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)

Myocardon (1 tablet=0.5 mg Nitroglycerin, 100 mg Euphyllin, 29.7 mg Papaverin-hydrochlorid and 0.3 mg Atropinmethylnitrat, without phenobarbital) was given in a dosis of 3 and 6 tablets in patients with acute myocardial infarction. According to the initial value of left ventricular filling pressure (LVFP) the patients were divided into 2 groups: Group I with a LVFP below 20 mm Hg and group II with a LVFP above 20 mm Hg. In group II there was clinical evidence of left ventricular failure. In both groups a decrease in pulmonary artery pressure and especially in left ventricular filling pressure was observed (in group I from 13 +/- 4 to 8 +/- 3 mm Hg and in group II from 26 +/- 7 to 16 +/- 4 mm Hg). Heart rate and mean arterial pressure did not change. In group II cardiac output increased from 3.5 +/- 0.6 to 4.3 +/- 1.31/min, whereas in group I it decreased from 5.1 +/- 0.9 to 4.6 +/- 0.91/min. Like isosorbid dinitrate Myocardon is useful in the management of left ventricular failure in patients with acute myocardial infarction. Side effects were observed: in two patients vomiting and in one patient sickness. The main effect of Myocardon is probably due to nitroglycerin, which is part of the substance. In higher dosis Myocardon has to be given without phenobarbital. Myocardon is especially useful if in the case of headache after nitrates the drug has to be changed.
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PMID:[The effect of nitroglycerin in patients with acute myocardial infarction. IV. Myocardon in patients with and without left ventricular failure (author's transl)]. 81 16

Pancopride ((+-)N-(1-azabicyclo-[2,2,2]-oct-3-yl)-2-cyclopropylmethoxy-4-ami no-5-chlorobenzamide) is a new potent and selective 5-HT3 receptor antagonist, orally and parenterally effective against cytotoxic drug-induced emesis. In vitro, pancopride displayed high affinity (Ki = 0.40 nM) for [3H]GR65630-labelled 5-HT3 recognition sites in membranes from the cortex of rat brains. In vivo, pancopride antagonized 5-HT-induced bradycardia in anaesthetized rats when administered i.v. 5 min (ID50 = 0.56 microgram/kg) or p.o. 60 min (ID50 = 8.7 micrograms/kg) before 5-HT challenge. A single oral dose (10 micrograms/kg) of pancopride produced a significant inhibition of the bradycardic reflex over an 8-h period. Pancopride dose dependently inhibited the number of vomiting episodes and delayed the onset of vomiting induced by cisplatin in dogs (ID50 = 3.6 micrograms/kg i.v. and 7.1 micrograms/kg p.o.). Pancopride was also effective in blocking mechlorethamine- and dacarbazine-induced emesis. Unlike metoclopramide, pancopride was shown to lack any measurable antidopaminergic activity both in vitro and in vivo. These results support clinical data, indicating that pancopride will be a useful drug for treating cytostatic-induced emesis in humans.
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PMID:Pancopride, a potent and long-acting 5-HT3 receptor antagonist, is orally effective against anticancer drug-evoked emesis. 145 37

Domperidone has been used as a gastrokinetic and anti-emetic drug within the frames of an intensive care programme in 57 patients with a history of 3-4 days of acute myocardial infarction. According to the observations, Motilium prevents the development of gastroduodenal complaints and nausea, vomiting in a period following the first days of acute therapy and promotes the start of bowel movement and defecation. It has no cardiac or other toxic effects and does not influence the action of other drugs.
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PMID:Role of domperidone in improving intestinal activity in acute myocardial infarction patients. 181 29

Between 1979 and 1989 17 patients aged two months to 12 years with acute myocardial infarction of any cause (other than after cardiac surgery) were seen at a children's hospital. Eight died from three days to three years after diagnosis (overall mortality 47%). The nine survivors, now aged 2-17 years, have been followed for one to 10 years (mean follow up five years) after infarction. The commonest causes of myocardial infarction in this series were anomalous origin of left coronary artery from the pulmonary artery (six patients (35%] and Kawasaki disease (five patients (27%]. The main symptoms of acute myocardial infarction were dyspnoea, vomiting, and difficulty feeding. Diagnosis was made in all patients by electrocardiography and confirmed by echocardiography, cardiac catheterisation, or at operation. All survivors were symptom free with excellent exercise capacity. The left ventricular ejection fraction in survivors ranged from 21% to 66%, and only one child was on regular cardiac medications. There were no cases of late sudden death. Twenty four hour Holter monitoring performed on survivors was normal (seven) or showed minor abnormalities only (one), suggesting that serious arrhythmia is rare after paediatric myocardial infarction. Myocardial infarction in children had a high early mortality; however, the incidence of serious arrhythmia was low in the survivors, who had a good exercise tolerance even when the left ventricular ejection fraction was low.
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PMID:Myocardial infarction in childhood: clinical analysis of 17 cases and medium term follow up of survivors. 205 43

We describe a girl aged 17 y who died after a cardiac arrest secondary to septic shock. At autopsy, the enlarged, soft, and flabby heart showed microscopic evidence of acute myocardial infarction, myocardial edema, myocardiocyte loss, replacement fibrosis in the interventricular septum, and right and left ventricular hypertrophic nucleomegaly. The pathological diagnosis was that of cardiomyopathy due to prolonged selenium deficiency. The patient had been on total parenteral nutrition for 17 mo, following extensive bowel resection for intractable pain, nausea, and vomiting caused by chronic idiopathic intestinal pseudoobstruction. Seven months before death, when severe biochemical selenium deficiency was diagnosed, supplemental selenium was added to the infusion, and plasma selenium concentrations increased. In long-standing selenium deficiency, sepsis may contribute the final insult to a damaged myocardium, triggering symptomatic cardiac failure and sudden death.
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PMID:Cardiomyopathy associated with nonendemic selenium deficiency in a Caucasian adolescent. 216 25

A 3 year-old Japanese girl had an acute onset associated with vomiting. The electrocardiogram (ECG) indicated changes similar to those of acute myocardial infarction (MI); there was no past history of kawasaki disease. Selective coronary angiography taken on the 28th day of illness revealed no abnormality. Thallium 201 scintigraphy was also performed and it revealed that the area of absent myocardial uptake was in the anterior wall. In serological findings, antibody titers against Coxsackie B-3 virus had risen significantly; therefore acute myocarditis caused by Coxsackie B-3 virus infection was diagnosed.
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PMID:Myocarditis with myocardial infarction like findings in a 3-year old girl. 302 50

The safety/tolerance of anisoylated plasminogen streptokinase activator complex (APSAC) versus heparin therapy in acute myocardial infarction has been studied in the first 65 patients treated in a multicentre study. A transient marked hypotensive effect was observed in 2 patients on APSAC given over 2 minutes. Primary ventricular arrhythmias during the first 4 hours after treatment occurred in 16 APSAC-treated patients and in 7 patients who received heparin; in 88% of the cases on APSAC these arrhythmias were reported by the investigators as being associated with reperfusion. Vomiting, shivering and fever were reported transiently in 2 APSAC-treated patients. Bleeding occurred in 7 patients in the APSAC group; none of these required transfusions, but the heparin dosage was adjusted in 1 patient. A reduction of blood haemoglobin was observed in 4 APSAC- and 2 heparin-treated patients; these were possibly drug-related. Three patients on APSAC died, while in the heparin group 4 deaths were reported.
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PMID:Preliminary safety and tolerance data obtained in the comparative study of anisoylated plasminogen streptokinase activator complex versus heparin. 331 11

Sixteen patients with acute myocardial infarctions who were either vomiting or nauseated were given an intravenous injection of prochlorperazine. All patients obtained relief with exception of one patient who was in acute renal failure. No patient developed symptomatic hypotension. Intravenous prochlorperazine in the dose of 2.5 mg is a rapid, effective, and safe method to relieve vomiting and nausea in patients who have sustained an acute myocardial infarction.
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PMID:Intravenous prochlorperazine for the rapid control of nausea and vomiting in acute myocardial infarction: a clinical observation. 354 40

A 55-year-old Caucasian woman suddenly developed substernal chest pain at rest accompanied by pallor, diaphoresis, nausea, and vomiting. Physical examination was otherwise unremarkable. The resting ECG showed T-wave inversion in all anterior leads which returned to normal 24 h after the onset of the symptoms. The pain was eliminated promptly by sublingual isosorbide dinitrate. "Impending" acute myocardial infarction was diagnosed. Coronary arteriography, however, failed to reveal any change in any major coronary artery but an apical aneurysm of the left ventricle was detected. As the complement-fixation test for Chagas' disease was positive, the diagnosis of chronic Chagas' heart disease was then established. This unusual clinical manifestation of Chagas' disease is thought to be the consequence of a transient imbalance in the cardiac autonomic nervous system, which is considered to play a central role in the pathogenesis of chronic Chagas' heart disease. In addition, the present case may alert clinicians to the thus far neglected atypical chest pain, which is frequently seen in chagasic patients but whose etiology remains obscure.
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PMID:Chronic Chagas' heart disease presenting as an impending myocardial infarction: a case favoring the neurogenic pathogenesis concept. 359 60

Continuous thoracic epidural infusion of bupivacaine 0.25% for the relief of pain in acute myocardial infarction (AMI) was studied. The method was only employed for patients, who could not obtain adequate pain relief by parenteral opioid analgesics without unacceptable respiratory depression and/or emesis. The method was effective in controlling pain. The systolic blood pressure was reduced significantly, while the diastolic blood pressure and the heart rate did not change.
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PMID:Continuous thoracic epidural analgesia for the control of pain in myocardial infarction. 366 72


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