Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clonidine, an alpha-2-adrenergic agonist, suppresses signs of opiate withdrawal in animals and in man. Electrical or chemical stimulation of the nucleus locus coeruleus (LC) increases noradrenergic activity and brain concentration of the noradrenergic metabolite MHPG, and produces many signs of opiate withdrawal. Thus, clonidine's ability to attenuate withdrawal might be due to the reduction of noradrenergic neuronal activity originating in the LC, but additional alpha-2-adrenergic receptors throughout the body and other mechanisms may also play a role. The present study explored the neuroanatomical and pharmacological selectivity of alpha-2-adrenergic receptors of the LC in the anti-withdrawal action of clonidine. Experiment 1 tested the hypothesis that behavioral and biochemical measures of naloxone-precipitated withdrawal from morphine would be blocked by infusions of clonidine (0.6 or 2.4 micrograms/microliters) into the LC. Significant reductions were observed in the occurrence of diarrhea, ptosis, weight loss and wet-dog shakes. Clonidine also reversed the naloxone-precipitated increase in hippocampus MHPG concentration. In experiment 2 subjects received an LC infusion or IP injection of a non-lipophilic alpha-2-agonist (ST-91), which does not penetrate the blood-brain barrier, or of clonidine into the dorsal parabrachial nucleus (DPB) to test the selectivity of the effects of clonidine infusions into the LC. ST-91 infusions into the LC reduced several of the observed withdrawal signs and increased others (e.g., jumping). Although peripheral injections of ST-91 attenuated some of the checked signs associated with naloxone-precipitated withdrawal, the frequency of wet-dog shakes was not reduced. ST-91 infusions into the LC, but not systemic ST-91 administration, prevented the withdrawal-induced increase in hippocampus MHPG concentration. Clonidine infused lateral to the LC into the DPB did not significantly attenuate withdrawal or reduce hippocampus MHPG levels. These results provide behavioral and biochemical evidence to support the suggestion that clonidine significantly attenuates naloxone-precipitated withdrawal through an interaction with noradrenergic neurons located in the vicinity of the LC.
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PMID:Clonidine infusions into the locus coeruleus attenuate behavioral and neurochemical changes associated with naloxone-precipitated withdrawal. 314 72

A prospective cohort study was designed to describe the patterns and to determine the factors associated with the risk of rectal prolapse in a commercial swine herd in California, USA. Thirty (1.0 per cent) of 2862 pigs prolapsed between 12 and 28 weeks of age with the peak incidence occurring in 14- to 16-week-old pigs. The overall prolapse rate was 9.1 cases per 100,000 days at risk. Prolapse rates were highest during the winter and autumn months. Other factors associated with an increased risk of prolapse were maleness (relative risk 2.3) birthweight less than 1000 g (relative risk 3.4) Yorkshire boar A (relative risk 2.8) and dams of litter number 1 (relative risk 14.9), 2 (relative risk 8.2) and 3 (relative risk 9.8). No evidence was found to support the hypothesis that diarrhoea and coughing are factors associated with a risk of prolapse.
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PMID:Patterns and determinants of rectal prolapse in a herd of pigs. 317 83

A double-wattled cassowary died following a clinical course of severe diarrhea, anorexia, and polydypsia. At necropsy, prolapse of the penis, severe enteritis, and swelling of the kidneys with subcapsular heavy deposits of urates were noted. Histologic lesions comprised nephrosis, interstitial edemia of the muscle, and sloughing of the intestinal villi. Leaves collected from the gizzard were identified as coast live oak (Quercus agrifolia). Diagnosis of oak poisoning was made based on the renal lesions and the finding of a high content of tannins in the liver and gastrointestinal tract. Oak poisoning has not been reported previously in avian species.
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PMID:A fatal case of oak poisoning in a double-wattled cassowary (Casuarius casuarius). 320 81

1. There is some evidence that benzodiazepine may modify the opioid withdrawal syndrome. We have investigated the effect of two different benzodiazepines, diazepam and flunitrazepam, on the morphine withdrawal syndrome experimentally induced in mice. 2. Opiate dependence has been induced by administration of morphine s.c. over a period of five days. Two hours after last morphine administration withdrawal syndrome was induced by s.c. injection of naloxone (5mg/kg). The number of jumps, wet-dog-shakes and paw tremor, and the presence or absence of ptosis, diarrhea, teeth chattering and body tremor were evaluated after naloxone injection. 3. All the signs of morphine withdrawal syndrome was antagonized by flunitrazepam and diazepam, only wet-dog-shake was strongly increased by flunitrazepam.
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PMID:Comparative study in mice of flunitrazepam vs. diazepam on morphine withdrawal syndrome. 324 76

The effects of two calcium channel blockers (verapamil and flunarizine) were evaluated on the naloxone-precipitated syndrome in morphine-dependent rats. The withdrawal signs in saline-treated rats were mainly diarrhea, body weight loss, jumping and ptosis. On i.p. administration, verapamil and flunarizine prevented diarrhea and body weight loss but not jumping. Verapamil also reduced the incidence of ptosis at the highest dose tested (40 mg/kg). Administered i.c.v., 160 micrograms verapamil reduced the body weight loss and the number of jumps without modifying diarrhea or ptosis. The results show that calcium channel blockers inhibit morphine abstinence syndrome manifestations through both peripheral and central mechanisms.
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PMID:Effects of peripheral and central administration of calcium channel blockers in the naloxone-precipitated abstinence syndrome in morphine-dependent rats. 360 36

The pharmacological properties of MO-8282 (1,2,3,4-tetrahydro-2-methyl-9H-dibenzo [3,4: 6,7]cyclohepta [1,2-c]pyridine maleate) as an antidepressant were investigated. At doses 10 times less than those of amitriptyline, MO-8282 showed similar potencies in reducing the duration of immobility during forced swimming in rats and in potentiating stereotype induced by L-DOPA. Intermediate doses of MO-8282 reduced the duration of immobility during forced swimming, in mice as well, suppressed muricide behavior of olfactory-bulbectomized rats and antagonized clonidine-induced suppression of exploratory activity in mice. MO-8282 moderately antagonized the ptosis but not the hypothermia induced by reserpine in mice. MO-8282 exhibited weak antagonism against the tremor, lacrimation and diarrhea induced by tremorine, but its activity was milder than that of amitriptyline. The uptake of noradrenaline into rat hypothalamic synaptosomes was inhibited by MO-8282 at concentrations 20 times less than equally effective doses of amitriptyline, but the uptake of dopamine or serotonin was unaffected by MO-8282. A single oral administration of MO-8282 at a dose of 30 mg/kg accelerated noradrenaline turnover, but did not affect dopamine and serotonin turnover in the rat brain. MO-8282 strongly inhibited noradrenaline-, histamine- or adenosine-sensitive adenylate cyclase activity of guinea pig brain. Its mode of action differed from that of imipramine, rather resembling that of mianserin. MO-8282 did not affect monoamine oxidase activity of rat liver. These results suggest that the pharmacological characteristics of MO-8282 are different from those of tricyclic antidepressants and rather similar to those of mianserin, but more potent. The results, therefore, indicate that MO-8282 is possibly a novel antidepressant.
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PMID:[Pharmacological properties of MO-8282, a novel antidepressant]. 379 61

A single injection of reserpine in an adult horse was believed to induce toxicosis for several days. Clinical signs included erratic, colic-like behavior followed by depression, bradycardia, miosis, ptosis, and paraphimosis. Diarrhea was not observed and may have been due to the effect of xylazine given with the reserpine. The horse was supported with IV fluids and intensive nursing care. Gradual improvement was noted 72 hours after the horse received the drug. Qualitative analysis via high-performance liquid chromatography was positive for reserpine. Methamphetamine is the recommended antidote but was not used in this case.
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PMID:Reserpine toxicosis in a horse. 399 54

Two different conditions are contrasted: mucosal prolapse in children aged between 2 and 5 years and total prolapse, which is very rare. Mucosal prolapse has become very rare in industrialised countries because of the excellent improvement in nutrition since the war, while this remains a very serious condition in under-developed countries. It is rapidly cured, provided the therapeutic errors are avoided, in particular cerclage. Sclerosis with quinine-urea is indicated in this situation. The various causes are discussed: in particular, the abnormal fixation of the rectum and the absence of the sacral curvature. The predisposing factors are essentially prolonged time spent on the pot, constipation and prolonged diarrhoea and, most importantly, malnutrition and prematurity. Total prolapse in very rare; it is about 15 centimetres long curved posteriorly and often incoercible. It occurs in younger infants and even neonates. It is often irreducible and therefore requires surgery in certain cases. It frequently disappears after the age of 8 years. There are a number of very different causes, not only malnutrition and prematurity and, in this clinical context, strain plays an important role and may be due to a vesical or urethral stone or to a congenital abnormality of these organs, but also abnormalities of the rectal segment with disorders of innervation, connective tissue diseases, any diseases affecting the internal sphincter, in particular congenital abnormalities. Abnormalities of the intrinsic rectal innervation with loss of sensitivity are frequent and can be due to denervations caused by a surgical operation (Hirschsprung's operation, for example). Abnormalities of the baso-receptors have also been observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anal prolapse in the child]. 409 98

In conscious spontaneously hypertensive (SH) rats, continuously infused with clonidine (500 micrograms/kg/day s.c.) for 12 days, yohimbine (3 or 10 mg/kg i.p.) dose dependently precipitated an overshoot of heart rate and other withdrawal symptoms, such as blood pressure upswings, diarrhea, ptosis, body shivering, jumping, and wet-dog shakes. Naloxone (3 or 30 mg/kg i.p.) or prazosin (1 mg/kg i.p.) did not evoke withdrawal signs in clonidine-treated SH rats. In SH rats treated for 12 days with guanfacine (10 mg/kg/day s.c.), the administration of yohimbine elicited a withdrawal pattern similar in severity and appearance to that observed in clonidine-treated rats. In methyldopa-treated (200 mg/kg/day) SH rats, the yohimbine-precipitated withdrawal symptoms were much less pronounced than those observed in the clonidine- and guanfacine-treated animals, despite the equipotency of the infusions in reducing mean arterial pressure. These results indicate that the clonidine-withdrawal syndrome can be precipitated by acute alpha 2-adrenoceptor blockade. The previously observed minor severity of the guanfacine-discontinuation syndrome in the rat should be attributed to the longer half-life of this drug as compared to clonidine. On the other hand, alpha-methylnoradrenaline much less intensively triggers the mechanisms underlying withdrawal symptoms than clonidine or guanfacine.
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PMID:Precipitation by yohimbine of the withdrawal syndromes of clonidine, guanfacine, and methyldopa in the spontaneously hypertensive rat. 618 94

A 17 year old high school boy experienced fever and diarrhea, which subsided within 4 days by appropriate medications. Six days later, however, he developed unsteadiness and limb spasm. On the morning of admission, he was found to have drowsiness, dysarthria, gait disturbance and involuntary jerks. When he was brought to the hospital, he was lethargic but could follow simple verbal commands. Frequent involuntary movements manifested by facial grimacings, limb spasms and twitchings with dystonic features were seen. Decorticate posturing was readily elicited by painful stimuli. There was no meningeal irritation sign or gross sensory impairment. The deep tendon reflexes were symmetrically exaggerated with bilateral Babinski signs. Bilateral lateral rectus muscle weakness was found together with mild ptosis and upward gaze limitation. Nystagmus was not present and the funduscopic examination was normal. Immediately he was placed on anticonvulsants, steroid hormone, gamma-globulin and antibiotics as well. A brain CT scan and a CSF examination revealed no abnormality. Meanwhile he continued to show a progressive deterioration associated with fever and status epilepticus, and within 24 hours he lapsed into coma in decorticate posture. An EEG obtained at the 3rd hospital day was compatible with spindle coma. In spite of aggressive treatment he remained febrile and comatous. Therefore, vidarabine (adenine arabinoside) was initiated from the 3rd hospital day for 5 days. Then he began to groan and show frequent choreic movements. For the subsequent 2 weeks he made a slow recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of brain stem encephalitis with complete recovery (Bickerstaff's encephalitis)]. 620 73


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