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Biomedical subjects

M Classen

Publications and source records attributed to M Classen.

At least 271 records · Page 15Linked to original sources
PubMed1988

Modulation of rat gastric mucosal prostaglandin E2 release by dietary linoleic acid: effects on gastric acid secretion and stress-induced mucosal damage.

We studied chronic intake of diets deficient in or supplemented with linoleic acid to determine whether it affects gastric acid secretion, release of prostaglandin E2, and stress-induced lesions. For 8-10 wk rats were fed three dietary regimens supplying 3.5% (control group), 0.3%, and 10% of total calories as linoleic acid. We found that diets deficient in linoleic acid (0.3%) reduced release of prostaglandin E2 into the gastric lumen (-77%) and increased basal (+133%) and pentagastrin-stimulated acid secretion (+93%) and the area of cold restraint-induced gastric mucosal lesions (+280%), when compared with the control group. Diets supplemented with linoleic acid (10%) increased prostaglandin E2 release into the gastric lumen (+106%) and reduced basal (-44%) and pentagastrin-stimulated acid secretion (-78%) and the area of cold restraint-induced mucosal.lesions (-80%). Prevention of these lesions by the 10% linoleic acid diet was confirmed by quantitative histology. Pretreatment with indomethacin (8 mg/kg intraperitoneally) abolished the effects of the 10% linoleic acid diet on prostaglandin formation, acid secretion, and mucosal injury. We conclude that in rats chronic intake of dietary linoleic acid reduces acid secretion and prevents cold restraint-induced mucosal lesions, possibly because of augmented synthesis of endogenous prostaglandins in the gastric mucosa.

Animals↗
PubMed1988

Preoperative staging of a distal common bile duct tumor by endoscopic ultrasound.

A 27-yr-old man with a long-standing history of primary sclerosing cholangitis presented with recurrent episodes of fever and progressive weight loss over 6 mo. The diagnosis of a distal cholangiocarcinoma was made by endoscopic retrograde cholangiography and transpapillary biopsy. The extent of the tumor could be reliably assessed by endoscopic ultrasound, whereas computed tomography scan, angiography, and transabdominal ultrasound failed to visualize the tumor. The intraoperative findings and histologic work-up of the resected specimen confirmed a T3N0M0 adenocarcinoma of the distal common bile duct.

Adenocarcinoma↗
PubMed1988

Effect of galanin on gastrin and somatostatin release from the rat stomach.

Galanin has been shown to be present in the gastrointestinal tract, pancreas and CNS. In the rat stomach, immunohistochemical studies have revealed the presence of galanin in the intrinsic nervous system suggesting a function as putative neurotransmitter or neuromodulator which could affect neighbouring exo- or endocrine cells. Therefore this study was performed to determine the effect of galanin on the secretion of gastrin and somatostatin-like immunoreactivity (SLI) from the isolated perfused rat stomach. The stomach was perfused via the celiac artery and the venous effluent was collected from the portal vein. The luminal content was kept at pH 2 or 7 Galanin at a concentration of 10(-10), 10(-9) and 10(-8) M inhibited basal gastrin release by 60-70% (60-100 pg/min; p less than 0.05) at luminal pH 7. At luminal pH 2 higher concentrations of galanin (10(-9) and 10(-8) M) decreased basal gastrin secretion by 60-70% (60-100 pg/min; p less than 0.05). This inhibitory effect was also present during infusion of neuromedin-C, a mammalian bombesin-like peptide that stimulates gastrin release. SLI secretion remained unchanged during galanin administration. The inhibitory action of galanin on gastrin secretion was also present during the infusion of tetrodotoxin suggesting that this effect is not mediated via neural pathways. The present data demonstrate that galanin is an inhibitor of basal and stimulated gastrin secretion and has to be considered as an inhibitory neurotransmitter which could participate in the regulation of gastric G-cell function.

Animals↗
PubMed1988

Substance P modulates lymphokine activities in supernatants of cultured human duodenal biopsies.

A duodenal biopsy culture technique was used to investigate the effect of substance P on lymphokine secretion by the human gut associated lymphoid tissue. Duodenal biopsies of 7 healthy volunteers were cultured in 1 ml medium each with Pokeweed mitogen (1 microgram/ml) for 4 days at 37 degrees C. Substance P (SP) was added in concentrations ranging from 10(-12) M to 10(-6) M. Media were changed every day. Interleukin (IL)-1 beta, IL-2 and IL-2-receptor activities were determined by means of specific ELISAs. Values were referred to 5 mg biopsy weight and expressed as per cent change of basal Pokeweed mitogen-pulsed supernatant activities. 10(-8) M and 10(-6) M SP led to a decrease of IL-1 beta activity (78 +/- 13.9% and 62.8 +/- 17.1%, respectively, alpha = 0.01 each). In contrast, 10(-8) and 10(-10) M SP showed an increase in IL-2 activity up to 182.9 +/- 94.5% and 295.6 +/- 144.7%, respectively. 10(-6) M and 10(-8) M SP enhanced IL-2 receptor activities by 81.5 +/- 70% and 40.9 +/- 11.8%, respectively (alpha = 0.05). The present data demonstrate for the first time distinct SP-mediated effects on lymphokine activities in supernatants of cultured human duodenal biopsies.

Adjuvants, Immunologic↗
PubMed1988

Effect of naloxone on vagally-induced gastric acid secretion in rats.

Previous studies in man and dogs have demonstrated that endogenous opioids participate in the stimulation of cephalic phase gastric acid secretion during indirect activation of the vagus. Since the effect of naloxone during direct vagal activation is unknown gastric acid secretion was assessed during electrical stimulation of the distal cut ends of both vagal nerves. In overnight fasted anesthetized rats the distal ends of the bisectioned cervical vagi were stimulated with 10V, 5Hz, 5 msec for 15 min. Vagal stimulation elicited an increase of gastric acid secretion by 5.6 mumol/min. Naloxone (1 mumol/kg.h) augmented gastric acid secretion significantly. Since this effect of naloxone was in contrast to previous data possible mechanisms of action of naloxone were examined that might help to explain this apparently inhibitory action of endogenous opioids on vagally-induced gastric acid secretion. The additional infusion of atropine or hexamethonium abolished the stimulatory effect of naloxone on vagally-induced acid secretion completely indicating that the action of naloxone depends on cholinergic background activity. Combined blockade of alpha- and beta-adrenergic receptors with phetolamine and propanolol reduced vagally-induced acid secretion in controls and during naloxone to a similar degree. Both adrenergic blocking agents also reduced the residual acid secretion observed during atropine or atropine + naloxone infusion. Measurements of plasma gastrin levels suggested that the naloxone-induced changes of acid secretion were not due to alterations of gastrin secretion. In summary these data demonstrate that vagally-induced acid secretion in anesthetized rats is largely due to cholinergic mechanisms with a small but separate contribution of adrenergic mechanisms. Endogenous opioids are activated during peripheral vagal stimulation attenuating vagally-induced acid secretion by modulation of cholinergic but not adrenergic mechanisms.

Animals↗
PubMed1988

Modulatory effect of glucose on VIP-induced gastric somatostatin release.

The present study was designed to examine the effect of increasing perfusate glucose concentrations on vasoactive intestinal peptide (VIP)-induced somatostatin (SLI) release from the isolated rat stomach. The stomach of overnight-fasted rats was perfused with Krebs-Ringer buffer containing 100, 150, or 200 mg/dl glucose, respectively. VIP was administered at 10(-12), 10(-11), 10(-9), and 10(-8) M. At a normal glucose concentration of 100 mg/dl, VIP at doses of 10(-12), 10(-11), and 10(-9) M elicited a small inhibitory effect on SLI release by 200-300 pg/min (P less than 0.01). As reported previously at 10(-8) M, VIP stimulated gastric SLI secretion by 500 pg/min (P less than 0.01). Increasing perfusate glucose to 150 mg/dl resulted in a stimulation of SLI release by all four concentrations of VIP with a maximal effect at 10(-9) M. During 200 mg/dl glucose, VIP had no effect in concentrations below 10(-9) M, and only the two highest doses (10(-9) and 10(-8) M) stimulated SLI release significantly. In the absence of VIP, glucose had no effect on gastric SLI release. In conclusion, the present data demonstrate for the first time that at normal glucose levels VIP has not only stimulatory but also inhibitory effects on gastric SLI, and second, a modest elevation of glucose has a modulatory effect on gastric D-cell function.

Animals↗
PubMed1988

Effect of somatostatin on skin lesions and concentrations of plasma amino acids in a patient with glucagonoma-syndrome.

A case of glucagonoma syndrome in a 58-year-old male patient who had the typical skin lesions associated with severe hypoaminoacidemia is described. The decrease in amino acids has been proposed to be causally related to the dermatosis. Furthermore, it has been shown previously that somatostatin rapidly improves skin lesions in glucagonoma patients. Therefore, plasma amino acid levels were determined before and during an infusion of somatostatin prior to surgical removal of the tumor in the tail of the pancreas. During somatostatin infusion in combination with total parenteral nutrition, 10 out of 22 amino acids were in the normal range. Thus it seems unlikely that normalization of amino acid levels is responsible for the rapid improvement in skin lesions in glucagonoma patients. On the other hand it cannot be excluded that partial normalization of amino acids contributed to the observed healing process. Nevertheless, somatostatin administered prior to surgery is a useful therapeutic regimen in these patients.

Adenoma, Islet Cell↗
PubMed1988

Effect of atrial peptide on gastric acid secretion in rats.

The effect of synthetic rat atriopeptin (AP) II was examined on basal, vagally and carbachol-induced gastric acid secretion in anesthetized rats. AP II infusion, at stepwise increasing doses of 2, 20 and 100 ng/kg/min, had no effect on basal acid secretion. At doses of 2 and 20 ng/kg/min, AP II augmented vagally induced acid secretion significantly. The secretory response to vagal stimulation + AP II 20 ng/kg/min was completely abolished by atropine. In contrast a higher dose of AP II (50 ng/kg/h) reduced vagally induced acid secretion significantly. This dose of AP II also reduced acid secretion during direct cholinergic stimulation by carbachol, while the lower dose of 20 ng/kg/min had no effect on carbachol-induced acid secretion. The present data demonstrate for the first time an effect of atrial peptide on gastric acid secretion. At lower doses AP II augments the vagal influence on parietal cell function perhaps by augmenting vagally induced acetylcholine release. At higher doses AP II exerts an inhibitory effect on parietal cell function during vagally and carbachol-induced acid secretion, suggesting different and as yet unknown mechanisms of action. These results raise the possibility that the heart can exert a hormonally mediated influence on the regulation of gastric acid secretion.

Animals↗
PubMed1988

Antral mucosal bile acids in two types of chronic atrophic gastritis.

Bile acids may damage the gastric mucosa, and they are cocarcinogenic in experimental colonic and gastric cancer. Chronic atrophic gastritis (CAG) and chronic atrophic gastritis with intestinal metaplasia (CAGIM) are associated with gastric carcinoma. We, therefore, analysed bile acids in the antral mucosa in controls (n = 10), in patients with CAG (n = 12) and CAGIM (n = 20). In both forms of chronic antral gastritis, total mucosal bile acid concentrations drop, caused mainly by lower primary bile acids. The proportions of secondary bile acids rise, in particular of toxic lithocholic acid. This is probably caused by bacterial activity in the stomach. Whether secondary bile acids, especially lithocholic acid, alone or in combination with other bacterial degradation products, influence gastric carcinogenesis remains to be elucidated in further studies.

Adult↗