Article

Laxatives in the horse - A review of the literature

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Abstract

After spasmodic colics, primary impactions of the large colon and caecum are the most common causes of colic in horses. In many of these cases, laxatives are routinely used in the field to resolve the impaction. Laxatives with different mechanisms of action and molecular composition are mentioned in the relevant literature. In clinical studies, intravenous or enteral fluid therapy seems to have become increasingly popular. However, the traditional use of oral or intragastric laxatives seems to be efficient in many cases and require much less effort and icur much lower financial costs. It is the aim of this paper to give an overview and summarize the results of studies, which have measured the effect of oral or intragastric laxatives in the horse. Where appropriate, results of publications in other species were included. After an introduction of the different classes and individual substances of the laxatives used in the equine species, the reported therapeutic benefits and possible side effects in the horse are described. Most of the literature refers to sodium sulfate (0.5-1 g/kg), magnesium sulfate (Epsom salt; 0.2-1 g/kg), mineral oil (paraffin oil; 0.5-10 ml/kg), dioctyl sodium sulfosuccinate (DSS) and lubricants of plant origin.

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Equine Nutrition and Feeding has become the standard work on the subject, covering every aspect of the nutrition of breeding, growing and working horses, describing the basis upon which scientifically derived conclusions for nutrition and dietary requirements are reached. Following the last edition in 1998, the book has been extensively updated, revised and rewritten with reference to well over 400 papers that have been published since 1998 on equine science. It has been made more practical by setting out the implications of new research for feeding programmes and it includes a full account of the toxicology and metabolic and other diseases, related to diet. Their causes and control are discussed and comprehensive lists of definitions of the terms and abbreviations used are given.
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Article
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Article
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Article
Dioctyl sodium sulfosuccinate (DSS) is an anionic detergent that is used widely as a laxative and promoted as a stool softener. Although many anecdotal reports attest to the laxative and stool softening efficacy of DSS, no controlled trials have been performed to document the effect of DSS on small or large bowel function in humans. We have compared, therefore, the effects of 100 mg of DSS three times daily (the maximum recommended dose) with placebo in a randomized, single blind, crossover study in two groups of subjects. First, 6 healthy ileostomates were studied while they ate a constant diet for 8 days. Dioctyl sodium sulfosuccinate administered for 4 days did not increase the daily ileal output of carbohydrate, total fatty acids, bile acids, nitrogen, or water. Cholesterol excretion was decreased while taking DSS (p less than 0.05). Second, 6 healthy volunteers were studied while eating a constant diet of 20 g of fiber plus 30 radiopaque markers daily so that mean daily transit time could be measured. After equilibration, a 7-day collection of stool was weighed and lyophylized to measure fecal water. Dioctyl sodium sulfosuccinate had no effect on stool weight, stool frequency, stool water, or mean transit time. We conclude that 300 mg/day of DSS does not increase ileal or colonic output of solids or water in healthy human subjects.
Article
An intestinal perfusion technique has been used to investigate the mechanism of action of the laxative, dioctyl sodium sulphosuccinate, in the human jejunum. Dioctyl sodium sulphosuccinate stimulated net secretion of water, sodium, chloride and potassium and inhibited net absorption of glucose and bicarbonate. These changes in water and solute transport were partially reversed by administration of indomethacin (4 mg/kg/day orally for three days), which suggests that they are mediated in part by endogenous prostaglandins.
Article
1. When castor oil was administered by gavage to rats, the duodenum and jejunum but not ileum and colon produced large amounts (5-6 fold greater than control) of platelet activating factor (Paf). 2. Intraluminal release of acid phosphatase (AP) was also markedly increased (5-6 fold greater than control) in the duodenum and jejunum of castor oil-treated rats and there was a correlation between the elevated release of AP and intestinal hyperaemia. 3. These findings support a role for Paf as a mediator of intestinal damage induced by castor oil.
Article
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Article
Intestinal tissues of man, rat, mouse, guinea-pig and rabbit were preincubated with laxatives, homogenised, and incubated with [14C]arachidonic acid. After extraction into chloroform, the eicosanoids were separated by thin layer chromatography. Metabolism of [14C]arachidonic acid into prostaglandins (PGs), and the lipoxygenase products LTB4 and 5-HETE, was stimulated by ricinoleic acid (100 micrograms/ml) or phenolphthalein (100 micrograms/ml), and to a lesser extent by picosulphate (125 micrograms/ml) and sulfosuccinate (200 micrograms/ml). Mannitol (500 micrograms/ml) had no effect. Indomethacin (1 microgram/ml) inhibited the stimulation of PG formation. The dual pathway inhibitor BW755C (1 microgram/ml) reduced the formation of prostaglandins, LTB4 and 5-HETE. In some experiments on rat colon, prostanoids were separated from lipoxygenase products, characterised by their chromatographic mobility and quantitated (relative amounts PGE2 greater than PGF2 alpha greater than TXB2 greater than PGD2). Their formation was enhanced by ricinoleic acid (100 micrograms/ml) and inhibited by either indomethacin or BW 755C (1 microgram/ml). The present results indicate that mammalian isolated gut tissue can convert [14C]arachidonic acid into both cyclo-oxygenase and lipoxygenase products, and support the suggestion that eicosanoids may participate in the laxative effect of some secretagogues.
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We describe a patient who survived a peak serum magnesium level of 9.5 mmol/L (23.0 mg/dL) after an oral cathartic overdose. The patient presented in coma but regained full consciousness over the next six hours with supportive therapy. His serum magnesium had returned to near-normal levels by the following morning at the time of his hospital discharge. This case represents an unprecedented extent of ingestion-related hypermagnesemia in a surviving patient, given that serum levels of more than 8 mmol/L are frequently associated with death from cardiac arrest.
Article
Twenty-five children with chronic constipation underwent serial monitoring of serum beta-carotene, retinol (vitamin A1), and alpha-tocopherol (vitamin E) levels during mineral oil therapy. Mineral oil was administered between meals. Patients were monitored for up to four months of therapy. Mean serum beta-carotene levels fell from 1.0 +/- 0.5 mumol/L (55.7 +/- 26.0 micrograms/dL) to 0.7 +/- 0.4 mumol/L (35.9 +/- 22.1 micrograms/dL) after the first month of mineral oil therapy and remained depressed throughout the remainder of the study. Serum alpha-tocopherol levels remained unchanged throughout the observation period. There was a modest increase in serum retinol levels during the study, especially after three months (from 1.48 +/- 0.84 mumol/L [42.3 +/- 24.1 micrograms/dL] to 2.22 +/- 0.77 mumol/L [63.5 +/- 22.1 micrograms/dL]). We conclude that while a short course of mineral oil can induce a reduction in the serum level of beta-carotene, the treatment has no adverse effect on serum levels of retinol and alpha-tocopherol.
Article
The effect of oral laxatives on the organisation of colonic motor complexes was investigated in four conscious dogs. Six strain gauge transducers were implanted on the colon of each dog. After a control period of two to three hours, dogs were orally dosed with 1, 2, or 4 ml/kg of castor oil, or 0.5 g/kg magnesium citrate. Oral olive oil, 4 ml/kg, was used as control. The recording was continued for another 10 hours or until defecation occurred. Each dog showed spontaneous cyclic bursts of contractions (contractile states) at all recording sites during the control period. Contractile states migrating orad or caudad over at least half the length of the colon were called colonic migrating motor complexes (CMMC). Castor oil and magnesium citrate significantly increased the period of colonic motor complexes, but olive oil had no significant effect. None of the above substances changed the percentage of orad migrating motor complexes, as compared with the control values. Periods in which colonic motor activity was completely absent for at least 60 min over at least three consecutive recording sites occurred more frequently after all of the substances. The occurrence of these periods of inhibition, however, was not a consistent feature and there seemed to be no relationship between the occurrence of inhibitory periods and defecation during the recording period. The dogs defecated within 10 hours after administration of magnesium citrate, 1, 2, and 4 ml/kg of castor oil in 12.5, 25, 37.5, and 88.8% of experiments respectively, but never with olive oil. Defecation was generally accompanied by giant migrating contractions in the colon. We conclude that oral laxatives, magnesium citrate and castor oil have a profound effect on colonic motor complexes and colonic motor activity. The period of CMMC is significantly prolonged after their oral administration because of an increased number of non-migrating motor complexes or periods of inhibition of motor activity.
Article
The effect of bisacodyl on intestinal electrolyte, glucose, and water transport, and transit was studied in 6 healthy volunteers by intestinal perfusion. A 5-lumen tube with an occluding balloon allowed constant perfusion (10 ml/min) of 30 cm of the upper jejunum and a rapid collection of the perfusate free of contaminants. A phenol red bolus was injected into the tube and its passage through the test segment was calculated by dye dilution formula. A 1-hour control period was followed by a test period with 6 mg/h bisacodyl and followed by 2 other 1-hour control periods. Net absorption of Na+ (0.35 +/- 0.08 mmol/min) and water (1.7 +/- 0.6 ml/min) changed to net secretion (Na+ -0.93 +/- 0.3 ml/min; water -6.6 +/- 1.9 ml/min), glucose absorption decreased from 25.4% +/- 1.1 to 6.3 +/- 0.5 mg/min and K secretion was enhanced. 62 +/- 2.1% of bisacodyl was absorbed in the 30-cm jejunal segment. Mean transit time decreased from 8.5 +/- 1 to 4.4 +/- 0.7 min and mean flow rate increased from 8.4 +/- 0.6 16.6 +/- 1.9 ml/min. There was an inverse linear relationship between mean transit time and mean flow rate. All the effects of bisacodyl were fully or at least partially reversible. Volume and calculated radius of the test segment remained constant and did not change under bisacodyl. It is concluded, that the secretory effect of bisacodyl is mainly responsible for the decreased mean transit time rather than a direct effect on motility.
Article
The purpose of this study was to determine some relationships between colonic myoelectric spiking activity and intraluminal propulsion when colonic peristalsis was stimulated by bisacodyl. Myoelectric recordings were obtained in 12 subjects by means of a 50 cm long Silastic tube equipped with four bipolar electrodes fixed at 10-cm intervals. The tube was introduced into the left colon by flexible sigmoidoscopy and the electrodes were located at 50, 40, 30, and 20 cm from the anal verge. A small polyethylene catheter opening at the proximal end of the Silastic tube was used for introducing the laxative into the colon. One hour recording sessions were obtained before and after bisacodyl administration (5 mL of 0.4% solution). The control tracings showed that colonic spiking activity was made of rhythmic stationary bursts that occurred at only one electrode site and of sporadic bursts that were either propagating over the whole colonic segment or nonpropagating. Administration of bisacodyl was followed by complete suppression of the rhythmic stationary activity; a considerable increase in the sporadic spiking activity, propagating as well as nonpropagating; the occurrence of abdominal cramps and urgency to defecate, both associated with the propagating sporadic spike bursts. It is concluded that colonic propulsion induced by bisacodyl may be dependent upon the production of the sporadic bursts, particularly the propagating ones, while the rhythmic stationary bursts do not seem to play a significant role in colonic transit.
Article
Two conjugated bile salts (10 mmol/l sodium glycocholate, 10 mmol/l sodium taurodeoxycholate) and three laxatives (30 mmol/l magnesium sulphate, 10 mmol/l ricinoleic acid, 2 mmol/l dioctyl sodium sulphosuccinate) were tested on seven subjects with no intestinal lesions in 14 experiments by intestinal perfusion of the jejunum. A 25 cm segment was studied. Each solution was perfused at the rate of 10 ml/min. Water and electrolyte fluxes, losses of deoxyribonucleic acid (DNA), and intestinal cell enzyme activity were measured in the fluids collected. All the laxatives and bile salts tested (except sodium glycocholate) induced water and electrolyte secretion, a rise in intraluminal DNA loss, and enzyme activity. It was possible to establish a significant correlation (p less than 0.001) between the amounts of water fluxes and DNA loss under the effect of dioctyl sodium sulphosuccinate and ricinoleic acid.
Article
Surfactants, a group of nonspecific membrane perturbating substances, can cause nerve damage. Various concentrations of the cationic surfactants benzalkonium chloride (BAC) and benzethonium chloride, the anionic surfactants sodium ricinoleate, dioctyl sodium sulfosuccinate and sodium lauryl sulfate and the nonionic surfactant Triton X-100 were applied to the serosal surface of the rat jejunum every 5 min for 0.5 hr and then rinsed off with saline. Thirty days after surfactant application, the treated and an untreated segment of jejunum were removed and examined histologically. All surfactants which were tested significantly reduced the number of ganglion cells in the myenteric plexus. In addition, sodium ricinoleate significantly reduced the number of ganglion cells in the submucosal plexus. Higher concentrations of the cationic agents BAC and benzethonium chloride caused a generalized tissue damage including disruption of the smooth muscle, lymphocytic infiltration, intestinal perforation and death. Using BAC as a prototype surfactant, peptidergic neuron distribution and gut electrical activity were examined. BAC treatment markedly reduced the immunoreactivity of somatostatin, substance P, met-enkephalin and vasoactive intestinal peptide in the myenteric plexus. In addition, the electric properties of the smooth muscle were altered. BAC treatment resulted in an erratic, markedly distorted basic electric rhythm and an alteration in spike potential generation. These studies demonstrate that surfactants in appropriate concentrations selectively ablate the myenteric neurons and alter peptidergic neuron distribution and gut electrical parameters in the rat jejunum.
Article
1. The effects of MgCl2 on the electrical characteristics and sodium and chloride transport in short-circuited rabbit terminal ileum in vitro were studied. 2. Increasing the magnesium concentration from a basal concentration of 1.1 mmol/l to either 2.5 or 10.3 mmol/l (mucosal or serosal addition) resulted in increases in the unidirectional flux of chloride from serosa to mucosa (JCl sm), short-circuit current (SCC) and transmucosal potential difference (p.d.). 3. Increasing the magnesium concentration from a low basal concentration (0.3 mmol/l) to 10.3 mmol/l (mucosal or serosal addition) abolished net sodium absorption and converted net chloride absorption into net secretion, as a result of a decrease in the unidirectional flux of sodium from mucosa to serosa (JNa ms), and increases in the unidirectional fluxes of sodium and chloride from serosa to mucosa (JNa sm and JCl sm). Increases in SCC and p.d. occurred after mucosal, but not serosal, addition of magnesium. 4. Incubation of stripped ileal mucosa with MgCl2 (10.3 mmol/l) did not result in increased mucosal concentrations of cAMP or cGMP. 5. These data suggest that at least part of the carthartic effect of magesium salts is likely to result from marked changes in ileal ion transport and provide a rational explanation for the watery diarrhoea commonly seen after the oral administration of magnesium salts to hypomagnesaemic patients.
Article
We studied possible mechanisms of magnesium sulfate (MgSO4)-induced diarrhea. In vivo perfusion of hamster small intestine with an isotonic electrolyte solution containing 50 mM MgSO4 produced nearly three times as much fluid secretion as did a solution containing an equiosmotic amount of mannitol. We found that magnesium was absorbed at a faster rate than mannitol under these conditions, suggesting that differences in solute permeability do not explain the differences in secretory rates. Magnesium ion rather than sulfate appeared largely responsible for the effect as replacement of sulfate with chloride did not diminish the response. MgSO4 perfusion of a proximal intestinal segment did not affect water transport in an isolated distal segment suggesting that release of cholecystokinin or alterations in serum levels of other hormones were not responsible. Intestinal permeability, morphology, and cyclic nucleotide levels were normal after MgSO4 perfusion. Thus, MgSO4-induced diarrhea cannot be explained by the usual mechanisms, and additional processes responsible for intestinal secretion must exist.
Article
We describe severe hypernatremia in a patient with hepatic encephalopathy, who was treated with lactulose. Lactulose produces hypernatremia via its osmotic effect and its degradation to organic acids. We recommend that patients who receive large quantities of lactulose and who lack access to free water have their electrolytes monitored and the dose tapered as quickly as possible.
Article
Meconium constipation is observed in a number of foals during every foaling period. The literature on the clinical picture, methods of treatment and complications, is reviewed in the present paper. In addition, the cases of seventy-five foals are reviewed, in which meconium constipation was suspected and which were submitted to the Internal Disease Department of Large Animals during the period from 1972 to 1982. The clinical picture was found to be due to another disorder in nine cases. Treatment with castor oil and alcohol resulted in discharge of the meconium in fifty-eight cases. Complications occurred in twenty-five foals, fifteen of which died from the effects.