laxative



References: Laxative






J Pharm Pharmacol. 1993 Nov;45(11):951-4.
Sennoside-induced secretion is not caused by changes in mucosal permeability or Na+,K(+)-ATPase activity.

Leng-Peschlow E.

Department of Pharmacology, Madaus AG, Koln, Germany.

The effect of sennosides (50 mg kg-1) on the rat colon in-situ was studied 6 h after oral treatment when the laxative effect was maximal. In a second experiment, rhein (4 x 10(-3) M), an active sennoside metabolite, was administered into the lumen of the colon for 1 h. Both sennosides and rhein reduced net H2O and Na+ absorption or reversed it to net secretion. Paracellular permeability, as measured using erythritol as a small marker molecule, was increased 2- to 3-fold; permeability to a large molecule, PEG 1000, was unchanged. The activity of Na+,K(+)-ATPase in the colon mucosa was not affected. There was no damage of the epithelial cells as determined by lactic acid dehydrogenase release. These results indicate that neither inhibition of Na+,K(+)-ATPase nor damage of the colon epithelium are involved in the secretory effect of sennosides or rhein. The increased paracellular permeability of small molecules fits into the concept of stimulation of active chloride secretion by sennosides, which is electrochemically and osmotically balanced by an increase in Na+ and H2O flow via the paracellular pathway.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7908035&dopt=Abstract constipation laxative



Arch Fr Pediatr. 1993 Nov;50(9):755-62.
[Severe complications and mortality in mental eating disorders in adolescence. On 99 hospitalized patients]

[Article in French]

Alvin P, Zogheib J, Rey C, Losay J.

Travail du Service de Medecine pour Adolescents, Departement de Pediatrie, C.H.U. Bicetre, Le Kremlin-Bicetre.

BACKGROUND. Subclinical medical complications frequently occur during the follow-up of anorexia nervosa and bulimia. This paper describes some of these. POPULATION AND METHODS. Charts of 99 adolescent patients (89 girls and 10 boys), aged 11.8 to 22 years (mean: 16.6 +/- 2.1 years), admitted for anorexia nervosa (N:92) or bulimia (N:7), were analyzed retrospectively. All severe or potentially severe, clinical and non-clinical, findings at admission were included in the study. RESULTS. Anorexic patients had a mean weight loss of 31.5% (22 of them were also vomiters or laxative abusers). Initial nasogastric tube feeding was necessary in 19 patients and parenteral nutrition in 2. Bradycardia and hypotension were common. A variety of ECG abnormalities were seen in 86% of the patients. Mitral valve prolapse was present in 14 of the 43 patients examined by echocardiography. Electrolyte imbalance was also common: hyponatremia in 7 patients, hypokalemia in 21, hypochloremia in 10 of the 12 vomiters, hypophosphatemia in 7, hyperazotemia in 24 and hypoglycemia in 22. Bone marrow hypoplasia was frequent, with leukopenia in 29 patients, anemia in 21 and thrombocytopenia in 5. No patient developed infectious complications. One patient presented with an acute gastric dilatation and another with spontaneous pneumomediastinum. One patient, 14 year-old, died 3 years after the onset of anorexia from acute water intoxication. CONCLUSION. These well-known complications are more common in anorexic than in bulimic patients. Their prevention requires rigorous and continuous medical supervision.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8060204&dopt=Abstract constipation laxative



J Pharm Pharmacol. 1993 Jan;45(1):59-62.
Stimulation of enterocyte protein kinase C by laxatives in-vitro.

Beubler E, Schirgi-Degen A.

Department of Experimental and Clinical Pharmacology, Karl-Franzens-University, Graz, Austria.

To elucidate the role of protein kinase C in the mechanism of action of stimulatory laxatives, experiments were performed with preparations of rat lysed enterocytes. The phorbol ester 4-beta-phorbol 12-myristate 13-acetate (PMA) concentration-dependently (2-200 micrograms mL-1) stimulated the activity of protein kinase C in this preparation. Ricinoleic acid, the active principle of castor oil, deacetylbisacodyl, the active principle of bisacodyl, and deoxycholic acid exerted the same effect, although less efficiently. This reflects their potency for inducing intestinal fluid secretion and prostaglandin release, effects that are also induced more potently by PMA. Accordingly, the potency of the three C18 fatty acids, ricinoleic acid, stearic acid and oleic acid on protein kinase C activity in-vitro, on prostaglandin E2 release and on net fluid secretion in-vivo runs in parallel. It is therefore concluded that stimulatory laxatives activate protein kinase C, leading to prostaglandin E2 release, thus resulting in net fluid secretion.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8094448&dopt=Abstract constipation laxative



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