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Biomedical subjects

K Kovács

Publications and source records attributed to K Kovács.

At least 19 recordsLinked to original sources
PubMed1992

Suboccipital cerebrospinal fluid and plasma concentrations of somatostatin, neuropeptide Y and beta-endorphin in patients with common migraine.

The somatostatin-like (SLI), the neuropeptide Y-like (NPY-LI), and the beta-endorphin-like (BE-LI) immunoreactivities of cerebrospinal fluid (CSF) obtained by suboccipital puncture, or plasma from patients suffering from common migraine or other neuropsychiatric disorders were analysed. The SLI concentration was tendentiously decreased in the migraine patients during the attack-free period compared to that of a 'mixed neuropsychiatric group'. During the migraine attack the level of SLI was further decreased. Similar alteration was found in the CSF BE-LI, while the BE-LI in the plasma showed only a tendentious decrease in common migraine patients. The NPY-LI did not change during the attack period in the CSF or plasma. These findings may indicate the possible role of somatostatin in the pathogenesis of common migraine, and support earlier observations that beta-endorphin is involved in the development in this disorder.

Adult↗
PubMed1992

Presynaptic inhibitory effect of TNF-alpha on the release of noradrenaline in isolated median eminence.

The effect of tumor necrosis factor-alpha (TNF-alpha) on the stimulation-evoked release of noradrenaline (NA) from isolated rat median eminence (ME) was investigated, using a low-volume perfusion system. Median eminence, loaded with [3H]noradrenaline, was superfused with Krebs solution and stimulated electrically (2 Hz, 120 shocks). The effect of TNF-alpha was studied on the S2/S1 ratio. It was found that stimulation-evoked release of NA from noradrenergic axon terminals in the isolated rat ME was inhibited by TNF-alpha and this effect was concentration-dependent. In contrast, TNF-alpha had no effect on the release of [3H]NA from the spleen. Since NA released in the ME might be involved in the modulation of corticotropin-releasing factor (CRF) production, it is suggested that TNF-alpha, through presynaptic modulation of NA release from noradrenergic nerve terminals in the ME, might regulate CRF and other neurohormone release in this hypothalamic structure.

Analysis of Variance↗
PubMed1992

Lipopolysaccharide is able to bypass corticotrophin-releasing factor in affecting plasma ACTH and corticosterone levels: evidence from rats with lesions of the paraventricular nucleus.

Stimulation of the immune system or experimental conditions (bacterial lipopolysaccharide (LPS) treatment) provoke a broad spectrum of physiological responses. It was recently shown that one of them is the activation of the hypothalamic-pituitary-adrenal (HPA) axis. The mechanism and the site or sites through which LPS stimulates the HPA axis are not well understood. To establish whether the effect of bacterial LPS is related in vivo to the presence of hypothalamic hypophysiotrophic peptides (corticotrophin-releasing factor-41, arginine vasopressin, etc.), plasma ACTH and corticosterone levels were monitored in intact and sham-operated rats, and in rats with paraventricular nucleus lesions in order to remove the main source of these neuropeptides. Evidence was obtained that 4 h after treatment, LPS was able to activate the hypophysial-adrenal system in the absence of hypophysiotrophic neuropeptides of paraventricular origin. It is suggested that, in vivo, LPS could have a direct effect on the pituitary gland or that it acts through an extrapituitary, non-paraventricular pathway to activate the HPA axis.

Acute-Phase Reaction↗
PubMed1991

Corticotropin-releasing hormone-containing neurons in the hypothalamo-hypophyseal system in rats six weeks after bilateral lesions of the paraventricular nucleus.

Corticotropin-releasing factor-like immunoreactive nerve fibers and varicosities are present in the pituitary stalk and median eminence 6 weeks after bilateral lesioning of the hypothalamic paraventricular nucleus. The total immunoreactivity may reach 10% of the control density. The origin of these fibers was investigated 3 days after hypothalamic transections in paraventricular-lesioned (6 weeks postoperatively) rats. Accumulations of corticotropin-releasing factor immunostaining were observed in the proximal portions of the transected axons and in neuronal perikarya. Fibers with retrograde labeling were seen lateral and dorsolateral from the sagittally oriented knife cuts which transected the retrochiasmatic area and cells were found in the supraoptic nucleus and in the perifornical nucleus (dorsal-dorsolateral to the fornix), ipsilateral to the lesion. No corticotropin-releasing factor immunostained cells were seen in other hypothalamic or preoptic nuclei which project to the median eminence or the posterior pituitary. Corticotropin-releasing factor containing cells in the supraoptic and perifornical nuclei may have an importance in stress response in rats with long-term paraventricular lesions.

Animals↗
PubMed1990

Platelet aggregation of migraineurs during and between attacks.

Platelet aggregation induced by ADP, collagen and platelet-activating factor was studied in common (migraine without aura) and classical migraine (migraine with aura) patients during and between attacks. The EC50* values for ADP and platelet-activating factor were significantly higher, whilst that for collagen was significantly lower in classical migraine patients during headache-free intervals compared to healthy volunteers. The EC50 values obtained for common migraine sufferers during symptom-free periods were similar to those of controls. During attacks, the EC50 value for ADP, but not for collagen and platelet-activating factor, was significantly higher than that of the controls. In healthy subjects a positive correlation was found between ADP and collagen-induced aggregation. In contrast, there was a U-shaped correlation matrix in classical migraine patients. The present observations show that platelet aggregation is altered in migraine patients and this raises the possibility that platelet-activating factor may be involved in the pathogenesis of migraine.

Adenosine Diphosphate↗
PubMed1989

[Clinical characteristics of cluster headache].

The authors describe in detail the clinical characteristics of 48 patients suffering from cluster headache. They investigate the question of nomenclature and survey the clinical forms of diagnosis. They deal with differential diagnosis comparing migraine, trigeminal neuralgia and headaches origin from systemic illness. They point out that the clinical characteristics of their patients co-responding to the data in the literature. They emphasize that the precise anamnesis can result the diagnosis of this type of headache which is the basis of the treatment.

Chronic Disease↗
PubMed1989

Cerebrospinal fluid (CSF) investigations in migraine.

A normal cell count as well as normal CSF pressure levels were found in both classic and common migraine patients during and between attacks. Total protein content was significantly lower in the migraine patients than in the controls, but no changes were found in the CSF protein fractions. The CSF 5-hydroxyindoleacetic acid level of the migraine patients proved to be higher than in the controls, whereas the homovanillic acid concentration was within the control limits.

Adult↗
PubMed1989

[Mammosomatotropic cells in the pituitary gland of the rat with and without adenoma. Immunoelectron microscopic study].

In non-tumorous adenohypophysis and in adenomas of adenohypophysis of rats the GN and PRL producing bihormonal mammosomatotroph cells were demonstrated by double marked immune-gold immuno-electronmicroscopic examinations. Cytogenesis and regulation of these cells are known, their clearing up is expected. Further examinations are needed to elicit, whether mammosototroph cells may occur also in nontumorous human adenohypophysises.

Animals↗
PubMed1988

Competitive mechanisms of basic peptides inducing transganglionic degenerative atrophy.

In addition to the classical microtubule inhibitors (antimitotic agents), transganglionic degenerative atrophy of central terminals of primary sensory neurons can be induced also by means of applying to a peripheral nerve basic polypeptides (Polymyxin B and Colimycin) and two basic derivatives of glutamic acid that do not exert any microtubule inhibition. This effect is independent of other pharmacological effects (histamine liberation, Ca2+ -binding, etc.) of the applied compounds, and probably it is based on a competitive reaction with nerve growth factor.

Animals↗
PubMed1987

Insulin-induced hypoglycemia activates the release of adrenocorticotropin predominantly via central and propranolol insensitive mechanisms.

The dynamic patterns of pituitary-adrenocortical and sympatho-adrenal hormone responses to insulin hypoglycemia as well as the relative importance of central vs. peripheral control of hypoglycemia-induced ACTH secretion were evaluated. In conscious rats bearing indwelling cannulae, the changes in hormone concentrations after insulin injection were dependent on the changes in blood glucose levels with respect to both time course and magnitude. ACTH, corticosterone, epinephrine, and norepinephrine levels were found to be maximal at 60 min after 2.5 IU kg-1 insulin injected ip, whereas earlier (20 min) but smaller increases were obtained in response to 0.5 IU kg-1 insulin injected iv. In rats 6-7 days after lesions of the medial basal hypothalamus (MBH), the rise of ACTH during insulin hypoglycemia was markedly inhibited and corticosterone levels were significantly reduced. Simultaneously, the hypoglycemia-induced increase in plasma epinephrine was unchanged and that in plasma norepinephrine was significantly enhanced in rats with the MBH destroyed. The beta-adrenoreceptor blocker propranolol did not inhibit ACTH and corticosterone responses to hypoglycemia in either sham-operated or MBH-lesioned animals. We conclude that the main factors triggering ACTH release during insulin-induced hypoglycemia are of central rather than peripheral origin. The high concentrations of circulating catecholamines occurring during insulin hypoglycemia are not responsible for pituitary-adrenocortical activation by direct, beta-adrenoreceptor mediated action at the pituitary level.

Adrenocorticotropic Hormone↗
PubMed1987

The possibilities of real-time sonography in the diagnostics of peripheral pulsating resistances. Our experiences of some cases.

Real-time sonography was performed in 5 patients in 7 cases for peripheral pulsating resistances. The change developed in the inguinal fold in one case after arteriography and in 3 patients following a vascular operation. In an additional case, a pulsating mass located in the neck proved to be the kinking of the subclavian artery. After a brief literary review of the ultrasound-diagnostics of the vessels, the authors have found sonography a suitable means for judging the relationship between the vessel or graft and the pseudoaneurysm, the size of the communication and eventual thrombus formation.

Adult↗
PubMed1987

Inhibition of electroshock-induced seizures by cholecystokinin-related peptides in mice.

The effects of several doses of cholecystokinin octapeptide sulphate ester (CCK-8-SE) and nonsulphated cholecystokinin octapeptide (CCK-8-NS), and two CCK-related peptide analogues Ac-Thr5-caerulein, and nonsulphated Ac-Thr5-caerulein were investigated on electroshock-(ES)-induced seizures after intraperitoneal administration in mice. As parameters, the duration of the tonic and clonic phase of the fit, and those of postictal coma and behavioural depression were measured. CCK-8-SE decreased the duration of the clonic phase; its highest dose, 3.2 mumol/kg, shortened the coma. CCK-8-NS antagonized only slightly the clonic phase of seizure. Ac-Thr5-caerulein did not influence ES-induced seizures in any dose, only increased the duration of behavioural depression. Similarly to CCK-8-NS, the nonsulphated form of Ac-Thr5-caerulein inhibited selectively the clonic phase of seizures. The reference drugs, diazepam and phenobarbital, antagonized dose-dependently and most effectively the tonic phase of ES-induced seizures, but in much higher doses than did the CCK-related peptides. Besides, diazepam increased and phenobarbital decreased the duration of postictal coma. The results showed that the tested CCK-related peptides inhibit prevalently the clonic phase of ES-induced seizures after peripheral administration.

Animals↗