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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nervous control of gastrointestinal motility is extremely complex, is regulated by the enteric system, the "brain of the gut", and modulated by extrinsic nerves. This system with its multiplicity of transmitters and receptors does not always allow a clear interpretation of experimental data, especially with compounds lacking specificity. In this review the complex situation is described particularly in relation to receptor populations (cholinergic, adrenergic, dopamine, histamine, 5-hydroxytryptamine, opioid, gamma-aminobutyric acid (GABA), prostanoid and dihydropyridine receptors), therapeutic aspects of drugs and their usefulness in children. Newer principles with known drugs and promising new compounds with a more appropriate kinetic or fewer side-effects, deriving from distinct pharmacological groups, as candidates for the treatment of gastrointestinal disorders are considered e.g. anticholinergics (prifinium or actilonium bromide), adrenergic alpha 2-agonists (clonidine, lidamidine) for diarrhoea in diabetic neuropathy, adrenergic beta-blockers for shortening postoperative ileus (propranolol), dopamine receptor antagonists (metoclopramide, domperidone, alizapride) and another prokinetic substance (cisapride) which may be useful for a number of applications as gastro-oesophageal reflux, gastro-paresis, intestinal pseudo-obstruction, cystic fibrosis and constipation, morphine derivatives (e.g. loperamide) for intractable diarrhoea and calcium antagonists (e.g. nifedipine) for achalasia. Increasing experience in digestive tract pharmacology and reliable clinical studies will furthermore be the basis for a more specific and better tolerated therapy of gastrointestinal motility disorders in adults and children.
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PMID:Rational pharmacotherapy of gastrointestinal motility disorders. 266 4

Parturient paresis (milk fever) is a hypocalcemic disorder caused by the onset of lactation in the dairy cow. In most cows a complete recovery follows a single iv calcium treatment to correct the acute hypocalcemia. However, about 20% of cows treated for parturient paresis experience recurring episodes of hypocalcemia (relapses) requiring further treatment. Analysis of plasma from 8 nonrelapsing parturient paretic and 11 relapsing parturient paretic cows revealed differences in plasma 1,25-dihydroxyvitamin D [1,25-(OH)2D] concentrations before and during the development of hypocalcemia. In nonrelapsing cows, plasma 1,25-(OH)2D increased to 4- to 5-fold as plasma calcium concentrations declined during the first stage of parturient paresis. In relapsing cows, decreases in plasma calcium concentrations during the first stage of parturient paresis were accompanied by just a 2- to 2.5-fold increase in plasma 1,25-(OH)2D. Plasma 1,25-(OH)2D eventually increased 4- to 5-fold in the relapsing cows, but this response was delayed 24-48 h compared with the response in the nonrelapsing cows. Plasma PTH concentration profiles were similar in relapsing and nonrelapsing cows, suggesting that renal 25-hydroxyvitamin D 1 alpha-hydroxylase was temporarily refractory to stimulation by PTH in the relapsing cows. In both groups of cows recovery from parturient paresis began about 12-24 h after plasma 1,25-(OH)2D concentrations had increased 4- to 5-fold. These data imply that lack of production of 1,25-(OH)2D is an important factor in predisposing the cow to relapses of parturient paresis and is critical for recovery from the hypocalcemia associated with the onset of lactation.
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PMID:Recurring hypocalcemia of bovine parturient paresis is associated with failure to produce 1,25-dihydroxyvitamin D. 273 59

Intravenously administered parathyroid hormone has recently been reported to prevent parturient paretic hypocalcemia in dairy cows. In the present study, Parathyroid hormone was administered intramuscularly prior to parturition to study its effects on Ca homeostasis and the incidence of periparturient hypocalcemia. Ten Holstein cows were fed a high Ca diet prepartum to predispose them to parturient paretic hypocalcemia. Five cows received intramuscular injections of synthetic bovine parathyroid hormone three times per day beginning about 6 d before parturition and continuing at a reduced dose for about 6 d after parturition. One of five control cows developed parturient paresis, and all five control cows exhibited hypocalcemia within 24 h of calving. None of the treated cows became paretic, and plasma calcium was normal or slightly elevated in these cows during the first 24 h after calving. Parathyroid hormone administration increased plasma concentrations of 1,25-dihydroxyvitamin D and hydroxyproline prior to parturition, suggesting that both intestinal Ca absorption and bone calcium resorption were increased by administration of the hormone. One hormone-treated cow became recumbent and required euthanasia. Although metastatic calcification of soft tissues was not observed, the death of this cow raises the possibility that there are unknown side effects of parathyroid hormone when administered intramuscularly.
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PMID:Periparturient hypocalcemia in cows: prevention using intramuscular parathyroid hormone. 274 25

High mortality in two flocks of 1900 turkey breeder hens accidentally fed 280 g monensin/ton of complete feed is described. Mortality attributed to the poisoning was 76% in flock 1 and 18% in flock 2. Clinically, turkeys were found dead, exhibited respiratory distress with wings extended laterally, had fine tremors, or showed posterior paresis and inability to rise. The most striking finding at necropsy was the almost complete absence of gross lesions. Some turkeys had severely congested lungs; however, many did not. A few birds had pale streaks within the adductor muscles of the legs. Microscopic lesions included myofiber degeneration and necrosis of skeletal and myocardial muscle. Serum phosphorus, lactate dehydrogenase, and creatine phosphokinase were markedly elevated, whereas potassium, chloride, and calcium values were lowered.
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PMID:Monensin toxicity in turkey breeder hens. 293 Apr

Forty-eight Holstein cows with two or more previous lactations and no history of parturient paresis were randomly assigned to one of four prepartum diets in a 2 x 2 factorial design to determine the effect of dietary supplementation with ammonium salts and Ca intake on serum Ca concentrations at calving. Four diets provided either 53 g total dietary Ca/d or 105 g Ca/d and were either supplemented with ammonium salts [100 g/d each of NH4Cl and (NH4)2SO4] or unsupplemented. Anion-cation balance of the diets, calculated as milliequivalents (Na + K)--(Cl + S), was -75 meq/kg DM with ammonium salts and +189 meq/kg DM without ammonium salts. Experimental diets were fed from 21 d prior to expected parturition until calving. Calcium intake during the feeding period did not affect the incidence of parturient paresis or serum concentrations of ionized Ca at calving. The incidence of parturient paresis was 4% with and 17% without the ammonium salts. Cows fed diets containing ammonium salts had higher serum ionized and total Ca concentrations at parturition. Serum concentrations of Mg, P, Na, K, and Cl on the day of parturition were unaffected by dietary treatment.
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PMID:Ammonium chloride and ammonium sulfate for prevention of parturient paresis in dairy cows. 323 32

Parturient paresis (hypocalcemia) is most likely to affect dairy cattle around the time of parturition. It causes progressive neuromuscular dysfunction and flaccid paralysis. Older dairy cows, cows with a history of parturient paresis during a previous lactation, high-producing cows, and cows from the Jersey and Guernsey breeds are at highest risk for developing parturient paresis. Nonparturient hypocalcemia may also occur and is related to events other than parturition, such as severe stress, that temporarily overwhelm the mechanisms of calcium homeostasis. Beef cattle, sheep, and goats are affected less frequently by hypocalcemia than are dairy cows. Because these species are not as stressed for milk production as dairy cattle, nonparturient hypocalcemia makes up a higher proportion of cases in nondairy ruminants. Clinical signs of hypocalcemia in beef cattle, sheep, and goats tend toward hyperesthesia and tetany rather than the classic flaccid paralysis that occurs in dairy cattle with parturient hypocalcemia. Prompt and effective treatment of hypocalcemia helps to reduce the incidence of secondary complications, such as muscle damage or mastitis. The standard treatment regimen of 500 ml of 23 per cent calcium gluconate, administered intravenously, will elicit a favorable response in approximately 75 per cent of recumbent cows within 2 hours of treatment. Relapses following successful initial therapy are common and may be prevented in part by supplementation of intravenous treatment with an additional 500 ml of 23 per cent calcium gluconate administered subcutaneously. Proper nursing care following treatment speeds recovery and reduces the incidence of secondary complications owing to hypocalcemia.
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PMID:Parturient paresis and hypocalcemia in ruminant livestock. 326 54

We studied the relationship of serum prolactin, estradiol-17 beta, and progesterone concentrations to plasma calcium, phosphorus, and free hydroxyproline concentrations, as well as to dry matter intake, in 14 aged dairy cows (mean of 4.5 parities), 7 of which became paretic, from 28 days before to 4 days after calving. Plasma calcium and phosphorus concentrations and dry matter intake decreased more at parturition in paretic cows than in nonparetic cows. Prolactin concentrations were not different between paretic and nonparetic cows, but were variable. Concentrations of estradiol were higher in paretic cows from 15 to 5 days before parturition, whereas hydroxyproline concentration was lower in paretic cows on days 10 through 3 before parturition. Progesterone concentration was lower in paretic cows and decreased earlier at parturition, compared with that in nonparetic cows. The findings suggested that high estradiol concentrations in late pregnancy inhibit bone resorption and predispose aged cows to parturient paresis. The earlier decrease in progesterone concentration at parturition and lower concentrations throughout late pregnancy might have contributed to the greater inappetence in paretic cows at parturition. The importance of prolactin in the pathogenesis of parturient paresis is not clear.
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PMID:Prolactin, estradiol, and progesterone changes in paretic and nonparetic cows during the periparturient period. 335 52

This article describes the general and specific interpretations of common laboratory tests used to evaluate bovine neurologic disease. Cerebrospinal fluid analysis is emphasized. Comments are made about general conclusions such as hemorrhage, inflammation, infection, and neoplasia as well as specific diseases like thromboembolic meningoencephalitis. Tests in commonly available serum chemistry profiles like total calcium concentration and aspartate aminotransferase activity are described in terms of their usefulness in diseases such as parturient paresis or hepatic encephalopathy. The indications for more specific tests like ionized calcium, blood ammonia concentration, or erythrocyte transketolase are included.
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PMID:Clinical pathology of bovine neurologic disease. 355 50

A study was conducted to determine the impact of dietary P intake on vitamin D metabolism and incidence of parturient paresis in aged dairy cows. Thirty dairy cows (10/group) were fed one of three experimental diets for approximately 28 d precalving. Phosphorus intake was .7, 1, or 3 times daily maintenance requirement and Ca intake was three times daily maintenance requirement for all cows. There was a 20% incidence of parturient paresis in each group. Prepartum dietary P intake had no effect on precalving or calving plasma Ca concentrations. Cows fed the low P (.7 times) diet had higher plasma Ca at 3 and 5 d postcalving than did cows fed P at 1 or 3 times maintenance. Plasma phosphorus concentrations reflected dietary P intake. Dietary P intake had no effect on plasma Mg, free hydroxyproline, 1,25-dihydroxyvitamin D, or 24,25-dihydroxyvitamin D concentrations. The range in dietary P from .7 to 3 times maintenance requirement had no effect on the incidence of parturient paresis. However, it did appear to influence Ca homeostasis during the postpartum period as cows fed the low P diet had higher plasma calcium concentrations postcalving. This may be a result of the low P diet enhancing intestinal C absorption by a vitamin D-mediated transport mechanism.
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PMID:Impact of prepartum dietary phosphorus intake on calcium homeostasis at parturition. 361 74

Based on the examination of 45 dead and 5 moribund female mice during a 2-year period, we are able to describe a new disease entity: ileus of the small intestine in lactating mice caused by a paresis of peristalsis. Diarrhoea was not observed and inflammation and infectious agents were not found. Females were affected during the 2nd week of their first lactation. The condition may have a mortality rate as high as 40%. It is assumed that exhaustion (calcium, glucose, etc.) is the cause of this condition. Consequently, the development of a dietary supplement or of a special diet for lactating mice may prove beneficial in preventing this disease. Endogenic (Clostridia) or exogenic toxic components may also play a role.
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PMID:Paresis of peristalsis and ileus lead to death in lactating mice. 375 26


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