Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Regional cerebral blood flow (CBF), mood states and somatic symptoms were measured before and after inhalation of amyl nitrite in 10 physically healthy volunteers with a prior history of using volatile nitrites for recreational purposes. CBF was measured with the same technique, under identical laboratory conditions, in an equal number of normal volunteers. During CBF measurements, blood pressure, pulse rate, respiratory rate and end-tidal levels of carbon dioxide were monitored. The amyl nitrite group and the control group were compared on CBF, rating scale scores and physiological indices via analysis of variance. Amyl nitrite inhalation was associated with significant global increases in CBF, while the control group did not show any change. Pulse rate increase was the only physiological change associated with administration of the drug. Subjects who received the drug reported significant decrease in anger, fatigue and depression and increased palpitation, breathing difficulty, dizziness and headache. Changes in the rating scale scores, physiological indices, and somatic symptoms after amyl nitrite did not correlate with regional CBF change.
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PMID:Regional cerebral blood flow changes associated with amyl nitrite inhalation. 270 85

The ferrihaemoglobin (HbFe3+) formation by amyl nitrite (AN) or sodium nitrite (NaNO2) was studied in different species including man, in vivo and in vitro. In in vivo studies AN was administered intravenously (i.v.), intramuscularly (i.m.), by inhalation, or orally. NaNO2 was injected i.v.. AN i.v. produced HbFe3+ much more rapidly than NaNO2 in dogs, cats, rabbits, and rats. In dogs, i.m. injection of AN was followed by a very slow linear increase in the HbFe3+ content. Inhalation of AN did not lead to HbFe3+ formation in dogs unless it was rebreathed in a closed (bag) or not completely open (gas mask) system. HbFe3+ was produced by oral AN in dogs, the effect being enhanced by addition of DMSO. Inhalation of AN by human volunteers in a gas mask and from ampoules crushed close to the nose did not induce haemoglobin oxidation to a practically significant extent, but it was associated with headache, tiredness, dizziness, and a fall in blood pressure. In in vitro studies, in contrast to NaNO2, AN produced HbFe3+ instantaneously in erythrocytes of various species and in purified human haemoglobin. AN 1 mol yielded 2 mol Fe3+. Only 20% of the oxygen released during the oxidation of haemoglobin by AN or NaNO2 was recovered. In 0.2 M phosphate buffer, pH 7.4, 0.01 mol O2/mol AN was consumed. CO2 was released in the presence of AN, but not of NaNO2, from blood, plasma, and 0.02 M NaHCO3 solution. The ratio (lactate)/(pyruvate) decreased when HbFe3+ was formed by AN or NaNO2.
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PMID:Ferrihaemoglobin formation by amyl nitrite and sodium nitrite in different species in vivo and in vitro. 290 49

A 65-year-old man complained chest oppression at rest and dizziness. Echocardiography showed subaortic stenosis with outflow gradient of 100 mmHg, although interventricular septal thickness was only 12 mm and left ventricular posterior wall thickness was 11 mm, and mild mitral regurgitation. Selective coronary angiography demonstrated 90% stenosis in left main truncus, 50% stenosis in first diagonal branch, and hypoplastic right coronary artery. Emergent coronary artery revasculization concomitant with left ventricular myotomy myectomy was performed. Immediately after weaning off the cardiopulmonary pump, IABP was employed for cardiac assistance, because of residual left ventricular outflow pressure gradient, which was provoked by cathecholamine and amyl nitrite. He was discharged in 1 month in NYHA class I. Echocardiography 3 months after operation showed no residual outflow pressure gradient, no systolic anterior motion of mitral anterior leaflet, and mild approximately mitral regurgitation. Careful operative management, including myocardial protection and avoiding perforation of ventricular septum and postoperative medical care are mandatory to this group of patients. This case is the first successful coronary artery bypass grafting and concomitant left ventricular myotomy-myectomy reported in Japan.
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PMID:[Successful aorto-coronary bypass grafting and concomitant left ventricular myotomy-myectomy in a patient with coronary artery disease associated with hypertrophic obstructive cardiomyopathy]. 866 82

Sodium azide poisonings occur very rarely. The mechanism of sodium azide toxic effect has not yet been fully explained. Despite the lack of an explicit procedure for the cases of sodium azide poisonings, in vitro tests and rare case reports suggest that treatment with antidotes for cyanide poisoning victims can be effective. This study describes two cases of suicidal sodium azide ingestion. Case 1. 30-year-old male ingested ca. 180 mg of sodium azide. On admission to hospital, within 4 hours from poisoning, the man complained of dizziness and anxiety. Physical examination revealed horizontal nystagmus, flapping tremor, HR 135/min. In laboratory tests, higher blood concentration of lactates (3 mmol/l) was detected, as well as lower potassium concentration (3.4 mmol/L) and increased transaminase activity (ALT 74 U/l, AST 90 U/l). Electrocardiographic tests showed a negative T wave in limb lead III. Other results were within normal. As the patient ingested a toxic dose of sodium azide, he was treated according to the therapy prescription for cyanide poisoning (amyl nitrite inhalation followed by intravenous administration of sodium nitrite and sodium thiosulphate). ECG record of the last day of hospitalization (7th day of treatment) showed negative T waves in lead III, V4-V6. He was discharged from hospital in good condition. Case 2.23-year-old male ingested 10 g of sodium azide 1.5 hours prior to admission to hospital. At the beginning, the patient's condition was good, but it changed to critical state within the first hours of hospitalization. He developed a deep coma, respiratory and circulatory insufficiency, metabolic acidosis, cardiac dysrrhythmias and anuria. Cardiac activity monitoring showed alternating tachycardia (140 beats per minute) and bradycardia (48 beats per minute), numerous additional supraventricular and ventricular extrasystoles and sinus dysrrhythmia. Cardiac arrest (asystolia) occurred twice, the second incident with fatal outcome. The patient received supportive therapy, he was also treated according to the therapy prescription for cyanide poisoning. Circulatory disturbances observed in both cases have been described in literature as symptoms of sodium azide poisoning. However, available literature data are scarce and lack systematization, most of them coming from several decades ago. The lack of patient's consent for detailed examination of circulatory system and liver made it impossible to gather further knowledge on the subject. The efficacy of treatment with antidotes for cyanide poisoning has not been unequivocally determined for this kind of intoxication.
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PMID:[Sodium azide--clinical course of the poisoning and treatment]. 1772 2