Effect of ethanol on acid secretion by isolated gastric glands from rabbit.

Isolated gastric glands from rabbit, as well as basolateral and microsomal membranes derived therefrom, were used to examine the effect of ethanol on several parameters related to acid secretion. Low concentrations of ethanol, 0.2%-5% (vol/vol), had no effect on basal aminopyrine accumulation by isolated gastric glands but significantly potentiated aminopyrine accumulation stimulated by histamine. In contrast, this dose range of ethanol inhibited aminopyrine accumulation stimulated by forskolin or dibutyryl-cyclic adenosine monophosphate. This dose range of ethanol produced a similar effect on adenylate cyclase activity of basolateral membranes from isolated gastric glands, with potentiation of histamine stimulation and inhibition of forskolin stimulation. Low-dose ethanol was found to produce increased proton permeability of the apical membrane of the parietal cell but had no effect on hydrogen-potassium-stimulated adenosine triphosphatase activity. Ethanol (10%) significantly inhibited all parameters of acid secretion studied. Ethanol has a biphasic effect on acid secretion with potentiation of histamine-stimulated aminopyrine accumulation and adenylate cyclase activity at low doses and inhibition of all parameters of acid secretion at high doses.

Effect of acetazolamide on rat gastric mucosal protection and stimulated bicarbonate secretion with 16,16-dimethyl PGE2.

The effect of pretreatment with acetazolamide, a carbonic anhydrase inhibitor, was studied on the mucosal protection provided by and the gastric alkaline secretion stimulated by 16,16-dimethyl prostaglandin E2. Using a model employing a chamber of the rat whole stomach, 16,16-dimethyl prostaglandin E2 (1 microgram/ml) was found to significantly (p less than 0.05) increase the secretion of bicarbonate by 31.1 +/- 4.1 mu Eq/hr over basal values. This stimulated secretion was inhibited (to 18.0 +/- 2.2 mu Eq/hr) by pretreatment with acetazolamide (50 mg/kg body weight). In a separate series of experiments, the ability of this concentration of 16,16-dimethyl prostaglandin E2 to protect the rat stomach from necrosis caused by absolute ethanol was not impaired by prior exposure to the same dose of acetazolamide.

Effect of adrenalectomy on prostaglandin protection of the rat gastric mucosa.

Prostaglandins can prevent damage to gastric mucosa by agents such as Aspirin and ethanol, but their mechanism of action is not known. The authors examined the role of the adrenal gland in prostaglandin protection. Fifty, male Wistar rats were subjected to bilateral total adrenalectomy or sham operation. Adrenalectomized rats with circulating cortisol were discarded. After allowing 2 weeks for recovery, the authors measured the susceptibility of the gastric mucosa to injury by ethanol in an ex-vivo chamber of the entire stomach. This model permits the mucosa to be bathed by a series of solutions and the damage to be measured by planimetry. Mucosal damage was induced by applying 40% ethanol for 10 minutes. The prostaglandin used was 16,16-dimethyl prostaglandin E2 (10 micrograms) given for 10 minutes before the ethanol was introduced. The results show that mucosal damage from ethanol is consistently higher in the adrenalectomized rat but that adrenalectomy does not prevent protection by prostaglandin. The authors conclude that the mechanism of prostaglandin protection against ethanol injury is not corticosteroid-dependent.

[Formation of plasmid pBR322 oligomers as depending on a tetracycline concentration]. / Bildung von Oligomeren des Plasmids pBR322 in Abhängigkeit von der Tetracyklinkonzentration.

Escherichia coli K12 strains containing the plasmid pBR322 often show varying contents of plasmid oligomers, in which the monomer units are arranged in tandem. When the concentration of the plasmid-selective antibiotic tetracycline in the medium becomes increased selection of cells containing largely higher oligomers occurs. The number of monomer units organized in the oligomers increases with tetracycline concentration. recA- mutants are unable to generate oligomers under the same conditions and show lower tetracycline resistance. This observations suggest a selective advantage of oligomer containing cells in the presence of tetracycline as a result of higher gene dosage. But E. coli cells transformed with monomers, dimers, trimers, as well as tetramers of pBR322 are characterized by roughly the same plasmid DNA content as well as plasmid coded beta-lactamase and resistance to tetracycline.

Percutaneous antegrade biliary drainage: a nonoperative approach to biliary obstruction.

Twenty-seven patients underwent percutaneous antegrade biliary drainage for obstructive jaundice. The serum bilirubin levels was elevated in all patients. Generalized pruritus was a major complaint. Twenty of the patients had had a laparotomy for malignant disease. Of the 24 patients in whom this method of drainage was successful, the obstructing lesion was found at the porta hepatis in 12 and in the extrahepatic bile ducts in 12. Metastatic disease was the commonest cause of obstruction. Following drainage the serum bilirubin level fell from a mean of 21.4 mg/dl (366 mumol/l) to a mean of 4.1 mg/dl (70.1 mumol/l) within a week. Pruritus was relieved. The major complications were transient cholangitis in five patients and inadvertent dislodgement of the catheter in four. In three of these patients another catheter was reinserted with ease. There was no peritonitis or uncontrolled bleeding. Twenty-one patients were able to leave hospital. Their mean survival time was 7.3 months. A multiperforated catheter manipulated through the obstruction has the advantage of permitting bile flow into the duodenum (antegrade) in contrast to external drainage (retrograde) by T- or U-tubes. Although the mean survival time with this method is similar to that with insertion of drainage tubes at the time of laparotomy, morbidity and mortality are reduced; this is important in view of the poor prognosis of bile duct obstruction due to malignant disease.