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Biomedical subjects

A Tarnawski

Publications and source records attributed to A Tarnawski.

At least 127 records · Page 7Linked to original sources
PubMed1982

Effect of secretin on gastric parietal cell ultrastructure in man.

The effect of secretin on parietal cell ultrastructure and on gastric mucosal potential difference have not been reported. In five healthy subjects, we studied the effect of intravenous injection of 2 clinical units per kg. of secretin on parietal cell canalicular and tubulovesicular membrane areas. In addition, we studied the effect of secretin on serum secretin levels and gastric mucosal potential difference. Biopsies of gastric mucosa for light and electron microscopy were obtained prior to and 15 and 30 minutes after secretin injection. Electron micrographs of 140 parietal cells were analyzed by the Loud quantitative method. Fifteen minutes following secretin administration, parietal cell canalicular membrane area decreased from a basal value of 4.37 +/- 0.43 per cent to 3.17 +/- 0.28 per cent (p less than 0.01). The number and length of microvilli also significantly decreased. Tubulovesicular membrane area increased from 9.32 +/- 0.7 per cent to 9.74 +/- 0.6 per cent (p greater than 0.05). The effect of secretin on canalicular membrane area was short lived, with recovery to nearly basal level at 30 minutes. Nuclear membrane area did not change at 15 and 30 minutes after secretin. After injection, serum secretin increased from a mean basal value of 15 to 2800 pg. per ml. at 15 minutes, falling to 130 pg. per ml. at 30 minutes. Gastric potential difference following secretin injection rose from -43 +/- 2 mv. to -54 +/- 2 mv. (p less than 0.01) within 10 minutes. In conclusion, a pharmacologic dose of secretin alters gastric parietal cell ultrastructure and causes significant elevation of gastric mucosal potential difference.

Adult↗
PubMed1981

Ethanol induced duodenal lesions in man. Protective effect of prostaglandin.

This study aimed: 1. to investigate quantitatively mucosal changes in the human duodenum after ethanol instillation, 2. to determine the effect of 16,16 dimethyl prostaglandin E2 (dmPGE2) pretreatment on these changes. In 11 healthy subjects were instilled into the postbulbar duodenum solutions of normal saline or dmPGE2 and 15 minutes later 20 ml 40% ethanol. Mucosal changes were evaluated endoscopically and histologically. Thirty minutes after ethanol and saline, hemorrhagic changes involved the entire mucosa (endoscopic lesion index: 4.8 +/- 0.2) and all histological specimens showed erosions. Pretreatment with dmPGE2 significantly prevented ethanol-induced mucosal changes (endoscopic lesion index: 2.17 +/- 0.17 p less than 0.01) and mucosal biopsies did not show erosions outside endoscopically abnormal areas. In conclusion, direct instillation of ethanol induced consistent damage to duodenal mucosa in man. This damage was significantly reduced by dmPGE2 pretreatment.

Adult↗
PubMed1981

Fine-morphology of chief cells in human gastric mucosa after secretin.

Quantitative ultrastructural studies of human gastric mucosal chief cells during secretory stimulation have not been reported previously. In five healthy subjects we studied the effect of intravenous administration of 2 CU/kg of GIH secretin on gastric chief-cell ultrastructure. Gastric biopsies for quantitative ultrastructural analysis were obtained before and 15 and 30 min after secretin administration. Electron micrographs of 150 chief cells were analyzed by the Loud quantitative method. After secretin administration the percentage area occupied by zymogen granules decreased significantly at 15 and 30 min. At corresponding times membrane profile concentration (rough endoplasmic reticulum) increased significantly over basal values. This study provides morphological evidence of increased activity of chief cells after secretin administration.

Adult↗
PubMed1981

Effect of glucagon on human gastric mucosa: histochemical studies.

We studied the effects of glucagon (2 mg intravenously) on the histochemical localization and staining intensity of 10 enzymes in human gastric mucosa. Glucagon caused a significant increase in the histochemical activity of glucose-6-phosphate dehydrogenase in the undifferentiated neck cells and mucous cells of the foveolae and of ATPase activity in and around the mucosal capillary walls. Glucagon also stimulated mucus secretion from the surface epithelial cells. These changes were observed 15 and 30 min after glucagon in the oxyntic, but no pyloric mucosa. they indicate that glucagon, in addition to its effect on parietal cells, also affects other structures in human gastric mucosa.

Adenosine Triphosphatases↗
PubMed1981

Prostaglandin protection of carbon tetrachloride-induced liver cell necrosis in the rat.

We studied whether 16,16--dimethyl prostaglandin E2 (dmPGE2) may prevent acute liver damage induced by carbon tetrachloride (CCl4) in the rat. One hundred thirty male rats were divided into the following groups: (1) controls, (2) rats given CCl4 6670 mg/kg body wt subcutaneously, (3) rats pretreated with 5 micrograms/kg dmPGE2 given subcutaneously 30 min before, and 8 and 24 h after CCl4 administration, and (4) animals given dmPGE2 only as in group 3. Liver damage was assessed by biochemical studies (SGPT, serum alkaline phosphatase, and bilirubin) and by histology. In rats receiving CCl4 alone, SGPT activities were significantly elevated to 1024 +/- 82 U/L, 1270 +/- 120 U/L, 386 +/- 48 U/L and 208 +/- 20 U/L at 24, 48, 96, and 120 h after CCl4 respectively. In animals pretreated with dmPGE2 before CCl4, SGPT activities were 201 +/- 24 U/L, 55 +/- 4.6 U/L, 28 +/- 4 U/L, and 24 +/- 4 U/L at 24, 48, 96, and 120 h after CCl4, respectively (p less than 0.01, versus animals receiving CCl4 only). Histologically, livers of rats treated with CCl4 alone showed severe centrilobular necrosis at 24 and 48 h. Livers of animals pretreated with dmPGE2 before CCl4 did not show necrosis. It is concluded that dmPGE2 protects the liver against cell necrosis induced by CCl4 in the rat.

16,16-Dimethylprostaglandin E2↗
PubMed1980

Effect of human gastrin infusion on gastric potential difference in man.

Human gastrin I heptadecapeptide, infused intravenously to healthy volunteers in a dose of 0.5 micrograms/kg/hr, caused a prompt, significant reduction in gastric potential difference (decrease of mucosal negativity), with the peak change at 6 min. This decline in potential difference occurred at a time when the serum gastrin level was between 24 and 83 pg/ml; at the same time, scanning electron microscopic examination of fractographs of parietal cells demonstrated marked increase in canalicular membrane area. This study shows that the decrease in potential difference after gastrin occurs with serum gastrin levels which are in the physiologic range.

Action Potentials↗
PubMed1980

Quantitative ultrastructural analysis of the human parietal cell during acid inhibition and increase of gastric potential difference by glucagon.

Glucagon inhibits gastric acid secretion and increases the negativity of gastric mucosal potential difference (PD) in man. To test the hypothesis that the increased negativity of PD after glucagon in man could be due to decreased parietal cell canalicular membrane area, a quantitative ultrastructural analysis was carried out. Four healthy volunteers with normal gastric mucosa were submitted to biopsy before and 20 minutes after intravenous injection of 2 mg glucagon (G). This time corresponded with the maximal change in PD and a decrease in gastric acid secretion. Canalicular and tubulovesicular membrane area of 80 parietal cells (40 cells before glucagon and 40 cells after glucagon) were quantified by the Loud morphometric method. After glucagon, the oxyntic cell canalicular membrane area was reduced by one-fourth (P less than 0.05), while tubulovesicular membrane area showed an increase (P less than 0.05) at the same time. The decrease in the area of parietal cell canalicular membrane caused by glucagon may in part be responsible for increased negativity of the gastric PD caused by this hormone.

Adult↗
PubMed1980

Cytoprotective effect of 16, 16' dimethyl prostaglandin E2 and some drugs on an acute galactosamine induced liver damage in rat.

Present experiment was aimed to study whether 16, 16' dimethylprostaglandin E2 (dmPGE2), Hepatofalk (HF), or Orotofalk (OF) may prevent an acute liver damage induced in rats with D-galactosamine (GalN). Fifty male rats were divided into 5 groups: 1. controls, 2. rats receiving GalN 750 mg/kg b. w. intraperitoneally, 3. animals pretreated with 5 microgram/kg dmPGE2 given subcutaneously 24 hours prior to, 30 min prior to and 6 hours after GalN. Rats of group 4 received HF 0,8 ml/kg intramuscularly and group 5 OF 0,3 caps/kg intragastrically 24 hours prior to, 30 min prior to and 6 hours after GalN. Animals were sacrificed 24 hours after GalN injection. Histological, histochemical and ultrastructural studies of the liver were performed. In rats receiving GalN alone (group 2) typical severe liver damage consisting of acidophilic necrosis of hepatocytes, periportal and intralobular inflammatory infiltration, hypertrophy and hyperplasia of Browicz-Kupffer cells has been observed. Histochemical investigations showed in this group fatty degeneration and a decrease in glycogen content in hepatocytes, irregular distribution of lysosomes, numerous cytolysosomes and uneven decrease in lysosomal enzymes activity (acid phosphatase and beta-glucuronidase). Ultrastructural studies revealed depletion in glycogen, fat droplets, hypertrophy of smooth endoplasmic reticulum and numerous autophagic vacuoles. Some of these vacuoles or residual bodies were dropping out into intercellular space. Focal accumulation of lamellar cytomembranes as well as condensation of heterochromatin in nuclei were also observed. Pretreatment of animals with dmPGE2 (group 3), HF (group 4) or OF (group 5) prior to GalN prevented liver cell necrosis. Histological, histochemical and ultrastructural picture of the liver was in these groups close to normal. Only very slight hypertrophy and hyperplasia of Browicz-Kupffer cells, was seen as well as depletion of glycogen and hypertrophy of smooth endoplasmic reticulum in hepatocytes. We conclude dmPGE2, HF and OF offered impressive cytoprotection against GalN induced liver damage in rat.

16,16-Dimethylprostaglandin E2↗
PubMed1980

The induction of gastric mucosal tolerance to alcohol by chronic administration.

Acute alcohol intake produces marked damage to gastric mucosa. Whether gastric mucosa develops tolerance to repeated alcohol administration is unknown. To test this, we compared the effects of acute and chronic alcohol administration in male rats. Thirty-one Sprague-Dawley rats maintained on Chow diet received the following: group A, water for 4 weeks; group B, 50% EtOH for 4 weeks; group C, water for 4 weeks, then 8 hr prior to sacrifice 50% EtOH; group D, 50% EtOH for 4 weeks, then alcohol 8 hr prior to sacrifice. Control animals did not show macroscopic or microscopic changes in fundic or pyloric mucosa. The percentage fundic mucosa showing lesions (49%) in the acute EtOH group (group C) was significantly greater than in control (0%), chronic EtOH group (group B, 8%), and chronic plus acute EtOH (group D, 14%). Pyloric lesions were not significantly diferent between treatment groups C (9%), B (4%), and D (8%). Histologic changes in group C (acute alcohol) consisted of superficial erosions accompanied by severe hemorrhagic changes in the upper part of the gastric mucosa. In group B (chronic alcohol) and group D (chronic + acute alcohol) changes consisted of small superficial erosions without hemorrhagic changes. Our study shows that damage in rat gastrc fundic mucosa following acute intragastric administration of EtOH is significantly less in rats receiving EtOH chronically than in rats receiving only acute EtOH. We conclude that rat gastric mucosa is capable of developing tolerance to repeated administration of 50% alcohol.

Adaptation, Physiological↗