnaire]. / Charakterizace vertebrogenní bolesti zkrácenou formou dotazníku McGill Pain Questionnaire.

A Czech translation of the short form McGill Pain Questionnaire was tested in a group of patients suffering from pain of vertebrogenic origin. The results support the hypothesis that the questionnaire will be an asset in various disciplines of medical practice. While taking up little time it provides a comprehensive and valid picture of the quality and intensity of pain experienced by the patient. The results indicated that the questionnaire can differentiate between different syndromes of pain and is sensitive to the effect of placebo.

Gradual increase in cutaneous threshold induced by repeated hypnosis of healthy individuals and patients with atopic eczema.

Gradual increase in cutaneous pain threshold was found in healthy subjects and patients with atopic eczema during repeated hypnotic sessions with specific suggestions. This increase was less in the former than in the latter group. Repeated threshold measurements did not influence the threshold. The analgesic effect outlasted the hypnotic sessions by several months. It could be, however, suddenly reduced by appropriate hypnotic suggestion.

Analgesia and impact induced by anticipation stress: involvement of the endogenous opioid peptide system.

Anticipation of an unavoidable painful stimulation, i.e. anticipation stress, induces analgesia. This analgesia may result from activation of the endogenous opioid peptide system as it is blocked by naloxone. The present paper characterizes the anticipation stress further by following the kinetics of the analgesia rise, the impact of the stress on the stress-sensitive organs and the involvement of the endogenous opioid peptide system in the anticipation stress effects. Adult male rats exposed repeatedly to placing into a conditioning box followed by a painful stimulation develop analgesia almost immediately after a transfer to the box. Anticipation acts as a specific trigger, no other side stressor is effective. Anticipation stress has a significant impact on stress-sensitive organs: weights of the adrenals increase while those of the thymus and spleen decrease. These changes are associated with a significant increase of plasma corticosterone. Blockade of the endogenous opioid system by naloxone before the exposure to anticipation stress potentiates these stress-induced impacts, especially the decrease of weight of the thymus. Plasma corticosterone levels are not affected by naloxone. During the anticipation stress, the amount of opioid receptors, i.e. of [3H]naloxone binding sites, in the hypothalamus, but not in the striatum, decreases. The possible biological role of stress-induced activation of endogenous opioid system, namely the maintenance of the intensity of stress reaction within certain limits and thus the prevention of the self-destructive effects of stress reactions, is discussed.

Ergot alkaloids inhibit 3H-naloxone binding to opiate receptors in the rat striatum and hippocampus.

The authors tested direct effect of selected ergot alkaloids (lisuride, terguride, DH-ergotoxine, DH-ergotamine and DH-ergocristine) on specific 3H-naloxone binding in the rat striatum and hippocampus. In the striatum they found that DH-ergotoxine (a substance with high affinity for noradrenergic receptors) inhibited specific 3H-naloxone binding much more strongly than lisuride and terguride (substances with a greater affinity for dopaminergic and serotoninergic receptors). DH-ergotoxine, which inhibited binding significantly more in the striatum than in the hippocampus, displayed the greatest activity. The results show differences in the degree of inhibition by the various groups of ergot alkaloids in the striatum. In the case of DH-ergotoxine there was also a difference in the degree of inhibition in the striatum and the hippocampus.

Effects of ergot alkaloids on stress-induced analgesia.

Repeated, thirty minute anticipation of unavoidable painful stimulation causes endorphin-induced analgesia in rats. This type of stress-induced analgesia (SIA) develops rapidly during the first minutes of the exposure to anticipation stress. SIA can be demonstrated during the whole period of anticipation stress. Ergot drugs (DH--ergotoxine, lisuride, trans-9,10 dihydrolisuride) administered 30 min before the onset of anticipation stress, blocked completely this form of SIA. On the other hand, no effect of ergot alkaloids in the tail-flick latency, as measured under resting conditions, was observed. Possible interactions of ergot alkaloids with opiate receptors as an important mechanism by which ergot drugs affect SIA are discussed.

Changes in the activity of rat cortical and hippocampal neurones after the iontophoretic administration of beta-endorphin, glutamate and GABA.

The effect of microiontophoretically administered beta-endorphin on the activity of 62 cortical and hippocampal neurones was studied in acute experiments on 14 rats. The effectiveness of beta-endorphin was first of all verified in the isolated guinea pig ileum, the mouse was deferens and in a study if its analgetic and catatonic effect in rats. Beta-endorphin only mildly depressed the spontaneous activity of cortical neurones, but markedly inhibited the activity stimulated by the microiontophoretic administration of glutamate. In the hippocampus, beta-endorphin stimulated the activity of all the studied neurones when only low ejection currents were used and activation persisted for 1-4 min after terminating administration. With higher ejection currents, the discharge frequency rose enormously and not even GABA blocked this effect. The excitatory effect of beta-endorphin on the hippocampal neurones may possibly be the basis of the epileptogenic action of this substance.

Analgesia induced by painful stimulation and/or anticipation of pain; different mechanisms are operating.

Various stresses (i.e. transfer stress, exposition of animals to a new environment, footshock stress, anticipation stress) were found to produce hypalgesia as judged from an increase of the tail - flick latency in rats. Hypalgesia induced by transfer stress was slightly reduced by diazepam (5 mg per kg), but very significantly by chlorpromazine (5 mg per kg). Footshock-stress-induced analgesia lasted less than 15 min. Because naloxone or dexamethasone did not block the footshock-induced analgesia, the participation of the endorphinergic system in this form of stress-induced analgesia is not probable. During the 30 min lasting conditioned reaction to footshock administration (called here anticipation stress), marked analgesia was observed. This anticipation-stress-induced analgesia was blocked by naloxone, dexamethasone and chlorpromazine; no blockade was observed after diazepam. These observations suggest that the endorphinergic system in this form plays a role in stress-induced analgesia. The comparison of the effects of naloxone and/or dexamethasone on the analgesia induced by footshock on the one hand and analgesia induced by anticipation stress on the other thus suggests that different antinociceptive mechanisms are activated by the unconditioned and/or conditioned stimulus.

Postnatal development of the energy supplying enzyme pattern in the rat brain.

The activity of seven enzymes connected with energy-supplying metabolism was followed from the second day of life till adulthood (87th day). The enzymes selected were: 1. Triosephosphate dehydrogenase (TPDH), 2. Lactate dehydrogenase (LDH), 3. Glycerol-3-phosphate: NAD dehydrogenase (GPDH), 4. Hexokinase (HK), 5. Malate: NAD dehydrogenase (MDH), 6. Citrate syntase (CS) and 7. 3-Hydroxyacyl Co A dehydrogenase. Although some variations occurred, the enzyme profiles were characteristic of those of the nervous tissue from the second day of life onwards until adulthood and displayed relatively high activities of HK, CS and MDH and low activities of TPDH, LDH, GPDH and HOADH. The activities of all enzymes studied here increased during postnatal development and some reached adult values on the 14th day, that of TPDH on the 27th day and HOADH on the 41st day of life. The activities of MDH and GPDH did not attain the adult values still on the 41st day of life. The anaerobic energy supply capacity seems to increase transiently on the 31st day of life, i.e. at a developmental stage where the resistance against hypoxia is known to increase transiently.

Changes of electrodermal properties in the "acupuncture points" on men and rats.

The measurements of skin resistance to electrical current performed in rats and men indicated the occurrence of small skin areas, in which the conductivity for DC and AC was sharply increased. In healthy men, the anatomical localization of these areas of increased skin conductivity (AISC) corresponded to the localization of the so-called "acupuncture points" (AP). In patients, the AISC were also found outside the ordinary AP, mainly in areas of referred pain. The measurements of the size of AISC by multiple electrodes indicated the approximate size of AISC cca 350 microM in the rat, ccs 450 microns in man. The recording of skin conductivity were taken from : a) AISC in man and the rat, b) skin in the close neighbourhood of AISC, c) from the sweating human skin.

Pattern of labelling of the rat brain stem after intraventricular administration of 3H-leucine; low and high resolution autoradiographic study.

The pattern of labelling of proteins of the periventricular grey matter was studied two hours after intraventricular administration of 3H-leucine by low- and high-resolution autoradiography. The pattern was investigated by computer-controlled densitometry. The deposition of radioactive, proteins in the periventricular grey surrounding the mesencephalic part of the aquaeductus Sylvii was compared with that surrounding the fourth ventricle. In the former case, the distribution, of grains was in a circular area 500-600 micrometer in diameter; the densitometric tracing revealed a homogeneous distribution of the label; in the latter case, the distribution was nonhomogeneous and was limited by the tissue components forming the wall of the fourth ventricle. A comparison of the intensity of labelling (performed by a combination of low- and high-resolution autoradiography indicated: a) relatively substantial labelling of proteins of ependymal cells, b) very sparce labelling of subependymal layers, c) very high labelling ot neurones, adjacent to the subependymal layers. The significance of these findings for the interpretation of studies using the intraventricular administration of labelled amino acids for investigating brain macromolecular metabolism is discussed.