Changes in electrical potential difference and sodium–potassium ATPase of canine mucosa after jejunal–ileal bypass surgery

1983 ◽  
Vol 61 (5) ◽  
pp. 512-515
Author(s):  
G. R. Grahame ◽  
J. P. Shoenut ◽  
S. Takeo ◽  
G. P. Sharma
Keyword(s):  
Atpase Activity ◽  
Bypass Surgery ◽  
Electrical Potential ◽  
Rectal Mucosa ◽  
Close Correlation ◽  
Potential Difference ◽  
Electrical Potential Difference ◽  
Sodium Potassium ◽  
Potassium Atpase ◽  
Ileal Bypass

Changes in electrical potential difference and sodium–potassium ATPase activity of rectal mucosa in dogs were examined before and after jejunal–ileal bypass surgery. The potential difference in the postoperative period was significantly higher (P < 0.05) than the preoperative value. The potential difference increased by 160% at the 3rd day after the surgery, and then gradually declined with prolonged recovery periods. Ouabain-sensitive sodium–potassium ATPase activity also increased at the 3rd day (160%) and at the 10th day (86%) after the surgery. Fourteen days after the surgery the sodium–potassium ATPase activity returned almost to the preoperative value. These results indicated a close correlation between changes in transmucosal potential difference and sodium–potassium ATPase activity of rectal mucosa, suggesting a significant participation of sodium–potassium ATPase in changes of potential difference induced by jejunal–ileal bypass surgery.

Sodium Potassium ATPase Activity in Human Rectal Mucosa With and Without Renal Insufficiency

1985 ◽  
Vol 5 (3) ◽  
pp. 177-181 ◽  
Author(s):  
Ronald J. Hené ◽  
Peter Boer ◽  
Hein A. Koomans ◽  
Evert J. Dorhout Mees
Keyword(s):  
Renal Insufficiency ◽  
Atpase Activity ◽  
Rectal Mucosa ◽  
Sodium Potassium ◽  
Potassium Atpase

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

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.

THE EFFECT OF ALDOSTERONE AND ADRENALECTOMY ON THE ELECTRICAL POTENTIAL DIFFERENCE OF RAT COLON AND ON THE TRANSPORT OF SODIUM, POTASSIUM, CHLORIDE AND BICARBONATE

1967 ◽  
Vol 39 (4) ◽  
pp. 517-531 ◽  
Author(s):  
C. J. EDMONDS ◽  
JANE C. MARRIOTT
Keyword(s):  
Electrical Potential ◽  
Latency Period ◽  
Potential Difference ◽  
Rat Colon ◽  
Electrical Potential Difference ◽  
Bicarbonate Secretion ◽  
Sodium Potassium ◽  
Ionic Fluxes ◽  
Descending Colon ◽  
Adrenalectomized Rats

SUMMARY The effect of adrenalectomy on the increase of the transmucosal potential difference (p.d.) of the colon of the rat induced by Na depletion, together with the action of aldosterone on the p.d. and on colonic Na+ and Cl− transport, and K+ and bicarbonate secretion have been investigated. Adrenalectomy increased the Na+ content in the stool, an effect reversed by treatment with aldosterone. When Na+-depleted rats were adrenalectomized and maintained on cortisone, the elevated p.d. fell to levels below those found in normal rats. Aldosterone given intravenously (i.v.) in physiological doses increased the p.d. in normal, adrenalectomized and Na+-depleted adrenalectomized rats after a latency period of 80–110 min., and the p.d. tended to rise further when injections were continued for several days. The p.d. gradient along the colon after treatment with aldosterone was similar to that of Na+-depleted rats, the highest p.d. being at the distal end of the descending colon. Cortisol intravenously increased the p.d. but the effect was small in comparison with that of aldosterone. Measurement of ionic fluxes in the descending colon of adrenalectomized rats showed that treatment with aldosterone produced an increase in Na+ and water absorption, and in K+ secretion, but had no effect on bicarbonate secretion. The effects of aldosterone on the transmucosal p.d. and ion transport were similar to those of Na+ depletion.

Adenosine Receptor Modulation of Hypoxic-ischemic Injury in Striatum of Newborn Piglets

2020 ◽  
Vol 17 (4) ◽  
pp. 510-517
Author(s):  
Santiago Ortega-Gutierrez ◽  
Brandy Jones ◽  
Alan Mendez-Ruiz ◽  
Pankhil Shah ◽  
Michel T. Torbey
Keyword(s):  
Oxidative Stress ◽  
Atpase Activity ◽  
Neuronal Injury ◽  
Receptor Activation ◽  
Adult Mortality ◽  
Vehicle Group ◽  
Sodium Potassium ◽  
Receptor Modulation ◽  
A2a Receptor ◽  
Potassium Atpase

Background: Hypoxic-ischemic encephalopathy (HIE) is a major cause of pediatric and adult mortality and morbidity. Unfortunately, to date, no effective treatment has been identified. In the striatum, neuronal injury is analogous to the cellular mechanism of necrosis observed during NMethyl- D-Aspartate (NMDA) excitotoxicity. Adenosine acts as a neuromodulator in the central nervous system, the role of which relies mostly on controlling excitatory glutamatergic synapses. Objective: To examine the effect of pretreatment of SCH58261, an adenosine 2A (A2A) receptor antagonist and modulator of NMDA receptor function, following hypoxic-ischemia (HI) on sodium- potassium ATPase (Na+, K+-ATPase) activity and oxidative stress. Methods: Piglets (4-7 days old) were subjected to 30 min hypoxia and 7 min of airway occlusion producing asphyxic cardiac arrest. Groups were divided into four categories: HI samples were divided into HI-vehicle group (n = 5) and HI-A2A group (n = 5). Sham controls were divided into Sham vehicle (n = 5) and Sham A2A (n = 5) groups. Vehicle groups were pretreated with 0.9% saline, whereas A2A animals were pretreated with SCH58261 10 min prior to intervention. Striatum samples were collected 3 h post-arrest. Sodium-potassium ATPase (Na+, K+-ATPase) activity, malondialdehyde (MDA) + 4-hydroxyalkenals (4-HDA) and glutathione (GSH) levels were compared. Results: Pretreatment with SCH58261 significantly attenuated the decrease in Na+, K+-ATPase, decreased MDA+4-HDA levels and increased GSH in the HI-A2A group when compared to HIvehicle. Conclusion: A2A receptor activation may contribute to neuronal injury in newborn striatum after HI in association with decreased Na+, K+-ATPase activity and increased oxidative stress.

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