Biomedical subjects

C Johansson

Publications and source records attributed to C Johansson.

At least 289 records · Page 16Linked to original sources

PubMed1985

Effect of graded doses of intraluminal H+, prostaglandin E2, and inhibition of endogenous prostaglandin synthesis on proximal duodenal bicarbonate secretion in unanesthetized rat.

The purpose of this study was to examine the effect of graded doses of intraluminal HCl and prostaglandin E2 on proximal duodenal bicarbonate secretion in unanesthetized rats. Basal bicarbonate secretion was approximately 14 mumol/cm . h and increased significantly in a dose-related manner to 50, 100, and 150 mM HCl as follows: 22.0 +/- 1.5, 29.2 +/- 4.0, and 42.0 +/- 4.3 mumol/cm . h, respectively (mean +/- SE). After a single 5-min infusion of 150 mM HCl, duodenal bicarbonate secretion remained significantly above basal for almost 3 h. The responses to 100 mM HCl and 10(-4) M prostaglandin E2 were similar (29.2 +/- 4.0 and 26.9 +/- 4.4 mumol/cm . h, respectively). Indomethacin (4 mg/kg, intraperitoneally) suppressed the bicarbonate response to 150 mM HCl; whereas the response to 10(-4) M prostaglandin E2 was unaltered. These studies in the in vivo rat indicate that (a) graded doses of intraluminal HCl produced graded increases in proximal duodenal bicarbonate secretion; (b) the bicarbonate output in response to a 5-min infusion of HCl persisted for almost 3 h; and (c) the bicarbonate response to HCl was essentially abolished by indomethacin pretreatment, suggesting that endogenous prostaglandins are at least in part involved in acid-induced proximal duodenal bicarbonate secretion.

Animals↗

PubMed1985

Acid instillation increases gastric luminal prostaglandin E2 output in man.

The capacity of the gastroduodenal mucosa to maintain integrity when exposed to acid and pepsin may require formation of endogenous prostaglandins (PG). The gastric mucosa is capable of PG biosynthesis, and PGE2 is present in the gastric contents of man. The purpose of this study was to examine if acidification of the human stomach affects the output of PGE2. Gastric perfusion was made with 150 mM HCl in seven healthy subjects pretreated with a histamine-2-receptor blocker (ranitidine). Gastric luminal PGE2 was measured by gas chromatography-mass spectrometry. Basal output of PGE2 was 1.42 +/- 0.24 pmol/min (mean + SEM), which increased to 5.37 +/- 0.91 pmol/min (p less than 0.02) during acid perfusion. Gastric acidification did not cause mucosal damage as judged by luminal DNA. We conclude that PGE2 is synthesized in the gastric mucosa even during nearly complete inhibition of parietal cell secretion. Luminal acid, a likely physiological stimulator of mucosal defense, induces a fivefold increase in PGE2 output from the intact mucosa.

Adult↗

PubMed1985

Randomised double blind trial of somatostatin in the treatment of massive upper gastrointestinal haemorrhage.

In order to evaluate the effect of somatostatin in the treatment of massive upper gastrointestinal bleeding a randomised double blind trial of 95 patients has been undertaken during a 28 months period. Patients with oesophageal varices have been excluded as well as patients with diabetes. All patients were endoscoped within eight hours of admission to the hospital, whereupon the source of bleeding and types of stigmata were assessed. Forty six patients, chosen at random, were given a 72 hour infusion of somatostatin, while the remaining 49 patients received infusion of placebo. The two groups were well matched for sex, age, and source of bleeding. On the day after admission, an additional endoscopy was performed at which eight patients in the somatostatin group and 16 in the placebo group were found to have a persistent bleeding. A total of five patients in the somatostatin group and 14 in the placebo group underwent surgery (Fisher's exact test, 2-tail, p = 0.04). Rebleeding occurred in six patients in the somatostatin group, of whom five experienced rebleeding after completion of the somatostatin treatment. In the placebo group, rebleeding occurred in five patients, of whom four rebled on the day after admission. The need for blood transfusions and the mortality rate did not differ significantly between the two groups. No toxic side effects were found as a result of the infusion of somatostatin. In this study, somatostatin reduced the number of patients needing surgery with massive upper gastrointestinal bleeding.

Adult↗

PubMed1985

Protection of the gastroduodenal mucosa by prostaglandins.

Like other nucleated cell populations in the body, the cells of the gastroduodenal mucosa are capable to metabolise arachidonic acid into prostaglandins, with prostaglandin E2 as the probable major metabolite. The production increases on demand and can be followed in the gastric lumen, where the output of prostaglandin E2 increases two to fourfold after exposure of the mucosa to hydrochloric acid. Exogenous prostaglandins, in particular of the E series, stimulate several identified mucosal defense factors in the upper gastrointestinal tract. Prostaglandins of the E series stimulate the transport of bicarbonate and the production and release of mucus glycoproteins from the gastroduodenal mucosa. They have trophic effects on gastrointestinal epithelia by increasing the survival time of mucosal cells and have cytoprotective properties. In addition, E2 prostaglandins suppress the gastric acid secretion and accelerate peptic ulcer healing. Non steroidal antiinflammatory drugs, which block the biosynthesis of prostaglandins, suppress the bicarbonate secretion, the production of mucus glycoproteins and cytoprotective properties. They interfere with the inhibitory feedback regulation of the gastric acid secretion and are ulcerogenic in experimental and clinical situations. These actions of PG biosynthesis blockers provide indirect information on the importance of local prostaglandin formation for maintenance of gastrointestinal mucosal integrity. It is hypothesised that biosynthesis of prostaglandins in the gastroduodenal mucosa is of importance and may be a key event in triggering the different components of the mucosal defense.

Animals↗

PubMed1984

Isolation and primary structure of human PHI (peptide HI).

The isolation of the human form of PHI (peptide HI) is described. The peptide was purified from human colonic extracts by using a chemical method for the detection of its C-terminal amidated structure. Human PHI consists of 27 amino acid residues and the complete amino acid sequence is: His-Ala-Asp-Gly-Val-Phe-Thr-Ser-Asp-Phe-Ser-Lys-Leu-Leu-Gly-Gln-Leu-Ser- Ala-Lys-Lys-Tyr-Leu-Glu-Ser-Leu-Met-NH2. The differences between the structures of porcine and human PHI are at position 12 (Arg/Lys replacement) and at position 27 (Ile/Met).

Amino Acid Sequence↗

PubMed1984

[Analysis of athletic injuries and the cost to society at a northern health care region. Soccer is the cause of most of the injuries but badminton is the most expensive].

Explore the source record for details and available documents.

Adolescent↗

PubMed1984

Intact and sympathectomized carotid bodies of long-term hypoxic rats: a morphometric ultrastructural study.

The ultrastructure of the carotid body after exposure to hypoxia (10% O2) for one, two or three weeks was investigated morphometrically. The study was performed on rats after unilateral removal of the superior cervical ganglion. The normally occurring bimodal distribution of type I cells, representing cells with small vesicle profile diameters (SVC) and large vesicle profile diameters (LVC) respectively, changed after one week of hypoxia into a unimodal population. After one or two weeks of hypoxia the diameter range of dense-cored vesicle (DCV) profiles in type I cells was not different from that of DCV profiles in control LVC. After three weeks of hypoxia the DCV vesicle size was intermediate between those of control SVC and LVC. The volume density of DCV decreased after one week but returned to initial values after two and three weeks of hypoxia. At two or three weeks of hypoxia, however, the total cell volume was increased about 1.4 times which should reflect an increase of the total content of DCV at these times of exposure to hypoxia. An increased mean area of cell profiles indicates a hypertrophy of the type I cells, but no signs of hyperplasia could be detected. The ganglionectomy did not cause any remarkable changes compared to the intact carotid body except for a higher volume density of DCV during the early periods of hypoxia. It is inferred from the study that the increased total mass of type I cell tissue during long-term hypoxia is due to a hypertrophy of the cells. Furthermore, the type I cells can increase their storage capacity for catecholamines during hypoxia by an increase in the size and number of DCV.

Animals↗

PubMed1984

Villous dysplasia. An ominous histologic sign in colitic patients.

Preoperative biopsies and colectomy specimens from 40 patients with long-standing ulcerative colitis (of whom 20 had adenocarcinoma at colectomy) were searched for the presence of villous adenomatous changes with or without cellular dysplasia. Villous adenomatous changes were found in available preoperative punch biopsies in nearly 70 per cent of the patients with carcinoma, but in none of the preoperative punch biopsies from the 20 patients without cancer. Only three of the preoperative biopsies from patients with carcinoma showed severe dysplasia, and also one of the 20 colitic patients without carcinoma. The mucosal tip in villous adenomatous changes was usually covered by columnar epithelium without dysplasia. In preoperative punch biopsies from patients with long-standing ulcerative colitis, the presence of structures compatible with villous adenoma--even those without cellular dysplasia--should be considered an ominous histologic sign and, thus, an indication for panproctocolectomy.

Adenoma↗

PubMed1984

Bioconversion of arachidonic acid in the human gastrointestinal tract.

The data presented demonstrate that the bioconversion of [14C]arachidonic acid in homogenates like these is very easily influenced by protein (enzyme) and substrate concentration as well as exogenous cofactors. This is not unexpected but variations will lead to artifactual differences. Neither quantitative nor qualitative differences could be detected between biopsies taken from healthy as compared to diseased individuals. No products other than PGE2, PGF2 alpha, TxB2, and 6-keto-PGF1 alpha (and metabolites thereof) could be demonstrated although special efforts were undertaken to determine whether there was any detectable lipoxygenase activity. Therefore it seems that future studies on the possible roles of prostaglandins in gastrointestinal physiology should be restricted to those compounds identified, primarily PGE2 and PGF2 alpha. The monotony in the pattern of products formed in homogenates from different tissues also suggests that in order to be able to detect possible differences between various conditions such studies should involve a minimum of tissue manipulation.

Adolescent↗

PubMed1984

Secretin, VIP, and PHI stimulate rat proximal duodenal surface epithelial bicarbonate secretion in vivo.

The surface epithelial cells of the stomach and duodenum secrete bicarbonate at rest and in response to a number of agonists including the gastrointestinal hormones, glucagon, and GIP. Since those hormones with structural homology may have similar effects, the purpose of the present study was to examine the effect of graded doses (6, 24, and 96 nmol/kg) of pure porcine secretin, VIP, and PHI on bicarbonate secretion by the proximal duodenum containing Brunner's glands. Experiments were performed in vivo on unanesthetized Sprague-Dawley rats with chronic Thiry-Vella type loops of the proximal 2 cm of duodenum. The order of testing was random and only one hormone was tested on a single day. Compared to the saline control, each dose of VIP produced a significant increase in duodenal bicarbonate secretion in a dose-response manner. The two higher doses of secretin and only the 96 nmol/kg dose of PHI significantly increased bicarbonate output. The responses to 96 nmol/kg dose of secretin and VIP were similar, and each was significantly greater than observed with PHI. It is concluded that secretin and VIP stimulate proximal duodenal bicarbonate secretion and are more potent than PHI.

Animals↗

PubMed1984

Lipoprotein abnormalities in patients with early primary biliary cirrhosis.

In twelve females with early forms of primary biliary cirrhosis (PBC) serum lipoproteins, the intravenous fat tolerance test ( IVFTT ) and the lecithin: cholesterol acyl transferase (LCAT) rate were determined and compared to healthy controls. The cholestatic LDL (LP-X) test was negative in all cases. PBC patients had lower very low density lipoprotein TG concentrations than controls and had levels of (high-density lipoprotein) HDL-TG, -cholesterol and -phospholipids that were about 50% higher than in controls. In PBC the HDL2-cholesterol concentration was double but the HDL3-cholesterol concentration was 60% of control values (P less than 0.001 for both). The LCAT rate and the IVFTT value did not differ between the groups. A typical finding on agarose gel electrophoresis was the appearance of a slow-moving alpha-band. Several interpretations of these results are possible. In PBC the hepatic lipase activity may be impaired leading to a shift of the HDL2/HDL3 relation. The transport of HDL2 to the liver lipase site may also be affected and HDL3 production reduced due to malabsorption in the intestine.

Adult↗

PubMed1984

Effect of graded 15(R)15 methyl prostaglandin E2 and of indomethacin on the gastric secretory and plasma gastrin response to modified shamfeeding.

Vagal stimulation by modified shamfeeding in healthy subjects induced about fourfold increases of gastric outputs of acid, chloride, sodium and potassium. Prior oral 15(R)15 methyl prostaglandin E2 inhibited dose-dependently the peak and total gastric acid response to modified shamfeeding by lowering both the secreted volumes and the acidity. The inhibition by 15 micrograms of the analogue exceeded 50% and the suppression was submaximal by 140 micrograms. Gastric output of chlorides decreased in a dose-related way. The hydrogen ion output was proportionally more reduced than the chlorides. The analogue did not affect the gastric output of sodium. Potassium decreased in a dose-related way. Indomethacin was without effect on the gastric acid response to shamfeeding but reduced the sodium output compared to in controls and in series with the analogue. Plasma gastrin was slightly but significantly elevated by the shamfeeding procedure. This elevation was absent or even reversed by 15(R)15 Me PGE2. No effect was recorded by indomethacin pretreatment. Vagal stimulation augments both the parietal and non-parietal components of the gastric secretion. Low doses of oral 15(R)15 Me PGE2 were effective in suppressing the vagally stimulated acid secretion. Neutralization by the gastric non-parietal secretion can contribute to reduce the acid response. Blocking of the prostaglandin biosynthesis decreased gastric sodium output, suggesting indirectly that endogenous prostaglandins may be involved in modulating the gastric non-parietal secretion.

Adult↗

PubMed1984

Prostaglandin E2 in basal gastric secretion and during stimulation of muscarinic receptors in man. Measurements with gas chromatography--mass spectrometry.

The physiological importance of prostaglandin E2 (PGE2) biosynthesis in the gastric mucosa is unknown. A role of endogenous prostaglandins in protecting the gastrointestinal epithelia has been suggested, but the evidence is insufficient and rarely supported by concomitant measurement of PG production. Amounts of PGE2 in luminal gastric contents which can be sampled atraumatically may reflect PGE2 synthesis in the gastric mucosa in vivo. To confirm earlier reported measurements made with radioimmunoassay we have measured by gas chromatography - mass spectrometry (GC-MS) PGE2 in gastric juice of five healthy men under basal conditions and during stimulation of muscarinic receptors with iv. bethanechol which in dog is reported to enhance PGE2 output. PGE2 was detected in all basal samples. The output was in median 32.1 pmol/15 min (range 17.0-105.4, 1 pmol = 0.352 ng), which is similar to results from earlier studies. Bethanechol infusion (60 micrograms . kg-1 . h-1) did not affect PGE2 outputs systematically in spite of a significant increase in outputs of acid and chlorides. Stimulation of muscarinic receptors does not seem to influence PGE2 synthesis in gastric mucosa in vivo. Alternatively changes in PGE2 synthesis may be masked by rapid chemical or enzymatical degradation or reabsorption of PGE2. Studies are under way to explore those phenomena.

Adult↗

PubMed1984

Production of nitric oxide in loam under aerobic and anaerobic conditions.

Measurements of gas flow through soil columns of loam from Kjettslinge, Uppland, Sweden, gave average NO production rates of 0.06 +/- 0.01 ng of NO N g of soil min in aerobic conditions and 3.7 +/- 0.6 ng of NO N g of soil min in anaerobic conditions at 25 degrees C. Approximately 30% of the NO(3) loss in anaerobic conditions was as NO. In aerobic conditions an equilibrium concentration for NO was found. Above this concentration there was uptake of NO. Autoclaved samples indicated that less than 10% of the NO production was abiological, and there was no abiological NO uptake. The NO production reached anaerobic rates at soil O(2) levels between 0.5 and 0.05%.

Journal Article↗

PubMed1984

Effects of 16,16 dimethyl prostaglandin E2 on irradiation damage of the small intestine.

The effects of oral 16,16 dimethyl prostaglandin E2 on irradiation induced damage of the small intestine was examined in the rat. Groups of Sprague-Dawley rats received graded doses of the analogue or placebo at 24, 8 and 0.5 hours before and at 16 and 24 hours following whole abdominal exposure to 10 Gy. Rats were killed 72 hours after irradiation. Pretreatment within the lower dose range had a moderate protective effect with better preserved crypts and crypts to villus ratio. Larger doses seemed to increase the intestinal damage. The prostaglandin treated sham irradiated rats had higher villous height and larger epithelial surface compared with controls.

16,16-Dimethylprostaglandin E2↗

PubMed1984

Gastric acid inhibition by antral acidification mediated by endogenous prostaglandins.

The effects of indomethacin on the basal and stimulated gastric acid secretion at controlled intragastric pH were examined. Four tests with modified sham feeding were made in nine healthy volunteers on different occasions, twice with acid and twice with alkaline perfusion of the stomach. Blocking of the prostaglandin biosynthesis with indomethacin preceded one of the tests at each pH. Plasma levels of gastrin were measured. Antral acidification suppressed the basal and vagally stimulated gastric secretion rate of H+ and Cl-. The inhibition was associated with a decreased plasma gastrin response. Indomethacin reduced the inhibition of the peak acid output and plasma gastrin levels induced by antral acidification. During alkalinization of the stomach indomethacin had no effect on the acid secretion rate or plasma gastrin levels. The results suggest that the pH-dependent inhibitory regulation of the gastric acid secretion is mediated by locally produced prostaglandins. The mechanism functions at least partially through modifying the release of gastrin.

Adult↗

PubMed1984

A quantitative method of estimating inflammation in the rectal mucosa. IV. Ulcerative colitis in remission.

Histological preparations of the rectal mucosa were analyzed quantitatively in 61 patients with ulcerative colitis in remission (UCR). Four histological variables were recorded: the diameter (minor axis) of the lumen of 10 consecutive (transversally cut) glands, the interglandular linear distance between 10 consecutive glands, the number of glands at high-power field examination, and the number of nuclei in 10 consecutive areas of lamina propria. The most important feature to differentiate UCR patients from non-colitic patients was the distance between glands and the number of glands per area. The sum of the values of the four variables demonstrated that 84% of the patients with UCR had scores of 22 or more, whereas only 1 of 124 non-colitic patients (that is, 0.8%) had similar scores.

Cell Count↗

PubMed1983

Evidence for a selective brain noradrenergic involvement in the locomotor stimulant effects of amphetamine in the rat.

Male rats received the noradrenaline neurotoxin DSP4 (50 mg/kg) 7 days prior to injection of D-amphetamine (10 or 40 mumol/kg i.p.). The hyperactivity induced by D-amphetamine (10 mumol/kg) was significantly reduced by DSP4 pretreatment. However, the increased rearings and the amphetamine-induced stereotypies were not blocked by pretreatment with DSP4. The reduction of amphetamine hyperactivity induced by DSP4 was blocked by pretreatment with the noradrenaline-uptake blocking agent, desipramine, which prevents the neurotoxic action of DSP4. The present results suggest a selective involvement of central noradrenergic neurones in the locomotor stimulant effect of amphetamine in the rat.

Animals↗