Biomedical subjects

K Kadzielawa

Publications and source records attributed to K Kadzielawa.

At least 19 recordsLinked to original sources

PubMed1993

Tc-99m sestamibi uptake by cerebellar metastasis from bronchogenic carcinoma.

Tc-99m sestamibi has been used to detect primary brain and lung tumors. The authors report a patient who underwent brain imaging to differentiate tumor from abscess in the cerebellum because of a ring-like enhancement lesion on a brain CT scan. An abnormal area of increased sestamibi uptake in the right cerebellum was demonstrated planar and on a SPECT imaging. The removed tumor was confirmed to be poorly differentiated metastatic carcinoma.

Aged↗

PubMed1983

Inhibition of the activity of sympathetic preganglionic neurones and neurones activated by visceral afferents, by alpha-methylnoradrenaline and endogenous catecholamines.

The responses of electrophysiologically identified sympathetic preganglionic neurones (SPGN) and neurones activated by visceral afferents (VA) to iontophoretic application of: (1) the intraneuronal metabolites of alpha-methyl-DOPA (alpha-MD): alpha-methylnoradrenaline (alpha-MNA) and alpha-methyldopamine (alpha-MDA); (2) noradrenaline (NA) and adrenaline (Ad); and (3) N-methyl-beta-hydroxy-phenylethylamine (NMPEA), were tested in the upper and lower segments of the thoracic spinal cord of the cat. alpha-Methylnoradrenaline, NA and Ad had an inhibitory action on the majority of spontaneously firing neurones. Inhibition of the activity of preganglionic neurones and neurones activated by visceral afferents induced by alpha-MNA was usually equal to the effect of NA, but in some neurones alpha-MNA was more potent. The transport numbers of both amines are similar. The alpha adrenoceptor antagonists, thymoxamine, piperoxan and yohimbine, antagonized the inhibitory effects of alpha-MNA in spontaneously-active preganglionic neurones and neurones activated by visceral afferents. Piperoxan antagonized also the inhibitory effects of NA. The inhibitory effect of alpha-MDA was weaker and that of NMPEA was much weaker than that of alpha-MNA and NA. The inhibitory effects of alpha-MNA and NA in the cerveau isolé preparation resembled those observed in anaesthetized animals. In reserpinized cats, with catecholamine levels in brain stem and spinal cord reduced by 98-99%, the inhibitory effects of alpha-MNA were preserved. It is postulated that alpha-MNA modulates the activity of preganglionic neurones and that this action, leading to a decrease in sympathetic output and mediated by alpha 1 and alpha 2 adrenoceptors, could be the most important factor in the antihypertensive effect of alpha-MD. The inhibition of the activity of neurones activated by visceral afferents by alpha-MNA indicates that alpha-MD may also attenuate the response of the central nervous system to the input from the heart and other organs.

Afferent Pathways↗

PubMed1983

Antagonism of the excitatory effects of 5-hydroxytryptamine on sympathetic preganglionic neurones and neurones activated by visceral afferents.

The responses of electrophysiologically identified sympathetic preganglionic neurones (SPGN) and interneurones activated by sympathetic visceral afferents (VA), to iontophoretic application of 5-hydroxytryptamine (serotonin) and serotonin receptor antagonists: methysergide and cinanserin, were tested in the T3 segment of the spinal cord of the cat. Serotonin had a definite and dose-dependent excitatory action on sympathetic preganglionic neurones and neurones activated by visceral afferents. This excitatory response to serotonin was characterized by the rapid development of tachyphylaxis. Methysergide antagonized the effects of serotonin in preganglionic neurones and neurones activated by visceral afferents. Cinanserin was less effective than methysergide. Preliminary data on the effect of inhibitors of serotonin uptake: chloroimipramine and fluoxetine are also reported. These findings support the idea that the sympathetic output and the activity of neurones activated by sympathetic viscero-afferents is modulated by an excitatory serotoninergic supraspinal input.

Afferent Pathways↗

PubMed1979

Inhibition of the action of anticonvulsants by lithium treatment.

The present study demonstrates that the effectiveness of anticonvulsants significantly decreases following lithium treatment (3 doses of 50 mg/kg of LiCl given every 12 hr). The anticonvulsant action of phenytoin, phenobarbital and of 3 carbonic anhydrase inhibitors: methazolamide, acetazolamide, ethoxzolamide, was assessed in rats subjected to maximal electroshock. In a chronic study on tolerance development to the anticonvulsant action of acetazolamide, lithium treatment (10 mg/kg per day) has been shown to inhibit gradually the action of acetazolamide. These results are consistent with the hypothesis that norepinephrine and dopamine are involved in the action of anticonvulsants.

Animals↗

PubMed1979

Ethanol-induced spontaneous norepinephrine release from the rat vas deferens.

Acute ethanol exposure increases norepinephrine (NE) turnover both centrally and peripherally. One of the mechanisms by which ethanol could increase NE turnover is by increasing spontaneous NE release. The effect of ethanol on spontaneous NE release was investigated using tritium release from l-[3H]NE-labeled vasa deferentia as an index of NE release. Ethanol, 65 mM, increased spontaneous tritium release by 8% and pargyline, 100 mg/kg b.wt., pretreatment increased the ethanol effect by 63%. Ethanol alone (22 mM) had no effect on tritium release; however, with pargyline pretreatment tritium release increased by 13%. Combined reserpine, 5 mg/kg, and pargyline, 100 mg/kg, abolished these ethanol effects. Preincubation with tyramine, 1.8 microM, and omitting calcium from Krebs-bicarbonate buffer also abolished the ethanol effect. Butanol and propanol were more potent and methanol less potent than ethanol in increasing spontaneous tritium release. The mechanism consistent with all the above observations is that ethanol increases spontaneous exocytosis due to a nonspecific effect on presynaptic and vesicular membranes.

Acetaldehyde↗

PubMed1976