A small study found that senna improved post-surgery OIC when taken daily for six days. You can buy dry senna leaves from a health foods store and brew them in hot water.
Or, you can purchase sennosides tablets Senokot from a grocery or drugstore. The usual starting dose for adults is 10 mg to 60 mg daily. Senna should be taken on a short-term basis. Long-term use can cause diarrhea and trigger an electrolyte imbalance. This herb may also increase the risk of bleeding when taken with warfarin Coumadin , a blood thinner. A few home remedies may also improve OIC or help you manage discomfort.
Try these along with medications or natural remedies:. Increase physical activity. Exercise and physical activity stimulate contractions in the intestinal tract and promote bowel activity.
Aim for 30 minutes of exercise most days of the week. Talk with your doctor before starting a new exercise routine. Drink plenty of fluid. Dehydration makes it difficult to have a bowel movement.
Drink glasses of fluid per day. Stick to:. Eat more fiber. Increase fiber intake naturally to normalize bowel activity. Add fruits, vegetables, and whole grains to your diet. Excellent sources of fiber include:.
Too much fiber can cause diarrhea and abdominal cramping. People use opioids to manage severe pain. However, treatment is often available through natural means or in the form of over-the-counter or prescription medication. Read on to learn more about the link between opioids and constipation. Opioids are a medication that are useful for treating severe pain, especially during the later stages of cancer.
Opioids bind to specific proteins in the body called opioid receptors. These are present in the brain, spinal cord, and gastrointestinal tract. However, opioids also depress, or slow down, the central nervous system. As constipation is a common side effect of opioid use, a doctor may prescribe medication to prevent it when they prescribe the opioid. This can prevent the problem from developing. Senna, for example, is available in teas, remedies, and pharmaceutical preparations.
However, doctors usually only recommend taking senna for occasional constipation. Also, aloe vera is a traditional ingredient in constipation remedies. However, these are no longer sold over the counter in the United States, because their safety and effectiveness are uncertain.
Speak to a doctor before taking an herbal remedy, because some remedies can interfere with medications. We studied whether pretreatment with fluoxetine suppressed morphine-induced constipation and the increase in AQP3 expression in the colon.
The colon was isolated to assess AQP3 protein expression levels. The results showed that the concomitant administration of morphine and fluoxetine increased the number and weight of fecal pellets compared with morphine administration alone Figs. However, these increases were smaller than those in the control group. Changes in the morphine-induced constipation score and the colon AQP3 protein expression by fluoxetine administration.
These findings confirmed that a SERT inhibitor suppressed the morphine-induced increase in AQP3 expression in the colon and constipation. Water transport in the colon primarily occurs via the transcellular route through AQPs because of the strong tight junctions of colonic epithelial cells Loo et al. AQP3 is predominantly expressed in mucosal epithelial cells in the colon, and a change in AQP3 expression or function affects fecal water content Ikarashi et al. This study assessed the role of AQP3 in the colon in morphine-induced constipation and revealed a novel pathogenesis.
We investigated the relationship between the degree of constipation and AQP3 expression level in the colon. These findings revealed that the AQP3 expression level in the colon increases during morphine-induced constipation. Why does constipation develop when the AQP3 expression level in the colon increases?
The following reason may underlie this effect. Water is transported from the luminal side to the vascular side through AQP3 because the osmotic pressure is lower in the colonic lumen than in the blood vessel, and the feces are concentrated. Too much water is absorbed from the intestinal contents when the AQP3 expression level increases. Consequently, feces within the colon harden and aggregate, which leads to difficult defecation and constipation.
We studied the number and weight of fecal pellets in the group where HgCl 2 , an inhibitor of the water permeability of AQP3, and morphine were co-administered to confirm this process.
The number and weight of fecal pellets increased significantly in the concomitant HgCl 2 and morphine group compared with the morphine alone group, and this increase was approximately twice the control group Fig. This result strongly supports the idea that increased and decreased AQP3 causes constipation and diarrhea, respectively. Current studies of morphine-induced constipation focus only on the inhibition of peristaltic movements of the bowel Kaufman et al.
Accordingly, an increase in water absorption in the intestinal tract has not been scientifically established as a possible causal factor for constipation. The results of this study revealed that increased water absorption from the colon was attributable to increased AQP3 expression in the colon, which is a causal factor for morphine-induced constipation. We investigated the mechanism by which morphine increases AQP3 expression.
We evaluated the possibility that morphine acts directly on mucosal epithelial cells of the colon using human colon cancer HT cells. The results suggested that morphine is unlikely to directly increase AQP3 expression Fig.
We then investigated whether AQP3 expression in the colon increased by an indirect action of morphine. We focused on 5-HT, which is a neurotransmitter that is present in the intestinal tract in large amounts Kim et al.
Actually, 5-HT-positive EC cells changed their morphology to a process form, and these cells were commonly distributed in the mucous layer above the crypts in rat colons after morphine administration Fig.
These changes in the distribution and morphology of EC cells in the colon after morphine administration strongly suggest that 5-HT secreted from EC cells increases AQP3 expression in vivo Fig. Therefore, we studied whether the increase in AQP3 expression with 5-HT results from actions through these receptors.
SERT is predominantly expressed in mucosal epithelial cells of the intestinal tract, and abnormalities in the function or expression level of SERT is one cause of various diseases, including irritable bowel syndrome and ulcerative colitis Coates et al. These findings strongly support our hypothesis.
We investigated whether fluoxetine pretreatment suppressed morphine-induced constipation. The results showed that fluoxetine pretreatment suppressed the morphine-induced increase in AQP3 expression in the colon Fig. However, this improvement effect of fluoxetine on morphine-induced constipation was weak. The relatively small dose of fluoxetine in this study was unable to lower the increased AQP3 expression level in the colon in the morphine group compared with the control group Ortiz and Artigas, This result is one reason why morphine-induced constipation could not be completely improved.
The administration of an adequate dosage of a SERT inhibitor, such as fluoxetine, may improve morphine-induced constipation. This study in rats could not evaluate MG Kuo et al. This result suggests that there may be a route in humans by which the production of MG following morphine administration acts directly on the colon and increases AQP3 expression levels.
In summary, the results of this study suggest that morphine increases AQP3 expression levels in the colon, which promotes water absorption from the luminal side to the vascular side, hardens stools, and causes constipation.
We considered that morphine promoted 5-HT secretion from EC cells, which subsequently inhibits peristaltic movements of the bowel and also increases AQP3 expression level to ultimately cause constipation. The results of this study suggest that a substance that controls the function and expression of AQP3 in the colon can act as a new therapeutic drug for morphine-induced constipation.
The results also show that a drug targeting SERT, which regulates the actions of 5-HT in the intestinal tract, may be an effective treatment for or prevention of morphine-induced constipation. These novel findings will be critical for the development of new drugs for constipation and in the proposal of new therapies. Supplementary data are available online at Supplementary Data. Ataee R. Ajdary S. Zarrindast M. Rezayat M. Hayatbakhsh M.
Anti-mitogenic and apoptotic effects of 5-HT1B receptor antagonist on HT29 colorectal cancer cell line. Cancer Res. Google Scholar. Baumgarten R. Van De Pol M. Wetzels J. Van Os C. Deen P. Glycosylation is not essential for vasopressin-dependent routing of aquaporin-2 in transfected Madin-Darby canine kidney cells.
Beubler E. Horina G. Gastroenterology 99 , 83 — Burks T. Mediation by 5-hydroxytryptamine of morphine stimulant actions in dog intestine. Long J. Release of intestinal 5-hydroxytryptamine by morphine and related agents. Camilleri M. Opioid-induced constipation: challenges and therapeutic opportunities. Coates M. Mahoney C. Linden D. Sampson J. Chen J. Blaszyk H. Crowell M. Sharkey K. Gershon M. Mawe G. Molecular defects in mucosal serotonin content and decreased serotonin reuptake transporter in ulcerative colitis and irritable bowel syndrome.
Gastroenterology , — De Luca A. Coupar I. Insights into opioid action in the intestinal tract. Dupont C. Laburthe M. Broyart J. Bataille D. Rosselin G. Cyclic AMP production in isolated colonic epithelial crypts: a highly sensitive model for the evaluation of vasoactive intestinal peptide action in human intestine. Gallardo P. Cid L. Vio C. Sepulveda F. Aquaporin-2, a regulated water channel, is expressed in apical membranes of rat distal colon epithelium.
Liver Physiol. Gill R. Saksena S. Tyagi S. Alrefai W. Malakooti J. Sarwar Z. Turner J. Ramaswamy K. Dudeja P. Hendriks G. Koudijs M. Oorschot V. Klumperman J. Glycosylation is important for cell surface expression of the water channel aquaporin-2 but is not essential for tetramerization in the endoplasmic reticulum.
Herndon C. Jackson K. II Hallin P. Management of opioid-induced gastrointestinal effects in patients receiving palliative care. Pharmacotherapy 22 , — Hoffman M. Smith C. Fanelli C.
Pascal V. Degaetano C. Meenan G. Lehrer M. Lesser M. Citron M. A pharmacodynamic study of morphine and its glucuronide metabolites after single morphine dosing in cancer patients with pain.
Cancer Invest. Ikarashi N. Baba K. Ushiki T. Tail-flick latency was used as an indicator of analgesia in the animal experiment; it was significantly increased 1, 2 and 3 h after oral administration of morphine 2. Thus, oral administration of naloxone in aqueous solution antagonized the constipating effect of morphine without interfering with the antinociceptive effect of morphine. Experiments carried out with oral administration to rats of slow-release naloxone instead of naloxone in aqueous solution have not so far been published.
The increase in tail-flick latency caused by morphine 2.
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