Rectal mucosal prostaglandin E2 release and its relation to disease activity, electrical potential difference, and treatment in ulcerative colitis.

The forces that drive transfer of solutes between maternal blood and embryo in early human pregnancy are poorly understood. The aim of this study was to determine whether there is an electrical potential difference (PD) between maternal blood and the exocelomic cavity and between maternal blood and the amniotic cavity in the normal human conceptus at or before 10 wk of pregnancy. We measured PD between a saline-filled catheter in a forearm vein of women undergoing termination of pregnancy for psychological reasons in the first trimester and a second saline-filled catheter in the exocelomic cavity or amniotic cavity of their conceptus. The mean (±SE) maternal blood/exocelomic cavity PD in eight women was 8.7 ± 1.0 mV and the mean maternal blood/amniotic cavity PD in four of the women was 6.7 ± 1.3 mV, embryo side negative for both sets of measurement. These data show that there is a PD between maternal and embryonic extracellular fluid in the first trimester that will directly influence exchange of ions between the two compartments.

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Changes in electrical potential difference of rectal mucosa and of gallbladder bile constituents of dogs fed chenodeoxycholic acid

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y86-190 ◽

1986 ◽

Vol 64 (8) ◽

pp. 1115-1118

Author(s):

J. Patrick Shoenut

Keyword(s):

Chenodeoxycholic Acid ◽

Dose Group ◽

Low Dose ◽

Electrical Potential ◽

Rectal Mucosa ◽

Gallbladder Bile ◽

Potential Difference ◽

Control Group ◽

Electrical Potential Difference ◽

Dissolution Studies

Eighteen dogs were studied for 54 days. Rectal mucosal electrical potential difference (PD), gallbladder bile acids, cholesterol, and phospholipids were measured. It was shown that feeding chenodeoxycholic acid (CDCA) for 24 days in dosages of 15, 30, and 60 mg/kg of body weight, all depressed PD equally but significantly (P < 0.05) in three groups of dogs compared with a control group. This depression was reversible 24 days after CDCA ingestion ceased in the two highest dosages. The low dose group was sacrificed after 24 days of CDCA feeding and the gallbladder bile was analyzed. CDCA and cholesterol were each significantly (P < 0.05) elevated over control values in the gallbladder bile of these dogs. Phospholipids were not significantly changed. The PD, a reflection of Na+–K+ ATPase activity, may be a useful indicator in maximizing dosages of CDCA in gallstone dissolution studies.

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Stimulation of HCO3- transport in isolated proximal bullfrog duodenum by prostaglandins

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1980.239.3.g198 ◽

1980 ◽

Vol 239 (3) ◽

pp. G198-G203 ◽

Cited By ~ 4

Author(s):

G. Flemstrom

Keyword(s):

Electrical Potential ◽

Potential Difference ◽

Electrical Potential Difference ◽

Morphological Examination ◽

Minimal Concentration ◽

Dependent Transport ◽

Dose Dependent Increase ◽

Dose Dependent ◽

Stimulation Of

An in vitro preparation of proximal duodenum from the bullfrog transported alkali into the luminal solution (approximately 1 mueq x h-1 x cm-2) and generated a transepithelial electrical potential difference (5-10 mV, lumen negative). Transport was inhibited by 2,4-dinitrophenol (10(-5) M), CN- (5 X 10(-3) M), indomethacin (5 X 10(-5) M), and acetazolamide (5 X 10(-3) M) indicating that metabolism is required. Both alkali transport and the electrical potential difference showed a dose-dependent increase on administration of the prostaglandins E2, 16,16-dimethyl E2, and F2 alpha. The minimal concentration stimulating transport was lower with the E-type prostaglandins (10(-8) M than with F2 alpha (10(-6) M), and the former also produced greater maximal responses. In addition to metabolic-dependent transport of alkali, there was passive transmucosal migration of HCO3-, amounting to approximately 40% of basal (unstimulated) transport and sensitive to variation of the transmucosal hydrostatic pressure. Morphological examination showed that the preparation is devoid of Brunner glands. Stimulation of duodenal epithelial HCO3- transport by prostaglandins may contribute to their previously demonstrated ability to prevent duodenal ulceration.

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