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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Varying reactions of the vegetative nerve system to various point combinations (for example: vomiting, dizziness, diarrhea, urge to urinate, fatigue or drowsiness, headache), especially to the needling of Tai Chong (Li 3), induced us to perform biochemical studies before and after acupuncture treatment. A group of children and a group of adults were studied. The material studied was urine and blood; from the children, urine only. The following were determined in the urine: indolacetic acid, 5-hydroxy-indol-3-acetic acid, homovanillic acid, and vanillic-mandelic acid; in the blood, tyrosine and tryptophan (free and bound). Individual points with wide influence (He Gu = LI 4; Zu San Li = St 36; Tai Chong = Li 3) and their combination with generally effective points were tested. The needling of Tai Chong especially showed a clear increase in indolamine metabolism. Isolated increases in metabolites of catecholamine metabolism could be correlated with the patient's increased physical activity after acupuncture. Noteworthy is the observation that no significant chemical reactions were evident if local reactions to the needling no longer appeared at the end of a series of acupuncture treatments.
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PMID:Manipulation of neurotransmitters by acupuncture (?) (A preliminary communication). 23 99

Ten patients with severe dementia due to Alzheimer's disease (AD) or multi-infarct dementia (MID) or both, were treated with the precursor amino acids of the neurotransmitters serotonin and dopamine. The precursor amino acids (PAA) were given orally in a preparation that included tyrosine (4 gm daily) and 5-hydroxy-tryptophan (5-HTP) (800 mg daily), plus carbidopa (100 mg daily) as an aromatic amino-acid decarboxylase inhibitor. Diagnosis was established by an electroencephalogram, brain scan, computerized axial tomographic scan, and in one case by necropsy findings. Serial clinical evaluations and measurements of neuropsychologic function were performed. Levels of homovanillic acid (HVA) and 5-hydroxyindole-acetic acid (5-HIAA) were determined before and after administration of probenecid. Side effects of the PAA therapy were diarrhea, drowsiness, nausea, vomiting and agitation, all of which were controlled by reducing the dosage. One patient with MID and one with AD+MID showed clinical and psychologic improvement, but the others did not improve. Analysis of the cerebrospinal fluid for HVA and 5-HIAA before and after the probenecid test indicated some improvement in the metabolic turnover of these acid metabolites of serotonin and dopamine after administration of their precursor amino acids.
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PMID:Neurotransmitter precursor amino acids in the treatment of multi-infarct dementia and Alzheimer's disease. 30 Nov 48

Renal excretion of xanthurenic acid without any tryptophan load, passage of 4-pyridoxic acid with diurnal urine and its excretion with urine collected during 1 hour in the morning on an empty stomach were investigated in 86 practically healthy infants and in 77 others with acute respiratory viral infections aged from two weeks to one year. Investigations of the tryptophan tolerance in infants yielded negative results, viz. on administering to them of D,L-tryptophan in a load dose the infants started vomiting. Practically healthy infants did not excrete xanthurenic acid, while the renal excretion of 4-pyridoxic acid remained within normal limits. In patients at the height of the disease the passage of 4-pyridoxic acid steeply increased. In 9 of them xanthurenic acid appeared in the diurnal urine. In the quiscent stage of the affection in two infants xanthurenuria continued against the general background of diminished excretion of 4-pyridoxic acid. There is no reason to relate the disclosed xanthurenuria in sick infants with the state of hypovitaminosis in them.
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PMID:[Renal excretion of xanthurenic acid as an index of vitamin B6 allowance in infants]. 98 46

Recent concepts in the etiology of Fusarium trichothecene mycotoxicoses have been reviewed. The effect of orally administered trichothecenes on tissue metabolism has been traced from the gastrointestinal tract to the liver and subsequently to blood. It is proposed that the hyperaminoacidemia resulting from trichothecene toxicoses contributes to the behavioral changes observed, including loss of appetite and vomiting. Studies with several species and several trichothecenes have shown that elevated brain tryptophan arising from trichothecene-induced aminoacidemia can subsequently alter regional brain serotonin concentrations. This may produce behaviors such as loss of appetite and muscle incoordination characteristic of the firing of serotonergic neurons. Support is also presented for the concept that other Fusarium metabolites such as fusaric acid may act synergistically with trichothecenes to produce these effects.
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PMID:Recent advances in the understanding of Fusarium trichothecene mycotoxicoses. 147 35

Fusaric (5-butylpicolinic) acid is a phytotoxin produced especially by Fusarium moniliforme, a mold commonly found in Canadian-grown corn. Experiments were conducted to determine the effects of acute doses of fusaric acid on brain neurochemistry and behavior in swine. A total of 40 crossbred barrows (initial weight 10 kg) were orally dosed with 0 or 200 mg of fusaric acid/kg of BW and five animals from each treatment were killed 4.5, 9, 18, or 36 h after dosing. All brains were dissected, and concentrations of indoleamine and catecholamine neurotransmitters and metabolites were determined. Animals in the group killed 36 h after dosing were observed for behavioral changes. Vomiting was noted in 60% of the pigs dosed with fusaric acid. These pigs also seemed more lethargic than controls and appeared sedated. The major neurochemical changes due to exposure to fusaric acid were seen in the hypothalamus 18 h after dosing. Brain tryptophan, serotonin, and 5-hydroxyindoleacetic acid all tended to be elevated by the action of fusaric acid. Brain catecholamine concentrations were largely refractory to treatment. It was concluded that exposure to acute doses of fusaric acid can cause vomiting and neurochemical changes in swine. Fusaric acid may, therefore, be acting synergistically with trichothecene mycotoxins to cause vomiting and feed refusal in pigs consuming trichothecene-contaminated feedstuffs.
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PMID:Effect of fusaric acid on brain regional neurochemistry and vomiting behavior in swine. 171 54

Epidemic eosinophilia-myalgia syndrome (EMS) associated with excess L-tryptophan (Trp) consumption in humans has been declared a major public health problem. The EMS problem has not been observed in pigs, nor has comprehensive pathology associated with EMS in humans been described. Experiments were therefore conducted to evaluate the pathology and effects of excess dietary L-Trp for finishing (79 to 119 kg) pigs and to determine an LD50 of Trp for pigs. In Exp. 1, addition of .1 or 1% Trp to corn-soybean meal diets had no effect on growth performance or leukocyte and relative eosinophil counts or on plasma aspartate transferase, creatine phosphokinase, and lactate dehydrogenase activities. Likewise, untoward pathological effects of Trp feeding were not observed in the animals under study. In Exp. 2, supplementing the basal diet with 0, 2, and 4% Trp caused linear (P less than .05) decreases in weight gain, feed intake, and gain:feed ratio. Mortality could not be produced by acute oral dosing in the LD50 study (Exp. 3), wherein Trp doses between 2.00 and 5.71 g/kg of BW were administered by stomach tube. Vomiting occurred at oral doses greater than 5.71 g/kg of BW. These results suggest that oral ingestion of Trp in pigs is safe and that pigs can tolerate considerable excesses of Trp.
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PMID:Safety of L-tryptophan for pigs. 188 5

It has been suggested that bingeing and vomiting behavior may be an attempt to suppress hunger or reduce dysphoria. Theoretically, such relationships could involve a mechanism whereby bingeing and vomiting change plasma amino acids which, in turn, enhance brain serotonin-mediated satiety and/or improvement in mood. This hypothesis is based on data showing that the intake of dietary carbohydrates increases the uptake of tryptophan (TRP), the precursor of serotonin, into the brain by increasing the plasma TRP ratio (the ratio of the plasma TRP concentration to the summed concentrations of other amino acids that compete with TRP for brain uptake). Plasma prolactin (PRL) release might reflect the activation of this system. We found that an increase in the TRP ratio during bingeing and vomiting was associated with satiety (i.e., cessation of bingeing and vomiting), but not change in mood. In other words, bulimic subjects who developed an increased plasma TRP ratio during bingeing and vomiting had fewer cycles of bingeing and vomiting and a greater increase in plasma PRL than did subjects who did not develop an increase in the plasma TRP ratio. This study raises the possibility that an increase in the TRP ratio may be associated with the termination of bingeing and vomiting, perhaps due to its effects on brain serotonin metabolism.
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PMID:Bingeing behavior and plasma amino acids: a possible involvement of brain serotonin in bulimia nervosa. 283 64

Deoxynivalenol (DON) produces two characteristic toxicological effects, decreased feed consumption (anorexia) and emesis. Both effects have been linked to increased central (CNS) serotoninergic activity. Although there has also been some indication of a peripheral involvement, the role of blood pools of serotonin and related compounds in mediating DON toxicity is not well defined. In this study, the effect of DON on plasma concentrations of serotonin (5-hydroxytryptamine, 5HT), 5HIAA (5-hydroxyindoleacetic acid) and tryptophan (TRP), as a reflection of an induced peripheral serotoninergic system, was investigated in swine. Typical values for the plasma concentrations of 5HT, 5HIAA, and TRP were established in pigs. Following administration of DON, either intragastrically or intravenously, concentration changes in these substances were measured over an eight hour period. The effect of low and high toxin doses were also compared. Analyses showed no effect on plasma levels of the compounds of interest, even at sufficient toxin doses to invoke emesis in the test animals. Any variation over the course of the study remained within acceptable control limits. These results indicated no peripheral effect by DON which could account for the increased serotoninergic activity associated with altered feeding behaviour or emesis.
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PMID:The effect of deoxynivalenol on serotoninergic neurotransmitter levels in pig blood. 752 34

A wealth of data support a role for serotonin (5-HT) function in the mediation of satiety responses, that are impaired in patients with bulimia nervosa. Testmeal results are presented in which 26 bulimic patients and 17 normal controls were given in randomized, double-blind-fashion, placebo, and the 5-HT agents m-chlorophenylpiperazine (m-CPP, 0.5 mg/kg p.o.) and L-tryptophan (L-TRP, 100 mg/kg i.v.). Three and one-half hours after drug administration, subjects were allowed to eat and lib from a standardized testmeal of 3,500 calories, after which postprandial vomiting was not allowed. M-CPP, but not L-TRP, significantly decreased meal size in the combined group, the controls, and to a lesser extent, the bulimics (P < or = .06). Maximum m-CPP concentrations were inversely correlated to the number of calories consumed in the total group. Following m-CPP, there were significant decreases in carbohydrate, protein, and fat intake in the total group of subjects. There were also trends for decreased carbohydrate and protein intake in the bulimics following m-CPP. There were trends for both m-CPP and L-TRP to reduce fat intake in the controls. Differences in the effects between m-CPP and L-TRP are likely due to differential involvement of 5-HT receptor subtypes at presynaptic and postsynaptic sites. These studies in humans confirm reports in animals that m-CPP decreases food intake, including carbohydrates, protein, and fat in a mixed testmeal.
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PMID:Testmeal responses following m-chlorophenylpiperazine and L-tryptophan in bulimics and controls. 794 45

Migraine and the eating disorders, particularly bulimia nervosa, share some common demographics, phenomenology, psychopathology, and treatments. Bulimics also appear to be more sensitive to the induction of severe migrainous headaches than controls following challenge with the 5-HT agonist, m-chlorophenylpiperazine (m-CPP), but not placebo or L-tryptophan. This supports a common pathophysiological relationship involving postsynaptic 5-HT dysfunction between these disorders. In order to further explore the possible relationship between eating disorders and migraine, we administered a modified version of the Diagnostic Survey of the Eating Disorders (DSED) and the Eating Disorders Inventory (EDI) to a group of female migraine patients attending the Medical University of South Carolina (MUSC) Neurology Clinic (n = 34). Of the 34 migraine patients surveyed, 88% reported dieting behavior, 59% reported binge eating, and 26% reported self-induced vomiting during their lifetimes. Compared to the responses of a group of normal female controls (n = 577), patients with migraine had elevated scores on four of the eight subscales of the EDI: Body Dissatisfaction (p < or = .02), Perfectionism (p < or = .01), Interpersonal Distrust (p < or = .02), and Ineffectiveness (p < or = .06). These findings support the hypothesis that common pathophysiological mechanisms, perhaps involving 5-HT dysregulation, may be involved in these two disorders.
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PMID:Is migraine related to the eating disorders? 833 2


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