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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study was conducted to obtain information on the recreational use of the vasodilators (RVs) amyl nitrite and butyl nitrite in Toronto. The results of 70 interviews (40 complete) indicate that sniffing these RVs gives a 'high' lasting from a few seconds to a few minutes with headache being the most common side effect. None of the more serious side effects mentioned in the literature were reported. RVs are used chiefly in conjunction with sexual activities and dancing. Their use is currently a craze amongst the male homosexual population.
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PMID:Poppers, a new recreational drug craze. 70 98

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

Thirty-seven employees were exposed to cyanide between 1956 and 1985. One was found dead. Thirty-six employees were treated; most were given nitrite and oxygen. Some received oxygen alone. All recovered completely. One-third of these employees were unconscious. One was convulsing. Most were discharged home at 6 h post-exposure. Some employees remained at the plant to work an additional shift. Amyl nitrite and/or oxygen were the only agents used with 33 employees. Forced oxygen was administered to the unconscious, apneic employees. Three employees were given sodium nitrite and sodium thiosulfate iv. Treatment generally began within 3 min. In 5 to 20 min all of the unconscious employees reacted positively to the use of forced oxygen and forced amyl nitrite or sodium nitrite. There were no residual effects except headache and transient loss of appetite. Amyl nitrite and oxygen have been effective tools in the treatment of cyanide intoxication at this plant site. There have been no intercurrent or residual drug effects that outweigh the life-saving capacity of these agents. Sodium nitrite should be employed if the use of oxygen and amyl nitrite fail to improve the cardiovascular status/level of consciousness in 5-10 min.
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PMID:Treatment of cyanide poisoning in an industrial setting. 882 51

It remains an open question as to whether cortical spreading depression (CSD) is the pathophysiological correlate of the neurological symptoms in migraine with aura. In the experimental animal, CSD is an electrophysiological phenomenon mainly mediated via NMDA receptors. However, according to case reports in humans, visual aura in migraine can be alleviated by vasodilator substances, such as amyl nitrite and isoprenaline. There is also circumstantial evidence that brainstem nuclei (dorsal raphe nucleus and locus coeruleus) may play a pivotal role in the initiation of aura. In this study, CSD was elicited in alpha-chloralose anesthetized cats by cortical needle stab injury and monitored by means of laser Doppler flowmetry. Topical application of isoprenaline (0.1-1%) and amyl nitrite (0.05%) onto the exposed cortex had no effect on the elicitation or propagation of CSD. Also, after supracollicular transection, subsequent CSDs showed no differences in the speed of propagation and associated flow changes. We conclude from these data that--given CSD probably exists in humans during migraine--spreading neurological deficits during migraine aura are independent of brainstem influence and have a primarily neuronal rather than vascular mechanism of generation.
Cephalalgia 1999 Jul
PMID:Vasodilator agents and supracollicular transection fail to inhibit cortical spreading depression in the cat. 1044 38

1. Nitroglycerine (NG) was discovered in 1847 by Ascanio Sobrero in Turin, following work with Theophile-Jules Pelouze. Sobrero first noted the 'violent headache' produced by minute quantities of NG on the tongue. 2. Constantin Hering, in 1849, tested NG in healthy volunteers, observing that headache was caused with 'such precision'. Hering pursued NG ('glonoine') as a homeopathic remedy for headache, believing that its use fell within the doctrine of 'like cures like'. 3. Alfred Nobel joined Pelouze in 1851 and recognized the potential of NG. He began manufacturing NG in Sweden, overcoming handling problems with his patent detonator. Nobel suffered acutely from angina and was later to refuse NG as a treatment. 4. During the mid-19th century, scientists in Britain took an interest in the newly discovered amyl nitrite, recognized as a powerful vasodilator. Lauder Brunton, the father of modern pharmacology, used the compound to relieve angina in 1867, noting the pharmacological resistance to repeated doses. 5. William Murrell first used NG for angina in 1876, although NG entered the British Pharmacopoeia as a remedy for hypertension. William Martindale, the pharmaceutical chemist, prepared '...a more stable and portable preparation': 1/100th of a grain in chocolate. 6. In the early 20th century, scientists worked on in vitro actions of nitrate-containing compounds although little progress was made towards understanding the cellular mode of action. 7. The NG industry flourished from 1900, exposing workers to high levels of organic nitrites; the phenomena of nitrate tolerance was recognized by the onset of 'Monday disease' and of nitrate-withdrawal/overcompensation by 'Sunday Heart Attacks'. 8. Ferid Murad discovered the release of nitric oxide (NO) from NG and its action on vascular smooth muscle (in 1977). Robert Furchgott and John Zawadski recognized the importance of the endothelium in acetylcholine-induced vasorelaxation (in 1980) and Louis Ignarro and Salvador Moncada identified endothelial-derived relaxing factor (EDRF) as NO (in 1987). 9. Glycerol trinitrate remains the treatment of choice for relieving angina; other organic esters and inorganic nitrates are also used, but the rapid action of NG and its established efficacy make it the mainstay of angina pectoris relief.
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PMID:A short history of nitroglycerine and nitric oxide in pharmacology and physiology. 1077 31

Clinical experience with hydroxocobalamin in acute cyanide poisoning via ingestion remains limited. This case concerns a 35-year-old mentally ill woman who consumed more than 20 apricot kernels. Published literature suggests each kernel would have contained cyanide concentrations ranging from 0.122 to 4.09 mg/g (average 2.92 mg/g). On arrival, the woman appeared asymptomatic with a raised pulse rate and slight metabolic acidosis. Forty minutes after admission (approximately 70 min postingestion), the patient experienced headache, nausea and dyspnoea, and was hypotensive, hypoxic and tachypnoeic. Following treatment with amyl nitrite and sodium thiosulphate, her methaemoglobin level was 10%. This prompted the administration of oxygen, which evoked a slight improvement in her vital signs. Hydroxocobalamin was then administered. After 24 h, she was completely asymptomatic with normalised blood pressure and other haemodynamic parameters. This case reinforces the safety and effectiveness of hydroxocobalamin in acute cyanide poisoning by ingestion.
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PMID:Hydroxocobalamin treatment of acute cyanide poisoning from apricot kernels. 2185 98

Clinical experience with hydroxocobalamin in acute cyanide poisoning via ingestion remains limited. This case concerns a 35-year-old mentally ill woman who consumed more than 20 apricot kernels. Published literature suggests each kernel would have contained cyanide concentrations ranging from 0.122 to 4.09 mg/g (average 2.92 mg/g). On arrival, the woman appeared asymptomatic with a raised pulse rate and slight metabolic acidosis. Forty minutes after admission (approximately 70 min postingestion), the patient experienced headache, nausea and dyspnoea, and was hypotensive, hypoxic and tachypnoeic. Following treatment with amyl nitrite and sodium thiosulphate, her methaemoglobin level was 10%. This prompted the administration of oxygen, which evoked a slight improvement in her vital signs. Hydroxocobalamin was then administered. After 24 h, she was completely asymptomatic with normalised blood pressure and other haemodynamic parameters. This case reinforces the safety and effectiveness of hydroxocobalamin in acute cyanide poisoning by ingestion.
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PMID:Hydroxocobalamin treatment of acute cyanide poisoning from apricot kernels. 2269 86