Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous man dives, in a series designed to evaluate the physiological effects of helium, nitrogen, and oxygen (trimix), investigated the comparative effects of 5% vs. 10% nitrogen with fast compression (12 h 20 min) to 460 m (1509 ft) and subsequent compression over 2.5 d to 650 m (2132 ft). In 1981 three divers were compressed twice as slowly as for these earlier dives to 650 m over a period of 6 d 8 h using 10% N2 in heliox. An extensive series of studies were made over 4 d 15 h at 650 m before further compression to 686 m (2250 ft) for a stay of 24 h with extensive tests of psychological and neurophysiological performance, pulmonary function, reflex, Doppler, and other studies. High pressure nervous syndrome (HPNS) tremors and EEG theta activity increases were effectively controlled with no nausea, vomiting, or somnolence (microsleep). Some euphoria was present. At 686 m there was a 20% to 30% impairment of concentration and attention; otherwise the physical condition of the divers was fine and they completed all tasks without difficulty. Slow compression prevented the initial large performance decrement of 40% to 50% on Day 1 as found in previous fast-compression dives. Otherwise the performance tests showed much the same decrement of 15% to 20% seen in earlier dives; deeper than 570 m (1870 ft), however, the addition test was worse, with a decrement of 35%. The results are discussed with respect to the previous two dives with faster compression, and the possible nonlinearity of nitrogen antagonism of HPNS is considered.
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PMID:Effect of compression rate on use of trimix to ameliorate HPNS in man to 686 m (2250 ft). 716 98

There studies examined the effect of dietary arginine deficiency in the mature dog. Deletion of arginine from the diet resulted in a slight but significant loss of body weight. Severe episodes of emesis were observed in all experiments. Muscle tremors and frothing around the mouth were also observed in the experiments where the arginine-free diet was force fed. Increasing the amount of diet force-fed to mature dogs accentuated the symptoms of emesis, muscle tremors and frothing. Elevated plasma ammonia and orotate were detected in dogs fed an arginine-deficient diet. Urinary citric and orotic acid was also increased in mature dogs fed a diet devoid of arginine. Nitrogen balance was not significantly altered by deletion of arginine from the diet. Based on the occurrence of emesis, loss of body weight and alterations in intermediary metabolism, we concluded that the mature dog does require a dietary source of arginine. Dietary inclusions of 0.28% arginine prevented the symptoms of arginine deficiency.
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PMID:Arginine: an indispensable amino acid for mature dogs. 724 Dec 23

In 1978 a series of deep trimix (He-N2-O2) dives was initiated to establish the relationship between a given nitrogen percentage and the rate of compression required to prevent the high pressure nervous syndrome (HPNS) at 460 m (1509 ft) and to determine the effects of inspired gas density, hydrostatic pressure, and narcosis o various circulatory and respiratory parameter, including the presence of dyspnea. In 1979, three human subjects were compressed to 460 m in 12 h 20 min with 5% N2 in He-O2. This resulted in nausea, vomiting, fatigue, tremors, and other signs and symptoms of HPNS that were especially prominent on arrival at that depth but had much improved by Day 2. In March 1980 the same profile was repeated but with 10% N2 in He-O2. The divers arrived at 460 m with virtually no symptoms of HPNS, but the psychometric performance, as for Atlantis I, still was decreased by some 40% on Day 1 and recovered to some 15% by Day 2. After 5-6 days at 460 m further extension of the dive to 650 m (2132 ft) with a 7.7% N2 mixture for 24 h showed similar control of symptoms of HPNS, although inspiratory resting dyspnea was present in one subject. The results are discussed in relation to the interactions of nitrogen percentage and rate of compression.
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PMID:Control of HPNS in humans during rapid compression with trimix to 650 m (2131 ft). 726 42

The effect of prolonged hypotensive anesthesia and surgery on renal function was studied in 8 dogs with decreased renal mass. Renal mass was reduced by unilateral nephrectomy and ligation of 4 of the 6 terminal renal artery branches of the opposite kidney. One week after reduction in renal mass, the dogs were azotemic with a serum urea nitrogen (SUN) value of 65.8 +/- 11.5 mg/dl. Glomerular filtration rate, as estimated by 14C-inulin clearance, was 0.66 +/- 0.19 ml/kg of body weight/hour. A mean arterial pressure of less than 75 mm of Hg was maintained for 4 hours in dogs given 2.3 +/- 0.7% halothane. An exploratory laparotomy lasting 1 hour was performed. The day after the hypotensive episode, 3 dogs began vomiting, became dehydrated, and had SUN values greater than 100 mg/dl. The SUN values returned to base-line values after the dogs were rehydrated. Eight days after the hypotensive episode, 14C-inulin clearance decreased 15.2 +/- 8.2% (P less than 0.005) compared with base-line clearance values. Light microscopic and electron microscopic observations of the kidneys did not demonstrate acute renal failure. Prolonged hypotensive anesthesia can cause a decrease in renal function, and may cause prerenal uremia and/or acute renal failure.
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PMID:Renal function after prolonged hypotensive anesthesia and surgery in dogs with reduced renal mass. 732 27

In a double blind study, 40 infants with cows' milk intolerance of various causes were randomised to receive a nutritionally complete formula in which nitrogen was supplied either as whey hydrolysate or amino acids. The median age of infants was 10 weeks (range 36 weeks' gestation to 108 weeks' postnatal age). After a median follow up period of 25 weeks there was no significant difference in dietary intake between the formulas. Twenty four weeks after entry, weight and weight for length improved equally on both formulas. Plasma albumin improved significantly on the hydrolysed whey formula but not in the amino acid group. Both milks were palatable and normal intakes of formula were maintained. Biochemical and haematological indices remained within normal limits. There was no difference in stool frequency and vomiting between the two formulas. Two infants developed a probable allergic colitis while receiving hydrolysed whey. Amino acid formula may have a role in the management of atopic infants with severe cows' milk intolerance who have already reacted to whey or casein hydrolysate formula.
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PMID:Comparison of an elemental with a hydrolysed whey formula in intolerance to cows' milk. 749 57

Ornithine transcarbamylase deficiency is an X-linked recessive disorder of urea biosynthesis characterized by recurrent, often fatal, hyperammonemic encephalopathy in affected males; carrier females are usually asymptomatic. We report here the clinical and laboratory findings in five symptomatic heterozygous females with ornithine transcarbamylase deficiency. In each case, the onset of symptoms occurred in the 1st year of life, but diagnosis was delayed by up to 15 years. Symptoms included recurrent vomiting with lethargy (five patients), dietary protein intolerance (five), irritability (four), severe acute encephalopathy (three), ataxia (three), and acute hemiparesis (two). All eventually showed evidence of developmental delay or learning difficulties. Two of the three who experienced severe, acute, hyperammonemic encephalopathy suffered serious, permanent neurologic sequelae. Three of the patients showed decreased ornithine transcarbamylase activity in liver obtained by needle biopsy, and the other two had marked orotic aciduria associated with hyperammonemia. Neuroimaging studies demonstrated persistent abnormal lobar attenuation and abnormal signal on computed tomographic scan and magnetic resonance imaging. All patients showed marked symptomatic improvement on treatment with dietary protein restriction supplemented by pharmacologic measures to increase nonprotein nitrogen excretion. Ornithine transcarbamylase deficiency should be considered in the differential diagnosis of acute or chronic encephalopathy in females at any age.
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PMID:Ornithine transcarbamylase deficiency in females: an often overlooked cause of treatable encephalopathy. 749 56

Chromogranin A (CgA) is present in high concentrations in enterochromaffin cells, where it is co-localised with serotonin in the storage granules. Plasma CgA has been reported to mark emesis and serotonin release associated with cisplatin treatment. However, it is not known whether plasma CgA could be an indicator of emesis and of serotonin release in patients receiving non-cisplatin chemotherapies. Therefore, in this study we evaluated, in cancer patients, the temporal relationships between the increases in plasma CgA and urinary 5-hydroxyindoleacetic acid (5-HIAA) and the development of vomiting following dacarbazine, nitrogen mustard and cyclophosphamide treatments. Metoclopramide was used as antiemetic. With dacarbazine, nitrogen mustard and cyclophosphamide the median time to the onset of emesis was 2.3, 2.8 and 5.3 h and the duration of intense emesis was 3, 2 and 6 h respectively. Plasma CgA and urinary 5-HIAA increased after dacarbazine- and nitrogen mustard-based chemotherapies, with maximal increases between 4 and 6 h after initiation of drug infusion. The time course for the increases in plasma CgA paralleled that of urinary 5-HIAA and the period of intense emesis. A highly significant (P = 0.0009) positive correlation (r = 0.68) was found between the increases in plasma CgA and in urinary 5-HIAA. Cyclophosphamide treatment was not associated with increases in plasma CgA and in urinary 5-HIAA, despite inducing emesis; this indicates that the increases in CgA and 5-HIAA after dacarbazine and nitrogen mustard are not due to the act of vomiting per se. In summary, plasma CgA is a marker of serotonin release (most likely from enterochromaffin cells) after dacarbazine and nitrogen mustard-based chemotherapies, exocytosis being the most likely mechanism for the release of serotonin. Serotonin released from enterochromaffin cells seems to trigger the emetic response to dacarbazine and nitrogen mustard; however, cyclophosphamide may release serotonin from a different pool (enteric serotonin neurons and/or CNS serotonin?).
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PMID:Plasma chromogranin A marks emesis and serotonin release associated with dacarbazine and nitrogen mustard but not with cyclophosphamide-based chemotherapies. 754 18

A series of (fluorobenzyl)triazolo[4,5-c]pyridines was synthesized and tested for activity against maximal electroshock-induced seizures in rodents. The most promising compound, 14 (BW 534U87), which is a carbon-nitrogen isoster of a purine anticonvulsant, has a profile in rodents that suggests 14 will be free of emesis and useful in the treatment of seizure disorders for which phenytoin is presently indicated.
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PMID:1-(Fluorobenzyl)-4-amino-1H-1,2,3-triazolo[4,5-c]pyridines: synthesis and anticonvulsant activity. 756 50

Single dose toxicity studies of T-3761 were carried out in mice, rats and dogs, and the following results were obtained. 1. The approximate lethal dose of T-3761 were more than 5,000 mg/kg for mice and rats, more than 2,000 mg/kg for dogs with oral administration, and more than 5,000 mg/kg for mice and rats with subcutaneous injection. LD50 values with intravenous injection were 783 mg/kg for male mice, 832 mg/kg for female mice, 341 mg/kg for male rats, and 403 mg/kg for female rats. Two dogs given 200 mg/kg did not die but one of the two treated with 400 mg/kg died after intravenous injection. The approximate lethal dose for dog was 400 mg/kg. 2. Neither abnormal symptoms and macroscopic findings nor deaths were observed in mice and rats treated orally. Granuloma around precipitates of T-3761 at the injection site was seen in mice and rats injected subcutaneously. Slight increase of white blood cell count, serum GOT, CPK and urea nitrogen were transiently found in dogs treated orally. Neither abnormal macroscopic findings nor deaths were observed in dogs treated orally. 3. Decreased motor activity and irregular breathing were observed in mice and rats injected intravenously. In dying animals, tonic or clonic convulsions were observed. Vomiting, hyperemia of ophthalmic mucosa, edema of face, decrease of motor activity, salivation and decrease in body temperature were observed in dogs injected intravenously. At higher doses, scream and tachypnea were observed while injecting. Hematological examinations disclosed that increases in red blood cell count, white blood cell count, hematocrit and hemoglobin were found transiently. In biochemical examinations, increases in serum GOT, GPT, urea nitrogen and creatinine were found transiently. One dog intravenously injected 400 mg/kg, showed tonic convulsion and died.
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PMID:[Single administration toxicity studies of T-3761 in mice, rats and dogs]. 766 80

A series of pyrido[1,2-alpha]indol-6(7-H)-ones was prepared and evaluated for 5-HT3 receptor antagonist activity. The structural requirements for the 5-HT3 receptor antagonist have been defined as an aromatic moiety, a basic nitrogen, and a linking acyl group. The (5-methylimidazol-4-yl)methyl group as a basic nitrogen moiety was an important element for high potency. The highest potency was observed for compounds which have 7- and 10-methyl substituents on the pyrido[1,2-alpha]indol-6(7H)-one ring. From this series, (+)-11b (FK 1052) was selected for further evaluation. FK 1052 was a potent 5-HT3 receptor antagonist in the Bezold-Jarisch reflex test in rats (ED50 0.9 microgram/kg, i.v.) and a very effective antiemetic agent against cisplatin-induced emesis in dogs (ED50 1.2 x 2 micrograms/kg, i.v. and 2.7 x 2 micrograms/kg, p.o.).
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PMID:New 5-HT3 (serotonin-3) receptor antagonists. I. Synthesis and structure-activity relationships of pyrido[1,2-a]indoles. 769 71


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