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C Johansson

Publications and source records attributed to C Johansson.

At least 253 records · Page 14Linked to original sources

Cisapride induces clustered spikes and irregular spiking of the small intestine of the rat.

The aim of the present study was to investigate the effect of cisapride on the myoelectric activity of the small intestine in the rat. Intestinal myoelectric activity of fasted conscious rats was monitored by three bipolar electrodes chronically implanted at 5, 15 and 25 cm distal to the pylorus and connected to an EEG amplifier. In the basal state, regularly occurring migrating myoelectric complexes (MMCs) and clustered spikes were registered. Cisapride at doses of 0.5-4.0 mg-1 i.v. did not affect the MMCs, but at 8 mg kg-1 i.v. the regular MMCs were replaced by irregular spiking activity (p less than 0.05). Concomitantly cisapride increased the occurrence of clustered spikes and abbreviated the interval between them in a dose-dependent manner (p less than 0.05), without affecting their duration. Hexamethonium at a dose of 10 mg kg-1 i.v. abolished the MMCs as well as the stimulatory effect of ciSapride (4 mg kg-1). Atropine at a dose of 1 mg kg-1 i.v. did not affect the MMCs but blocked the stimulatory effect of cisapride (4 mg kg-1). It is concluded that cisapride induces clustered spikes and irregular spiking. These effects require intact cholinergic pathways, involving both muscarinic and nicotinic receptor mechanisms.

Animals↗

Alternating proliferative capacity in the rat gastrointestinal mucosa. Effects of E2 prostaglandins and indomethacin.

Having previously observed an apparent uneven distribution of proliferating cells in the gastric corporic mucosa of the rat, we examined the mitotic distribution along 8-mm sections of gastric and jejunal epithelia. Metaphases were arrested with vincristine to facilitate mitotic count, and the effects of treatment with a prostaglandin E2 analogue and a cyclooxygenase blocker were examined. Clusters of mitotic figures alternating with non-proliferating areas were observed in the gastric corporic epithelium of control rats. During 4 h mitotic activity was absent over 21% of the corporic mucosa. Extending the examined area to about 240 glands reduced substantially the error of mitotic counts. An uneven distribution of mitoses was found in the antral and jejunal epithelium, but areas without proliferating cells were uncommon. Treatment with the prostaglandin E2 analogue reduced the number of mitosis-free areas in the gastric corpus to 13%, and clusters were less easily identified. The total mitotic count was unaffected by treatment. In the jejunum prostaglandin increased the absolute number of mitoses. The mitotic span was also increased, reflecting the uneven distribution. Indomethacin produced the opposite effects to the prostaglandin analogue, including reduction of epithelial height. Of the gastric corporic mucosa 35% was non-proliferating during the observation period, but the clustering phenomenon was still apparent. Absence of dose relationship was attributed to ulcerogenic actions of high doses of indomethacin. It is concluded that mitoses are unevenly distributed in the upper gastrointestinal epithelium of the rat and that safe estimates of mitotic count require examination of large corporic areas.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Removal of Langerhans cells from human epidermal cell suspensions by immunomagnetic particles.

The possibility of eliminating the class II antigen-expressing and antigen-presenting Langerhans cells from normal human epidermal cell suspensions was investigated. Cell suspensions containing 1.7-2.8% Langerhans cells were prepared by enzyme treatment of human skin obtained at plastic surgery. The cells were incubated with mouse monoclonal antibodies directed against the CD1 antigen present on Langerhans cells and were further incubated with magnetic particles, 4.5 micron in diameter, coated with sheep anti-mouse IgG. The optimal ratio between particles and target cells was found to be 40:1. The rosetted Langerhans cells were removed by a cobalt-samarium magnet. In six experiments immunoperoxidase staining revealed 0-0.1% (mean 0.03%) CD1-reactive Langerhans cells in the depleted cell fraction. The alloantigen presenting capacity of the depleted cell fraction, measured by [3H]thymidine incorporation, was abolished.

Antigen-Presenting Cells↗

A simple in vitro technique for studies on induction of class II transplantation antigens on keratinocytes.

A new technique is described for evaluation of the induction and kinetics of class II transplantation antigens on keratinocytes. By culturing small rat or human skin specimens for 2-5 days in media containing gamma-interferon, class II antigens were detected on keratinocytes by immunohistochemistry. This technique is rapid and technically simple compared to keratinocyte cultures and raises the possibility of studying other cells in the skin.

Animals↗

DL-propranolol inhibits the vascular changes in the rat carotid body induced by long-term hypoxia.

Two groups of rats were exposed to hypoxia (10% O2) for 1 and 3 weeks with or without daily injections of DL-propranolol (0.66 mg.kg-1 ip). The structure of the carotid body was analyzed by light microscopical morphometry and the catecholamine content was assayed by high performance liquid chromatography. Exposure to hypoxia induced enlargement of the carotid body due to enhanced vascularity and hypertrophy of glomic and interstitial tissues. The dopamine and norepinephrine content were increased at both 1 and 3 weeks of hypoxia and reached levels 40-50 times those of the controls. The DL-propranolol treatment abolished the vasodilatory effect of hypoxia within the first week but did not prevent the other structural changes or the rise in catecholamine content. The data suggest that 1. the vasodilation elicited by long-term hypoxia may be controlled by beta-adrenoceptors and 2. the structural and biochemical events occurring in rat carotid body during long-term hypoxia do not influence each other and thus seem to be controlled by different mechanisms.

Animals↗

Gastric secretion in massive obesity. Evidence for abnormal response to vagal stimulation.

Studies in animals and man suggest involvement of the vagal nerve in the pathophysiology of massive obesity. An abnormal vagal response pattern has been found in the obese rat, but corresponding functional studies in obese man are nonexistent. The gastric acid secretion was therefore examined in 13 nondiabetic grossly obese patients (average body weight 120 kg) and compared to 16 age-matched controls of normal body weight. The gastric acid response to modified sham feeding was significantly (P less than 0.05) reduced in obese patients, being on average 60% of the control output. The obese patients had a higher maximal gastric acid response to graded intravenous pentagastrin, 36.6 +/- 2.9 mmol/hr, compared to 27.1 +/- 2.4 mmol/hr in controls (P less than 0.05). In addition, the patients seemed to need less pentagastrin to reach a secretory plateau. Basal acid secretion rates were similar in obese and control groups. Plasma gastrin and blood glucose were not significantly different in obese patients and controls, but patients had significantly elevated plasma insulin levels. The change of plasma insulin during the sham-feeding procedure correlated with the magnitude of the secretory response in obese and control subjects. The reduced gastric acid response to vagal stimulation in the absence of impaired parietal cell function in obese patients is indicative of an association between massive obesity and altered vagal function in man.

Blood Glucose↗

Sprinters and marathon runners. Does isokinetic knee extensor performance reflect muscle size and structure?

In order to evaluate relationships between structure and concentric function of the quadriceps muscle, isokinetic maximum knee extensor output at different velocities of angular motion (30-180 degrees s-1), integrated electromyographic activity (iEMG), cross-sectional area (CSA) of m. quadriceps and fibre composition of m. vastus lateralis were analysed in five sprinters and five marathon runners (all males). Both output and input parameters, concerning peak torque (PT), instantaneous power (IP), contractional work (CW) and the summed iEMG were closely correlated to the m. quadriceps CSA, as well as to the calculated absolute type II (A + B), IIA and IIB fibre areas of m. vastus lateralis. When PT, IP, CW and the summed iEMG were corrected for CSA, such relationships were found only at 180 degrees s-1 and only for type IIA fibre area. The electromyographic findings indicate that m. vastus lateralis was representative for the total mechanical output. The calculated mean power output (CW s-1) and output/input balance (CW/iEMG) describe similar relationships with the velocity of angular motion and were not related to the CSA or to the absolute area of any fibre type. The calculated optimal CW per second and CW/iEMG occur for sprinters at about 450 degrees s-1 and for marathon runners at about 270 degrees s-1, that is, velocities well above the capacity of the isokinetic dynamometer. Our observations indicate that the peak torque or instantaneous power, during single maximum knee extensions, at least at 180 degrees s-1, express characteristics of the muscle structure.

Adult↗

Fatigue and endurance of lower extremity muscles in relation to running velocity at OBLA in male orienteers.

At three occasions during a year, the ratio of contractional work (output)/integrated electromyographic activity (input), that is, CW/iEMG, was measured during repetitive maximum isokinetic manoeuvres for m. quadriceps and m. triceps surae in male elite orienteers. Running velocity at the onset of blood lactate accumulation (VOBLA), which was considered as a measure of running performance, and maximal oxygen uptake (VO2max) were analysed at each test. Type and amount of training were continuously registered. For m. quadriceps there was a decline in CW/iEMG during the first 30 manoeuvres, followed by an unchanged plateau level. In contrast, m. triceps surae showed a plateau level of virtually unaltered CW/iEMG ratio from the start to the end of the experiment. The differences might be explained by structural causes, but also by local muscle adaptation to training. The plateau level of CW/iEMG of m. quadriceps was positively correlated to VO2max. An increase in the plateau level of CW/iEMG was found for both tested muscle groups after the winter training period (mainly low intensity road running) when both VOBLA and VO2OBLA increased. During the competition period (mainly high intensity forest running), the whole group increased while some orienteers lowered their VOBLA. During this period, no changes in the plateau level of CW/iEMG of any muscle group or in VO2OBLA occurred. The changes in the plateau level of CW/iEMG might express local muscle adaptations to changes in running technique and aerobic/anaerobic demands during low intensity road running versus high intensity forest running.

Adult↗

Biliary lipid metabolism in chronic pancreatitis: influence of steatorrhoea.

Kinetics of [24-14C] cholic acid and [24-14C] chenodeoxycholic acid and biliary lipid composition were determined in patients with chronic alcoholic pancreatitis with (n = 8) and without (n = 8) steatorrhoea. Pool sizes, syntheses and fractional catabolic rates of the two bile acids were not significantly different from corresponding values in healthy controls. Biliary lipid composition was normal in patients without steatorrhoea. Patients with steatorrhoea, on the other hand, had lower cholesterol saturation of bile than corresponding controls. This is probably because of malabsorption of cholesterol.

Adult↗

Cell proliferation of the rat gastrointestinal mucosa after treatment with E2 prostaglandins and indomethacin.

The frequency of arrested mitoses after vincristine injection was studied in the gastrointestinal mucosa of rats treated with either natural prostaglandin E2 (0.2-5.0 mg X kg-1, b.d.), 15-R-15 methyl prostaglandin E2 (2 mg X kg-1, b.d.) or indomethacin (1.0-3.0 mg X kg-1, b.d.). In addition to the mitotic index, morphometric measurements including the mucosal thickness and the thickness of the proliferative and functional zones of the gastric corpus, antrum and jejunum were performed. Natural prostaglandin E2, at the highest dose range, reduced significantly the mitotic index in the gastric antrum. Normal values were found in the gastric corpus and jejunum and in the antrum with the lower doses. The mitotic index was unaffected by treatment with 15-R-15 methyl prostaglandin E2. Natural prostaglandin E2 produced trophic changes (i.e. increased thickness and/or hyperplasia) in the antrum, functional epithelial zone of the gastric corpus and in the jejunum. More pronounced trophic changes were observed in the mucosa of rats treated with the analogue. Indomethacin reduced the mucosal thickness in all examined epithelia and lowered the mitotic index in the jejunum. It is concluded that the trophic effects of E2 prostaglandins on gastrointestinal epithelia are not caused by increased production of new cells. The reduced mitotic index observed in the antral mucosa of prostaglandin-treated rats could be secondary to a negative feedback from the hyperplastic epithelium. The antitrophic effects of the prostaglandin-synthesis blocker (indomethacin) indicates that endogenous prostaglandins may participate in the epithelial cell regulation of the gastrointestinal tract.

Animals↗

Fatty acid composition in serum lipids and adipose tissue in patients with morbus Crohn after ileal resection.

In 36 patients with Crohn's disease who had been operated with ileal resection but were in a stable clinical condition, the fatty acid composition in the circulation and in adipose tissue was correlated to resection length. Fatty acid composition was also compared to data from a group of randomly selected healthy men and women of similar age. In plasma Crohn patients had reduced circulating levels of unsaturated fatty acids. On the other hand, increased proportions of these fatty acids were found in adipose tissue. It is unlikely that in this group of patients these data are unspecific reflections of disease activity. A more reasonable explanation seems to be an increased demand for precursors of local prostaglandin synthesis in the remaining bowel.

Adipose Tissue↗

From sagittal distance to area. A study of transverse, vocal tract cross-sectional area.

In speech articulation studies, data on the pharynx are scarce. Still, the pharynx is an important part of the vocal tract. The present paper reports on an attempt to use computed tomography for investigating the pharynx. Axial computed tomograms were taken at four levels in the pharynx of a male and a female subject sustaining the vowels [u:, i:, a:, oe:]. From the tomograms the lateral width and the cross-sectional area were measured and their relations to the sagittal distance from the back pharynx wall to the midline of the tongue examined and compared with previously published data. In addition, some previous results derived from plaster casts are presented showing the corresponding distance-to-area relationship in the mouth region of some male and female subjects.

Female↗

Cell cycle distribution of proliferative and functional cells of the rat jejunum after treatment with oral E2 prostaglandins.

Proliferative and functional epithelial cells were isolated from jejunal specimens of the rat by means of vibrational treatment combined with differential air insufflation. This method gave a good separation between superficial cells of the villi and the crypt cells, as evaluated by flow cytometry, morphology, cytology, and incorporation of radioactive thymidine into DNA. Groups of Sprague-Dawley rats (260 g) were treated twice daily for 11 days with oral placebo, 15(R)15-methyl-prostaglandin E2 in the range of 0.125-2 mg X kg-1, or 5 mg X kg-1 natural PGE2. Isolated crypt cells and superficial cells of the jejunal villi were then analysed by flow cytometry. Morphometric measurements were performed on sections of some jejunal specimens not submitted to vibrational treatment. The cell cycle distribution of crypt cells was unaffected by treatment with the prostaglandin analogue despite the presence of trophic changes. The proportion of crypt cells in G2/M phase was slightly but significantly reduced in rats given natural PGE2 compared with controls. The cell cycle distribution of villus cells was not affected by prostaglandin treatment. Trophic changes in the absence of increased DNA synthesis (S phase) or increased mitotic activity suggests that the hyperplasia observed after prostaglandin treatment is due to a reduced cell loss and/or slower migration time of epithelial cells.

Administration, Oral↗

Myoelectric motility patterns during mechanical obstruction and paralysis of the small intestine in the rat.

The purpose of the present study was to analyze changes of the myoelectric activity in experimental mechanical obstruction and paralytic ileus of the small intestine. Myoelectric activity was recorded in the upper small intestine of conscious, fasted rats by three bipolar electrodes implanted 10 cm apart. In the basal state regular myoelectric motility complexes (MMCs) were registered in all experimental animals. Obstruction of the small intestine (n = 13) was produced by a ligature between the middle and distal electrodes. Proximal to the obstruction regular MMCs continued. After 45 +/- 15 min at the middle (p less than 0.01), and 85 +/- 10 min at the duodenal electrode (p less than 0.01), MMCs disappeared. Another motility pattern was established, characterized by clusters of spikes, occurring regularly with 2-min intervals, separated by short silent periods, and a rapid aboral migration (p less than 0.01). Distal to the obstruction the propagation of MMCs was immediately disrupted. After a quiescent period of 13 +/- 3 min irregular spiking occurred and continued throughout the experiment (p less than 0.01). Intraperitoneal instillation of 0.1 M hydrochloric acid (n = 8) produced a prompt and long-lasting inhibition of the MMCs. The quiescence lasted for 70 +/- 23 min, until the MMCs reappeared (p less than 0.01). It is concluded that complete intestinal obstruction is followed by a series of significant and well-defined changes of myoelectric activity on both sides of the obstruction. Nociceptive stimulation of the peritoneum produces intestinal paralysis. The immediate inhibition of the motility indicates that the paralysis is not secondary to inflammatory reactions.

Animals↗

Prostaglandin synthesis in the human gastrointestinal mucosa.

Prostaglandins derive from polyunsaturated fatty acids, of which arachidonic acid is the most abundant. Arachidonic acid occurs in all cell membranes, where it is bound to phospholipids and can, once liberated by phospholipases, be metabolized by cyclooxygenase into prostaglandins and thromboxanes and by lipoxygenases into hydroxyacids, leukotrienes and lipoxins. In most studies on prostaglandin formation in the human gastrointestinal mucosa PGE2 and PGF2 alpha seem to be the regularly occurring products. Quantification of mucosal prostaglandin synthesis in vivo is problematic. Mechanical handling of tissues immediately activates arachidonic acid metabolism, and the determination of "tissue levels" of prostaglandins or prostaglandin biosynthesis in biopsy specimens ex vivo thus becomes unreliable as a measure of in vivo formation. A more reliable approach may be to measure prostaglandins in gastrointestinal luminal contents, which can be obtained atraumatically. Most measurements are made by radioimmunological methods, but the specificity of most assays has not been satisfactorily examined. More specific methods such as gas chromatography-mass spectrometry should be used to validate of a radioimmunoassays. Prostaglandin E2, which can be measured by gas chromatography-mass spectrometry, is regularly found in human gastroduodenal luminal contents. Exposure of the mucosa to hydrochloric acid increases the output of PGE2 to the lumen, indicating increased mucosal PGE2 formation during physiological activation of mucosal defense mechanisms.

Arachidonic Acid↗

Ulcerogenic drugs and antiulcer compounds: effects on gastroduodenal mucosa.

Nonsteroidal antiinflammatory drugs (NSAID) and steroids are ulcerogenic to the gastroduodenal mucosa in man although the exact incidence of drug-induced lesions is unknown. It is assumed that NSAID are ulcerogenic because they block the biosynthesis of prostaglandins, thereby reducing the mucosal resistance to acid peptic digestion. NSAID inhibit recognized mucosal defense factors, such as bicarbonate transport and mucus glycoprotein production and release; they reduce the thickness of the pH-mucus barrier, interfere with cytoprotection and have antitrophic actions. Prostaglandins reverse the inhibition of defense factors by NSAID and prevent their ulcerogenic actions; they stimulate secretion of bicarbonate and glycoproteins and have trophic and cytoprotective properties. Challenge of the mucosa stimulates defense factors and prostaglandin formation in parallell; pretreatment with NSAID impairs the defensive response and reduces local prostaglandin formation. Mucosal lesions, produced by NSAID may be prevented by agents that neutralize or inhibit gastric acid, such as H2-receptor blockers, antacids and acid antisecretory prostaglandins. Compounds, which stimulate--or simulate--mucosal defense factors are also effective such as sucralfate, colloidal bismuth and prostaglandins devoid of acid antisecretory properties. Of these, several may work by increasing local prostaglandin concentration.

Animals↗