Inhibition of catecholamine and 5-hydroxytryptamine induced enzyme secretion from the guinea-pig submandibular gland by 2-bromo-d-lysergic acid diethylamide.
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Biomedical subjects
Publications and source records attributed to A Danielsson.
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1. The effects of dopamine, 5-hydroxydopamine (5-OHDA) and noradrenaline on amylase secretion from the guinea-pig submandibular gland were investigated under in vitro conditions. 2. All three amines greatly enhanced amylase secretion. Blockade of dopamine beta-hydroxylase did not inhibit the response to dopamine. 3. Noradrenaline and dopamine stimulated amylase release from salivary glands of reserpine-treated animals, whereas 5-OHDA had no stimulatory effect on secretion in guinea-pigs pretreated with reserpine. 4. Haloperidol completely inhibited dopamine-induced enzyme discharge, but did not affect noradrenaline-initiated secretion. 5. Apomorphine caused a slight enzyme release by itself; it diminished the dopamine secretory effect, but did not modify that of noradrenaline. 6. Pimozide and fluspirilene attenuated the dopamine-induced enzyme discharge, but compared with haloperidol they were less effective. 7. It is concluded that dopamine exerts a secretagogic action different from that of noradrenaline. The possible presence of a specific dopamine receptor in salivary glands is discussed.
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Cell-mediated lymphocyte cytotoxicity in ileum and colon of patients with ulcerative colitis (UC), Crohn's disease (CD) and controls was investigated. Frequencies of cells expressing perforin and Fas-ligand (FasL) were determined by immunomorphometry. mRNA expression of perforin, granzyme B and FasL in T cells and subsets was assayed by reverse transcriptase-polymerase chain reaction. Cytotoxicity of intraepithelial and lamina propria lymphocytes was analysed without ex vivo activation in three functional assays: (1) anti-CD3-dependent T-cell receptor (TCR)-/CD3-mediated redirected cytotoxicity, (2) Fas-/FasL-mediated TCR-/CD3-independent cytotoxicity and (3) natural killer (NK) cell cytotoxicity. Inflammation in ileum of CD patients caused increased frequency of perforin-expressing cells and enhanced perforin-dependent TCR-/CD3-mediated cytotoxicity. In contrast, lymphocytes in the inflamed colon of UC or Crohn's colitis patients did not display this cytotoxicity nor did lymphocytes of normal colon. Normal colon lymphocytes showed spontaneous Fas-/FasL-mediated cytotoxicity. This activity was retained but not enhanced in inflamed UC colon. In contrast, a significant increase of FasL-expressing cells was seen in situ. Inflammation did not induce NK cell activity in colonic lymphocytes. Intestinal lymphocytes comprise effectors active in two different cytolytic processes. 'Classical' cytotoxic T lymphocytes in small intestine and lymphocytes executing TCR-/CD3-independent FasL-/Fas-mediated killing of unknown biological role present throughout the intestinal mucosa. Ongoing normal cytolytic processes seem to be enhanced by chronic inflammation.
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An analysis was made of the symptom diaries of 65 patients with primary sclerosing cholangitis (PSC) who recorded their symptoms of itching, pain and fever during a 3 year period. Symptoms occurred in 84% of the patients, with considerable individual variations in symptom load. Symptoms were usually intermittent. "Itching only" and "pain only" were the most frequent episode features. Most episodes lasted only 1-2 days. Fever seemed to be the most embarrassing symptom. Apart from close correlations between pruritus and serum ALP levels, there were no significant correlations between the symptom load and serum biochemistry or eleven different histological features. Even daily symptoms over a period of several months could disappear spontaneously. We conclude that most symptom episodes in PSC are mono-symptomatic and brief. Biochemical or histological data do not predict the appearance of symptoms.