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)

1. The cardiovascular and behavioural effects of cholinomimetic drugs injected through a cannula chronically implanted into a lateral cerebral ventricle were examined in unanaesthetized dogs.2. Acetylcholine (ACh) (10-20 mug) produced an increase in arterial pressure and heart rate, the dogs became more alert, moved their heads, licked and swallowed and then became drowsy.3. The responses to ACh were potentiated by intraventricular physostigmine (5 mug), were abolished by intraventricular atropine (100 mug) but were unaffected by intraventricular mecamylamine (250 mug). The responses to ACh were reproducible on any one day if injections were given again after a 30 min interval but tolerance developed when ACh was injected repeatedly over periods of several days.4. Methacholine (40 mug) produced similar behavioural and cardiovascular effects to ACh but of a longer duration. The responses to methacholine were abolished by intraventricular atropine (100 mug).5. Nicotine (20-60 mug) produced a biphasic cardiovascular response of an initial brief pressor response and tachycardia followed by a secondary increase in arterial pressure and heart rate which was greater in magnitude and duration. The secondary cardiovascular effects were associated with restlessness and vomiting.6. The responses to nicotine were abolished by prior injection of mecamylamine (250 mug) but were unaffected by atropine (100 mug). The responses to nicotine were not reproducible if injections were repeated on the same day but could be again produced if a few days were allowed to elapse between injections.7. An increased heart rate occurred during the pressor response to the cholinomimetic drugs but when a comparable pressor response was produced by intravenous infusion of noradrenaline in the same unanaesthetized dogs pronounced reflex bradycardia resulted.8. The results indicate that the activation of both muscarinic and nicotinic cholinergic mechanisms leads to cardiovascular and behavioural effects in the conscious dog although the site of action and peripheral mechanisms have not been determined.
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PMID:Cardiovascular responses to injections of cholinomimetic drugs into the cerebral ventricles of unanaesthetized dogs. 472 36

The purpose of the present study was to develop a controllable experimental model in the dog that would consistently and predictably produce a malignant hypertensive crisis, and to determine the sequential changes in renal function, salt and water balance, and hormones that are involved in the transition from benign to accelerated hypertension. Norepinephrine (NE) was infused continuously into the renal artery of unilaterally nephrectomized dogs that were maintained on 50 mEq sodium/day. The infusion rate of NE was increased each day according to the following schedule: 0.05, 0.1, 0.2, 0.3, 0.4, and 0.5 microgram/kg/min. During the first 4 to 5 days of intrarenal NE infusion, there was a progressive decrease in glomerular filtration rate (GFR) and effective renal plasma flow (ERPF), and increases in plasma renin activity (PRA), mean arterial pressure (MAP), and filtration fraction. At the end of this period of benign hypertension, MAP had risen from a control value of 91 +/- 4 to 132 +/- 8 mm Hg, in association with approximately a 10-fold increase in PRA and a 40% reduction in renal function. Then, suddenly, during the subsequent 24-hour infusion period, the MAP increased abruptly in all animals (MAP = 156 +/- 8 mm Hg), and a hypertensive crisis occurred. This crisis was associated with the following: salt and water depletion, hyponatremia, hypovolemia and hemoconcentration, polydipsia, marked activation of the renin-angiotensin-aldosterone system, increased plasma cortisol concentration, hemolysis, marked impairment in renal function, lethargy, and vomiting.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Malignant hypertensive crisis induced by chronic intrarenal norepinephrine infusion. 637 96

Octoclothepin, 8-chloro-1-(4-methylpiperazino)-10,11-dihydrodibenzo (b,f) thiepin, is a very potent neuroleptic drug with pronounced central antidopaminergic and antiserotonin actions. In most animal experiments, its plharmacological profile resembles that of perphenazine. Octoclothepin reveals an intensive central depressant action in a series of observational and instrumental procedures in rodents. Its active oral doses are within the range of 0.54 to 2.2 mg kg-1 in mice and of 0.1 to 4.8 mg kg-1 in rats. Octoclothepin possesses high cataleptogenic and anti-apomorphine activities in rats; it is able to exert full protection against apomorphine-induced emesis in dogs after the dose of 0.1 mg kg-1 s.c. Octoclothepin reduces some actions and toxicity of d,l-amphetamine and phenmetrazine in rodents. In the rat corpus striatum, octoclothepin in doses of 0.5 and d1.5 mg kg-1 s.c. reduces the DA level and raises the HVA and DOPAC levels significantly. Octoclothepin has antihistamine, antiserotonin and antianaphylactoid actions, it exhibits a high protection against the lethal action of adrenaline and noradrenaline in mice and rats, respectively. Acute toxicological data in mice, rats, rabbits and dogs are given. Clinical antipsychotic effectiveness of octoclothepin has been verified in a large population of psychiatric patients.
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PMID:Pharmacological properties of a potent neuroleptic drug octoclothepin. 689 91

Intracerebroventricular injection of dopamine (0.5-4.0 mg) produced dose-dependent and short-lasting emesis (1-8 min) in cats, which was abolished after ablation of the area postrema. Relatively selective alpha 2-adrenoceptor antagonists (yohimbine and idazoxan) and a mixed alpha 1- and alpha 2-adrenoceptor antagonist (tolazoline), but not a non-selective alpha 1-adrenoceptor antagonist (prazosin), injected intracerebroventricularly inhibited the emesis induced by intracerebroventricular dopamine. However, dopamine receptor antagonists (chlorpromazine, droperidol, spiperone, domperidone, triflupromazine, sulpiride and metoclopramide), an antimuscarinic drug (atropine), a ganglionic blocking agent (mecamylamine), an opioid receptor antagonist (naloxone) and a 5-HT receptor antagonist (methysergide), all injected intracerebroventricularly, had no significant effect on emesis evoked by intracerebroventricular dopamine. The emetic response to intracerebroventricular dopamine was attenuated in cats pretreated with intracerebroventricular reserpine, 6-hydroxydopamine, alpha-methyl-p-tyrosine and hemicholinium-3. It is postulated that dopamine-induced emesis is mediated through the release of noradrenaline acting at alpha 2-adrenoceptors and that it depends on the integrity of monoaminergic and possibly cholinergic structures within the area postrema. It appears, therefore, that the emetic effect of intracerebroventricular dopamine is mediated by adrenergic rather than dopaminergic mechanisms in the area postrema, at least in the cat.
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PMID:The role of alpha-adrenergic mechanisms within the area postrema in dopamine-induced emesis. 771 46

Despite the postulated tumour affinity of Lipiodol is liver dysfunction after chemoembolization of hepatic malignancies common. Vasoconstricting action of noradrenaline to protect non malignant tissue was studied. 70 patients with unresectable HCCs (UICC IV: 61%) were treated via percutaneous catheter. After noradrenaline (0.1-0.8 mg) induced and documented vessel constriction a suspension of Lipiodol (5-8 ml) and Mitomycin C (10-20 mg) was injected. In addition minced dehydrated dura suspended in Lipiodol occluded the major tumour feeding vessels. 120 (73%) of a total of 164 chemoembolizations were performed after intrahepatic noradrenaline (0.1-0.8 mg) bolus injection. Arterial perfusion of non malignant liver parenchyma was significantly reduced in 95%. 24 hours later selective tumor retention of lipiodol was noticed in 67%. Side effects were fever (79%), thoracoabdominal pain (67%), nausea and emesis (43%) and tachycardia (15%). There were two treatment related deaths: one each from liver failure and cardiac arrest. By WHO response criteria there were 17 (23%) partial remissions (PR), 34 (49%) stable diseases (SD) and 20 (28%) patients had progression (PD). The median survival time from initiation of treatment was 312 days. Bilobal and multiple tumors reduced survival time (90 days). These findings suggest that noradrenaline guided chemoembolization is feasible in Europe and even in patients with pylethrombosis well tolerated.
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PMID:[Noradrenaline-assisted selective chemoembolization of hepatocellular carcinoma]. 784 57

The effect of carmoxirole, a presynaptic dopamine (DA2) receptor agonist, on blood pressure, plasma catecholamines, renin-aldosterone and atrial natriuretic peptide and the intracellular concentration and transmembrane fluxes of Na+ and K+, in erythrocytes and platelets was studied in 24 normal men, using a double-blind, parallel study design. After a run-in period of 1 week, the subjects were treated with either placebo (n = 8) or 0.5 mg carmoxirole (n = 16) once daily for 1 week. Blood pressure and heart rate were not changed during carmoxirole administration in these normal men. Surprisingly, no significant effect of carmoxirole was found on the circulating plasma concentration of noradrenaline, adrenaline or dopamine. Other hormones such as renin, aldosterone and atrial natriuretic peptide were also not changed during carmoxirole administration. No significant effect of carmoxirole could be demonstrated on the intracellular concentration of Na+, K+, Mg2+ and Ca2+ and on the transmembrane fluxes of Na+ and K+ in erythrocytes and platelets. In the carmoxirole-treated subjects (n = 16), 6 subjects reported spontaneously adverse events such as syncope, dizziness and vomiting tendencies and/or fatigue.
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PMID:Erythrocyte and platelet cationic concentrations and transport systems in normal volunteers treated with carmoxirole. 790 90

The relation between pretreatment night-time urinary catecholamine excretion and chemotherapy-induced nausea and vomiting was studied. The first cohort included 17 women and three men with various cancer forms receiving low or moderately emetogenic chemotherapy. The second cohort included 42 women receiving cisplatinum (50 mg m-2) for ovarian cancer and ondansetron as an antiemetic (8 mg i.v. x 3 at chemotherapy and 8 mg p.o. x 3 for 5 days). Relatively higher noradrenaline, but not adrenaline, excretion was associated with an increased intensity of delayed nausea following treatment. Vomiting was not consistently related to the excretion of either catecholamine. The results indicate that noradrenaline modulates delayed nausea resulting from chemotherapy.
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PMID:Delayed chemotherapy-induced nausea is augmented by high levels of endogenous noradrenaline. 759 61

Total intravenous anaesthesia (TIVA) using a combination of a hypnotic and an analgesic agent is gaining increasing popularity as an alternative to balanced anaesthesia with volatile anaesthetics for abdominal surgery. Among the required characteristics of the drugs used in this technique are a good correlation between dose, plasma concentrations, and effect as well as rapid elimination from the circulation, allowing close control of anaesthetic depth. Two hypnotic drugs with similar pharmacokinetic and pharmacodynamic profiles are propofol and methohexitone, both of which can be employed as a component of a TIVA technique. Two TIVA combinations utilising either of these drugs with alfentanil were tested against isoflurane-nitrous oxide in a balanced regimen. METHODS. Twenty-seven healthy women undergoing hysterectomy for non-malignant diseases participated in the study after having given written consent. They were randomly allocated to receive either isoflurane (Iso), methohexital-alfentanil (M-A), or propofol-alfentanil (P-A). Blood samples for determination of cortisol, prolactin, catecholamines, glucose, lactate, non-esterified fatty acids, and pharmacon concentrations were drawn repeatedly from before induction until 360 min after surgery. Anaesthesia was induced in group Iso with fentanyl 0.1 mg and M 1.5 mg.kg-1 and maintained with Iso-N2O. In the TIVA groups M or P was given in a two-step infusion to load peripheral compartments and then maintain plasma concentrations within the hypnotic range. A was given as a continuous infusion in an identical dose (0.1 mg.kg-1 initial, 0.125 mg.kg-1.h-1 maintenance) in both groups. If signs of insufficient depth of anaesthesia occurred (heart rate or systolic blood pressure > 25% above baseline), then first A (0.5-1 mg), and if that was ineffective, then 50 mg hypnotic was administered. The A infusion was stopped 30 min before the end of surgery, and Iso or the hypnotic was stopped at skin closure. Recovery time was the time until the patients were able to give their birth date after stopping the Iso or hypnotic. RESULTS. The three groups were comparable with regard to age, weight, and duration of surgery. The total doses of M and P were 1,357 +/- 125 mg (mean +/- SEM) and 1,315 +/- 121 mg, respectively, and the total A doses were 20.7 +/- 2.5 mg (M-A) and 23.4 +/- 3.5 (P-A). The peak plasma concentrations were P 10.6 +/- 1.5 micrograms.ml-1 and M 12.4 +/- 2.6 micrograms.ml-1. At the end of surgery the P concentrations were in the projected range while those of M were somewhat lower than expected (P 3.7 +/- 0.4 microgram.ml-1; M 3.5 +/- 0.6 microgram.ml-1). Three patients each in the P-A and M-A groups required supplementary A injections. Five patients in the P-A group required additional bolus injections of the hypnotic as compared to 2 in the M-A group. The median recovery times were Iso 15 min, M-A 50 min, and P-A 25 min (P < 0.05). The incidence of shivering was Iso 3/9, M-A 5/9, and P-A 0/9 (P < 0.05); vomiting occurred with equal frequency in all groups (Iso 33%, M-A 33%, P-A 22%). The patients were somewhat more restless in group M-A. Systolic blood pressure dropped in a similar manner in all groups after induction of anaesthesia (Iso -31%, M-A -37%, P-A -36%) but recovered during surgery. The intraoperative response of cortisol (Iso + 216%, M-A +92%, P-A +43%) and catecholamines (noradrenaline Iso +56%, M-A +30%, P-A -21%) was lower in the TIVA groups, whereas prolactin increased after induction in all groups. Plasma concentrations of glucose, lactate, and fatty acids were lower in the TIVA groups than in the Iso group intraoperatively, but increased to comparable postoperative levels. CONCLUSIONS. Both TIVA regimens are acceptable alternatives to balanced anaesthesia with Iso N2O. (ABSTRACT TRUNCATED)
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PMID:[Total intravenous anesthesia with methohexital-alfentanil or propofol-alfentanil in hypogastric laparotomy. Clinical aspects and the effects of stress reaction]. 797 86

The pharmacological properties of AD-5423 [2-(4-ethyl-1-piper-azinyl)-4- (4-fluorophenyl)-5,6,7,8,9,10-hexahydrocycloocta[b]pyridine] were studied in biochemical and behavioral tests. In vitro, AD-5423 bound preferentially to dopamine (DA)-D2 (Ki, 14.8 nM; cf. haloperidol, 8.79 nM; and clozapine, 149 nM) and serotonin (5-HT)-S2 (Ki, 3.98 nM; cf. haloperidol, 26.8 nM; and clozapine, 8.66 nM) receptors. It displayed low affinity for adrenaline (Ad)-alpha-1 (Ki, 56.3 nM) receptors and was virtually devoid of binding to DA-D1 (Ki, 2870 nM), 5-HT-S3, Ad-alpha-2, Ad-beta, muscarine, tau-aminobutyric acid and benzodiazepine receptors. In addition, AD-5423 was only a weak inhibitor of DA, 5-HT and noradrenaline uptake systems. When administered p.o., AD-5423 (0.3-10 mg/kg) increased brain contents of the DA metabolites 3,4-dihydroxyphenylacetic acid and homovanillic acid in mice and rats and the 5-HT metabolite 5-hydroxyindoleacetic acid in mice. Behaviorally, AD-5423 (0.2-2 mg/kg p.o.) decreased exploratory activity in mice, suppressed conditioned avoidance responding and methamphetamine-induced hyperactivity in mice and rats, antagonized apomorphine-induced gnawing in rats and vomiting in dogs and reduced hostile responses in monkeys. In these effects, AD-5423 was more or less equi-potent to haloperidol. However, AD-5423 (10 mg/kg p.o.), unlike haloperidol, did not antagonize SKF38393-induced vacuous oral movements in rats. Head twitches induced by 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane in mice and by para-chloroamphetamine in rats were antagonized by AD-5423 at much lower doses (0.5-2 mg/kg p.o.) than those of haloperidol and clozapine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacological profile of AD-5423, a novel antipsychotic with both potent dopamine-D2 and serotonin-S2 antagonist properties. 809 23

We report an impressive case with Zollinger-Ellison syndrome (ZES), in which stress-induced sympathetic discharge influenced serum gastrin. Our patient was a 35-yr-old female who complained of frequent and massive vomiting (more than 4000 ml of gastric juice) which was aggravated especially by psychosocial stress. Basal hypergastrinemia (1900 pg/ml) was found after the admission. The most striking finding was that laboratory stress dramatically increased serum gastrin (from 1900 to 5400 pg/ml) and plasma noradrenaline (from 180 to 1130 pg/ml). Mental arithmetic stress further enhanced hypergastrinemia (5800 pg/ml) with a concomitant increase in plasma noradrenaline (1240 pg/ml). Neostigmine (10 micrograms/kg im) also increased serum gastrin up to 6100 pg/ml but propranolol (40 micrograms/kg i.v.) reduced these elevations (noradrenaline: 990 pg/ml, gastrin: 5000 pg/ml). In this case, the effect of stress on serum gastrin mimicked the effect of catecholamine infusion in ZES. These findings suggest that psychological stress induces serum gastrin secretion via beta-adrenoceptor with exacerbation of symptoms in some cases with ZES.
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PMID:Impact of stress on serum gastrin in Zollinger-Ellison syndrome. 836 43


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