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Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The amputation of the prolapsed rectum of 102 pigs of a fattening unit was carried out by means of a 5-10 cm piece of a plastic hose inside and a ligation around the prolapse. The pressure necrosis due to the ligation leads to the amputation of the prolapse. The positive effect of this method on the performance of the pigs was demonstrated by comparing the 102 treated pigs with a group of pigs that were not treated and with the non-diseased control group. Additionally the influence of diarrhoea and coughing on the frequency of rectal prolapses was investigated.
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PMID:[The surgical treatment of intestinal prolapse (prolapsus recti) in fattening swine under practice conditions]. 785 Dec 96

The destruction of N-methyl-D-aspartate (NMDA) receptor-bearing neurons by insulin-induced hypoglycemia has long been known to be due to excessively released aspartate and glutamate. In this study, the effects of NMDA-bearing neuron destruction by insulin-induced hypoglycemia on the development of morphine (M) physical dependence, which was found related to functional states of NMDA receptors, were investigated. NMDA receptor antagonists CGP 39551 and MK-801 were used to see whether they could change intensity of precipitated abstinence syndrome by preventing destruction. Therefore, two groups of fasting rats injected IP with physiological saline, and another two groups given IP 10 mg/kg CGP 39551 and 0.5 mg/kg MK-801 received 15 IU/kg crystalline zinc insulin IP. After 2 h, the rats were orally given 2 x 4 ml of 5% glucose solution. On the third day, two pellets containing 75 mg base M were SC implanted to all rats. On the sixth day, they were IP given 2 mg/kg naloxone (NL). Then jumps, wet-dog shakes, and defecation were counted while diarrhea and ptosis were rated for 15 min. The rats given insulin manifested significantly more intense NL-precipitated abstinence syndrome than controls. The rats administered CGP 39551 showed a less intense physical dependence than those injected with only insulin. But, the intensity was still significantly higher than controls. In the rats that received MK-801, the abstinence syndrome was more or less equal to that in controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Morphine physical dependence intensification by hypoglycemia: NMDA receptor involvement. 793 7

Helminth and schistosome infections occur in the same geographical areas as does malnutrition. These parasitic infections can occur already in malnourished persons. Hookworm infections reduces food intake and/or increase nutrient wastage via vomiting, diarrhea, or blood loss. These effects exasperate protein energy malnutrition, anemia, and other nutrient deficiencies. Hookworm infection reduces the work capacity and productivity of children and adults; increases maternal and fetal morbidity, premature delivery, and low birth weight, as well as the susceptibility to other infections; and reduces the rate of cognitive development. These social and economic consequences in turn reduce the ability of people and families to raise crops or earn enough money to buy food and other essentials. As many as 90% of the children in some areas of the developed world are infected with roundworm. More than 100,000 deaths in 1987 resulted from complications of roundworm infection (e.g., intestinal obstruction). Roundworm infection reduces the body's ability to use protein and to absorb fat, which worsens protein energy malnutrition. Other nutrient effects of roundworm infection are exacerbation of vitamin A deficiency and lactose and milk intolerance. Whipworm infection can effect prolapse of the rectum and nutritional problems. Treatment of children with whipworm improves hematocrit, growth rates and anthropometry, and serum albumin, and reduces diarrhea and bacterial and protozoan infections in the bowel. Schistosomiasis causes nutritional effects similar to those of helminths. Studies in Kenya show that, in children, 1 treatment against worm, infections improves growth and fitness within 4 months. Other studies in Kenya show that treating children for worms or anemia improves weight gains per month at least as much as and usually more than school feeding programs, a more labor intensive, complicated, and expensive effort. Deworming programs should operate in areas where undernutrition exceeds 25% and worms are prevalent.
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PMID:Helminth parasites, a major factor in malnutrition. 801 83

The evaluation of strength of morphine withdrawal syndrome in rats after the 17th day i. p. morphine administration is proposed as calculation of individual indexes in "open field" test. It is found, that injection 1, 5 or 10 mg/kg of morphine 30 min before testing, decreases the withdrawal syndrome in dose dependent manner. Disappearance of particular withdrawal signs took place in different doses of morphine pretreatment. According to this effect all the signs were divided into four groups and signs of each group were given by the specificity coefficient (from 0 to 3). The total individual index of the withdrawal syndrome was calculated as a sum of particular signs, multiplied by the particular coefficient. Specificity of significant signs decrease according to the order: "wet dog" shakes, diarrhea, writhings, dyspnea, paw shakes, ptosis, piloerection and teeth chattering.
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PMID:[A method for the quantitative assessment of the withdrawal syndrome in morphine-dependent rats]. 820 55

Butorphanol has been shown to act on mu-, delta-, and kappa-opioid receptors. However, the relative involvement of different opioid receptor subtypes in butorphanol dependence is not known. In the present study, nor-binaltorphimine, a long-acting non-peptide kappa-opioid receptor antagonist, was employed to mask central kappa-opioid receptors before and during the induction of butorphanol dependence in rats, so that the involvement of kappa-opioid receptors could be elucidated. The results revealed that treatment with nor-binaltorphimine markedly blocked naloxone-precipitated withdrawal signs of escape behavior, teeth-chattering, wet shakes, ptosis, body weight loss, and hypothermia at all doses tested, and attenuated the withdrawal symptoms of forepaw tremors (24 nmol: P < 0.001) and diarrhea (12 nmol: P < 0.05; 24 nmol: P < 0.01). In contrast, nor-binaltorphimine had no effect on yawning, ejaculation, nor urination in butorphanol-infused rats undergoing withdrawal. Three days of butorphanol infusion significantly increased KD values (in the cortex and striatum), decreased Bmax (in the cortex only) of [3H]U-69,593 binding, and shifted Ki of nor-binaltorphimine against [3H]U-69,593 (4.5 nM) binding in the cortex by more than 10-fold. Treatment with nor-binaltorphimine blocked the effects of butorphanol on kappa-opioid receptors. It is therefore concluded that kappa-opioid receptors are involved in mediating escape behavior, teeth-chattering, wet shakes, forepaw tremors, ptosis, diarrhea, weight loss, and hypothermia in butorphanol-dependent rats undergoing withdrawal. Furthermore, kappa-opioid receptors become desensitized to agonists (in the cortex and striatum), down-regulated (in the cortex), and supersensitive to antagonists in butorphanol-dependent rats.
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PMID:Effects of nor-binaltorphimine on butorphanol dependence. 822 88

The effect of perinatal lead exposure (at 300 and 1000 ppm in the maternal drinking water from conception to postnatal day 14) on the opioid withdrawal syndrome in adult offspring has been studied to assess if lead produces long term disruption of opioid systems manifested as altered morphine dependence. Dependence was induced in 50 day old rats by administration of morphine in osmotic mini-pumps implanted subcutaneously and delivering 5, 15 or 40 mg/kg/day. At postnatal day 55 an opioid withdrawal syndrome was precipitated by administration of naloxone (4 mg/kg i.p) and withdrawal behaviour scored over the next 30 min. Both objective (jumping, weight loss, weight of excreta, wet dog shakes, mouthing and face washing) and subjective (teeth chatter, ptosis, diarrhoea, irritability) measures were scored. 60 min after naloxone animals were killed and plasma corticosterone measured as a biochemical index of withdrawal. Morphine withdrawal scores and plasma corticosterone exhibited a clear dose relationship and there were no significant differences between 0 and 300 ppm lead-exposed groups. However withdrawal scores in 1000 ppm lead-exposed animals were lower in 15 and 40 mg/kg morphine treated rats, predominantly associated with lower weight loss, wet dog shakes and mouthing responses. Paradoxically corticosterone levels were elevated in the 40 mg/kg morphine dose group. The results support other evidence that perinatal lead exposure can induce disruption in opioid functioning which persists to adulthood and suggest a possible link between lead and opioid addiction.
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PMID:Effect of perinatal lead treatment on morphine dependence in the adult rat. 824 87

Clinical studies have suggested that patients who take morphine for pain relief do not show a high degree of dependence. The present study examined the development of naloxone-precipitated withdrawal in rats receiving morphine in the presence or absence of formalin-induced pain. Morphine (10 mg/kg, i.p.) or saline was administered for 4 consecutive days 10 min after a subcutaneous injection of 50 microliters of 2.5% formalin or saline into the hind-paw. On the 5th day, rats were injected with naloxone (1 mg/kg, i.p.) and observed for signs of precipitated withdrawal (ptosis, teeth chattering and excretion/diarrhea). Naloxone-precipitated withdrawal symptoms were significantly greater in rats that received morphine in the absence of pain than in rats that received morphine in the presence of pain.
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PMID:Formalin-induced pain antagonizes the development of opiate dependence in the rat. 827 66

The opiate abstinence syndrome is comprised of motivational symptoms and physical correlates. In rats, physical correlates have been characterized as intense hyperactivity together with jumping, ptosis, teeth chattering, wet dog shakes, and diarrhea. Motivational symptoms have often been associated with the development of place aversions. The search for the neural substrates for the motivational symptoms and physical correlates of the opiate withdrawal syndrome has not reached a consensus as to the existence of a common or separate neural basis responsible for them. In our laboratory, we have gathered evidence that microinjection of morphine into the DPAG inhibits defensive behaviors. However, DPAG microinjections of high doses may produce a 'fearful' hyperactivity as measured in a circular arena or produce anxiogenic-like effects as measured in the elevated plus maze. The antiaversive effects of morphine result from its action on mu receptors and the aversive ones may be associated with its action on other opiate receptors. These findings implicate the PAG as an important structure of the neurobiological substrate of the emotional and physical correlates of the opiate abstinence syndrome.
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PMID:Involvement of opioid mechanisms in the dorsal periaqueductal gray in drug abuse. 827 78

Butorphanol, a synthetic agonist/antagonist, has been shown to act on mu-, delta- and kappa-opioid receptors. However, the relative involvement of opioid receptor subtypes in mediating butorphanol dependence is not known. In the present study, naltrindole, a delta-selective non-peptide antagonist, was administered intracerebroventricularly (i.c.v.) to mask supraspinal delta-opioid receptors before and during the induction of butorphanol dependence. Treatment with naltrindole (0.1, 1, or 10 nmol/5 microliters per rat) significantly blocked naloxone-, a nonspecific antagonist, precipitated butorphanol withdrawal behaviors (escape behavior, teeth-chattering, wet shakes, forepaw tremors, ptosis, diarrhea, body weight loss, and hypothermia) at all doses tested, and decreased ejaculation at 0.1 nmol in butorphanol-infused rats. In contrast, naltrindole treatment had no effect on yawning, nor urination. These results indicate that central delta-opioid receptors are involved in mediating butorphanol dependence in rats.
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PMID:Involvement of delta-opioid receptors in physical dependence on butorphanol. 840 23

Pregnant rats were SC injected with physiological saline (control) or 10 mg/kg morphine (morphine group) or 2 mg/kg naloxone (naloxone group) three times daily during the last 5 days of gestation. Three weeks after birth, male young rats of each group were taken and placed in separate cages. When their body weight reached 130-150 g, 10 rats from control, morphine, and naloxone groups were SC implanted with two pellets containing 75 mg morphine base (total 150 mg). Three days following implantation, rats were IP given 2 mg/kg naloxone for precipitated abstinence syndrome. Immediately after naloxone injection, rats were strictly observed for 15 min and jumping, wet-dog shakes, teeth-chattering, diarrhoea, defecation, and ptosis counted or rated. All abstinence syndrome signs were significantly higher in the morphine or naloxone group than in control. On the basis of the previous experimental findings supporting the idea that opiate physical dependence is related to the binding of opiate, possibly other than their own, to NMDA receptors and the upregulation and/or supersensitivity associated with the binding, the intensification of morphine dependence has been attributed to the long-lasting NMDA receptor upregulation and/or supersensitivity.
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PMID:Prenatal exposure to morphine or naloxone intensifies morphine dependence at maturity. 846 3


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