Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-four healthy male subjects participated in a study comparing plasma concentrations of nitroglycerin generated by single applications of Nitradisc 32 mg, Transiderm-Nitro 50 mg and Nitro-Dur 104 mg patches and from one inch of Nitrobid 2% ointment. The three patch preparations are designed to release 10 mg nitroglycerin systemically over a 24 h period. Nitrobid ointment is intended to deliver 15 mg nitroglycerin per inch of ointment, and to be reapplied at least every 8 h. Blood was taken for nitroglycerin assay up to and including 24 h after each application. Assay for nitroglycerin was performed using a gas chromatography-mass spectrometry technique. Plasma concentrations of nitroglycerin were sustained up to the 24 h mark with all three patch preparations, but not with application of Nitrobid ointment. Nitrobid was associated with a rapid rise in nitroglycerin plasma concentrations maximal 1 h after application. Plasma concentrations of nitroglycerin absorbed from Nitrobid ointment fell below those absorbed from all three patch preparations after 8 h. Clinically, all four formulations were similar with respect to side effects, with headache and dizziness being the most common.
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PMID:Plasma levels of nitroglycerin generated by three nitroglycerin patch preparations, Nitradisc, Transiderm-Nitro and Nitro-Dur and one ointment formulation, Nitrobid. 308 98

In a study of GTN absorption during exercise and high ambient temperature, 12 healthy volunteers carried 10 mg glyceryl trinitrate (GTN, nitroglycerin) transdermal patches for 6 hours during each of 3 days. During a control day the mean plasma GTN concentration ranged from 1.0 nmol/L (SD +/- 0.8 nmol/L) to 1.5 nmol/L (SD +/- 1.0 nmol/L), whereas during a bicycle ergometer day mean GTN concentration was increased to 3.1 nmol/L (SD +/- 1.7 nmol/L, p less than 0.001). During a sauna day volunteers stayed for 20 minutes in a sauna, and mean GTN concentration in plasma rose to 7.3 nmol/L (SD +/- 1.7 nmol/L, p less than 0.001). Systolic blood pressure increased during exercise (p less than 0.01) but decreased significantly in the sauna (p less than 0.01). Headache was noted frequently (9 of 12 subjects) and dizziness by a few (3 of 12). The demonstrated increased transdermal absorption in our study may infer an increased effect during workload. Whereas the increase in transdermally absorbed GTN may be beneficial to the exercising angina patient, increased effects of GTN may be undesirable in hot surroundings. A study on angina patients is justified to assess whether this phenomenon bears clinical relevance.
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PMID:Increased uptake of transdermal glyceryl trinitrate during physical exercise and during high ambient temperature. 309 10

Intravenous nitroglycerin is frequently used in the treatment of acute myocardial infarction for its vasodilating effect on lowering both preload and afterload and in the control of ischemic heart pain. The end point for doses of nitroglycerin infusion is either relief of persistent or recurrent angina or controlling congestive heart failure by lowering left ventricular end diastolic pressure and volume. Nitroglycerin accomplishes these end points primarily through its venodilating property. Intolerable headaches or symptomatic hypotension may prevent achieving the clinical end point. Nevertheless, high doses of intravenous nitroglycerin may need to be administered to achieve a desired hemodynamic and therapeutic effect. Changes in mental status, i.e., lethargy and confusion, should be a warning sign of possible ethanol intoxication. An alcohol blood level verifies the clinical impression and gradually withdrawing the intravenous nitroglycerin is all that is necessary to effect a total recovery from this reaction.
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PMID:An unusual complication of intravenous nitroglycerin. 309 6

15 chronic cluster headache patients in whom pain was induced by nitroglycerin received acute intravenous treatment with a calcium entry blocker. At the time of peak pain we noted a sudden decrease after the Verapamil injection. The mechanism by which the calcium entry blocker afforded relief is unlikely to have been vasodilatation in patients whose blood vessels had just been dilated by nitroglycerin. A more probable mechanism is blockade of the release of the pain-inducing neurotransmitters. The vasodilatation phase is not a primary factor in the onset of pain.
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PMID:Calcium entry blocker: treatment in acute pain in cluster headache patients. 310 Apr 76

Forty-seven patients with chronic stable angina pectoris entered a thirteen-week open-label study with a transdermal therapeutic system of nitroglycerin in order to evaluate its clinical efficacy, safety, and patient acceptance. In 19 patients, a beta-blocker and in 17 patients a calcium-channel blocker were continued throughout the study period without alteration of their doses. The study consisted of a two-week run-in period and an eleven-week active drug period. Acute titration was done with nitroglycerin patches on the basis of weekly patient diaries on frequency of angina and sublingual nitroglycerin consumption. Overall, reductions in frequency of angina and in nitroglycerin consumption were statistically significant (p less than 0.05). Adverse reactions were common but tolerable. The reported side effects were headache in 32, skin rash in 18, dizziness in 10, palpitation and itching in 9 each, nausea in 7, flushing in 3, and vomiting in 1 patient. In conclusion, the present study demonstrates that individual dose titration with nitroglycerin patches for obtaining significant antianginal effect is essential. The present therapeutic system is convenient to use and well tolerated and had acceptable side effects in our study population.
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PMID:Clinical experience with a transdermal nitroglycerin system. 310 41

Nitrate usage worldwide is on the increase as the indications for therapy expand. Present indications for nitrate therapy include chronic stable angina pectoris, unstable angina pectoris, complications of acute myocardial infarction, and 'unloading' therapy for acute and chronic congestive heart failure. Nitrates are also being used in the operating suite by anaesthesiologists to control systolic blood pressure during various surgical procedures. New nitrate delivery systems have recently become available which provide considerable dosing flexibility, further increasing the interest in this group of compounds. The dominant action of nitrates is a direct effect on vascular smooth muscle, producing vasodilation of the veins and arteries. These drugs decrease myocardial work by lowering systolic blood pressure, systemic vascular resistance, and reducing intracardiac dimensions. In addition, nitrates have a potent effect on cardiac preload as a result of systemic venodilatation. There is also some evidence that nitrates exert direct effects on the coronary circulation (vasodilatation of coronary arteries and coronary collateral vessels, and direct atherosclerotic stenosis dilatation). These actions may play a role in relieving myocardial ischaemia. Adverse sequelae of nitrate therapy are well known and serious adverse reactions are uncommon. Headache and dizziness are the most frequent side effects. Nitrate tolerance is a definite problem - present evidence indicates that long acting formulations, high doses, or frequent dosing regimens are particularly likely to induce vascular tolerance to nitrates. Consequently, provision of a nitrate-free interval has taken on increasing significance as a strategy to avoid tolerance. Nitrate delivery systems are numerous. Although availability varies from country to country, in most countries there are a wide variety of formulations of glyceryl trinitrate (nitroglycerin) available, including sublingual and oral tablets, oral spray, topical ointment as well as discs or patches for transdermal administration, a transmucosal tablet and an intravenous formulation. Similar formulations of isosorbide dinitrate, except buccal tablets, are available in some countries. Isosorbide 5-mononitrate, a potent metabolite of isosorbide dinitrate, is achieving increasing popularity as an antianginal drug. Optimum nitrate therapy requires a good understanding of the properties of the various formulations, particularly onset and duration of action and propensity to induce tolerance.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Glyceryl trinitrate (nitroglycerin) and the organic nitrates. Choosing the method of administration. 311 8

A previous study verified the antianginal efficacy of 0.025 mg nitroglycerin without it having any effect on heart rate and blood pressure. In a randomized double-blind study, 40 patients with coronary heart disease received intravenously either 0.025 mg nitroglycerin or placebo. Before and 1-2 min after injection, the aortic and left ventricular (n = 20) pressures were recorded and coronary angiography performed. Mean heart rate, systolic and diastolic aortic pressure, left ventricular filling pressure and the pre- and poststenotic diameter of the coronary arteries, as well as the diameter of a distal coronary artery segment, showed no significant changes (p greater than 0.05). The stenotic segment diameter of the coronary artery remained unchanged after placebo administration (1.01 +/- 0.5 to 1.13 +/- 0.49 mm; p greater than 0.05) but increased significantly after the injection of nitroglycerin (from 1.15 +/- 0.68 to 1.32 +/- 0.73 mm; p less than 0.01). These results support the hypothesis that dilatation of coronary stenoses is an important aspect of the antianginal action of nitroglycerin. This may have practical consequences in the treatment of patients with angina and low blood pressure or severe headaches after the administration of conventional doses of nitroglycerin.
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PMID:[Coronary-dilating effect of minimal doses of nitroglycerin]. 312 Apr 36

Fifty-six patients with cardiac disease participated in a study to determine the effect of site placement on patient reports of headache and flushing after topical nitroglycerin ointment placement. Nitroglycerin was placed on the upper arm, chest, and pelvis in random order. Approximately 30 minutes after application, patients were asked to evaluate their headache and flushing using a visual analogue scale. No significant difference in the severity of side effects was found when the three sites were compared by multivariate analysis of variance with repeated measures. The clinical practice of instructing patients to vary the site placement of nitroglycerin ointment to avoid side effects was not supported.
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PMID:Effect of nitroglycerin ointment placement on the severity of headache and flushing in patients with cardiac disease. 313 14

The antianginal effects of sustained-released oral nitroglycerin were evaluated in patients with chronic stable angina using a double-blind randomized protocol. Nineteen patients were inducted into the trial and 17 of these completed the study. Two doses of oral nitroglycerin were used; 2.6 mg and 6.5 mg given three times daily for a period of 2 weeks, the patients crossing over to the alternative dose at the end of each period. Evaluation of effect was carried out 2 hours after the morning dose using graded treadmill exercise testing with on-line computer analysis of the electrocardiogram (EKG) (CASE, Marquette Electronics, Inc.). Various exercise parameters were measured and the results compared to placebo values and between the two dosages. The aim was to demonstrate an antianginal effect and to look for a dose-response relationship and for attenuation of effect if any on continued administration. The mean +/- SEM exercise time on placebo was 6.7 +/- 0.6 min, increasing to 8.6 +/- 8 min (p less than 0.02) with 2.6 mg tds dosage and 8.4 +/- 0.7 min (p less than 0.01) with 6.5 mg tds of oral nitroglycerin. None of the other exercise-derived indices were altered significantly by oral nitroglycerin. Two patients were withdrawn because of severe headaches and both were receiving the higher dose. The data did not demonstrate any dose-response relationship but confirmed the anti-anginal efficacy of sustained action oral nitroglycerin. This efficacy did not show any significant attenuation of effect on continued administration, indicating a possible lack of development of tolerance.
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PMID:Oral nitroglycerin in angina pectoris--evaluation of effect by computerized exercise testing using two different doses. 315 16

Ocular sympathetic function, facial flushing and the presence or absence of lachrymation and rhinorrhoea were examined in 30 patients during spontaneous or nitroglycerin-induced cluster headache. In 27 cases measurements were also obtained during the headache-free interval. Ocular sympathetic function was impaired on the symptomatic side between cluster attacks and function was reduced further during cluster headache. Greater heat loss from the orbital region on the symptomatic side was associated with ocular sympathetic dysfunction both during and between attacks, and with lachrymation during attacks. Heat loss from the cheek and side of the nose was greater on the symptomatic side in patients whose attack was accompanied by lachrymation, but heat loss from these areas was unrelated to the extent of ocular sympathetic deficit. These findings suggest that parasympathetic overactivity in the greater superficial petrosal nerve provokes facial flushing and lachrymation. Parasympathetic overactivity could also cause dilatation of the internal carotid artery and compression of the periarterial plexus of sympathetic fibres, producing a sympathetic deficit with release of vasoconstrictor tone in the eye. Thus autonomic disturbances in cluster headache may be explained by the unitary hypothesis of parasympathetic hyperactivity being responsible for ocular sympathetic deficit.
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PMID:Autonomic disturbances in cluster headache. 317 90


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