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

Nitroglycerin ointment (Nitrong 2%, 5 cm) and an identical placebo ointment were tested in a double-blind crossover study in five healthy volunteers to determine its influence on heart rate, blood pressure, and venous distensibility during supine rest and at 45 degrees tilt. Two hours after administration, a significantly higher venous distensibility was observed with the active ointment than with placebo. There were insignificant changes in heart rate and blood pressure. Three of the five subjects experienced headache for 6 h or more after active ointment.
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PMID:Circulatory effects of nitroglycerin ointment (Nitrong) with special reference to venous distensibility. 642 58

The sensitivity to nitroglycerin-induced dilatation of large intracranial arteries was studied in 17 patients with migraine without aura, 17 age and sex-matched healthy subjects and 9 patients with episodic tension-type headache. Nitroglycerin in the doses of 0.015, 0.03, 0.25 microgram/kg/min was successively infused for 15 min per dose. Blood velocity (Vmean) in the middle cerebral artery (MCA) was recorded with transcranial Doppler before and at the end of every infusion period, and 30 and 60 min after end of the last infusion. In all three groups Vmean decreased with increasing doses (p < 0.001). The response was more pronounced in migraine patients at the two higher doses (p < 0.05). Since nitroglycerin acts as an exogenous source of nitric oxide (NO), these data support that NO supersensitivity may be an important molecular mechanism of migraine pain.
Cephalalgia 1993 Dec
PMID:Arterial supersensitivity to nitric oxide (nitroglycerin) in migraine sufferers. 790 2

Nitroglycerin, which may be regarded as a prodrug for nitric oxide, induces a mild to moderate headache in healthy subjects. In order to study whether migraine patients are more sensitive to nitric oxide than non-migrainous subjects, four different doses of intravenous nitroglycerin were given in a double blind design to 17 migraine patients, 17 age and sex matched healthy controls and 9 subjects with tension-type headache. The nitroglycerin-induced headache was significantly more severe in migraine sufferers, lasted longer and fulfilled diagnostic criteria for migraine more often. We have previously shown a similar supersensitivity to histamine which in human cerebral arteries activates endothelial H1 receptors and causes endothelial production of nitric oxide. Migraine patients are thus supersensitive to exogenous nitric oxide from nitroglycerin as well as to endothelially produced nitric oxide. It is suggested that nitric oxide may be partially or completely responsible for migraine pain.
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PMID:Nitric oxide supersensitivity: a possible molecular mechanism of migraine pain. 824 57

The responses in cervicogenic headache to four different agents have been studied. Nitroglycerin was given sublingually to 27 patients. Eighteen patients got more than 20% increase of their headache. Of those with any headache increase at all, 12 got bilateral and 12 unilateral pain. The typical late cluster headache response to nitroglycerin was not seen in cervicogenic headache. The provocative effect of nitroglycerin seemed less marked in cervicogenic than in cluster headache. Oxygen inhalation, a frequently used treatment for cluster headache, was given to 14 patients with cervicogenic headache. In general, the effect seemed uncertain and probably clearly inferior to the effect in cluster headache. Ergotamine treatment (given to 13 patients) also seemed to be of little avail in cervicogenic headache. Morphine injections given to 11 cervicogenic headache patients resulted in "marked" improvement in 4, but complete pain freedom was only seen in 2 cases. In our opinion, the present results add further evidence to the view that different etiologic and pathogenetic factors underlie cervicogenic headache and cluster headache.
Headache 1993 May
PMID:Cervicogenic headache: responses to nitroglycerin, oxygen, ergotamine and morphine. 832 Jan

Nitroglycerin-(NTG)-induced headache and dilatation of the radial artery were followed in a double blind, randomized, placebo-controlled, cross-over study in 6 healthy volunteers. NTG 0.5 microgram.kg-1 x min-1 or saline were infused i.v. for 7 h, and subsequently the infusion rate was doubled for 10 min. The radial artery diameter was measured repeatedly with high frequency ultrasound and pain was scored using a 10 point verbal scale. After 5 min of NTG infusion both headache and the arterial diameter differed significantly from baseline, and no further significant change occurred. The intensity of the headache was mild to medium (median headache score 3, range 1-7). The mean dilatation of the radial artery was 36%. The dilatation in each individual, was stable over time, both during NTG and placebo, and it did not change with the double infusion rate. The headache score in each individual was more fluctuant. No tolerance either to the NTG-induced headache or arterial dilatation was observed.
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PMID:Lack of tolerance of headache and radial artery diameter during a 7 hour intravenous infusion of nitroglycerin. 843 54

Nitroglycerin (NTG) in situ reduces the pressure of the upper anal sphincter (UAS). We have tested the effects of NTG on the UAS of patients with terminal constipation. We studied two groups of constipated patients. Group 1 consisted of 11 patients (nine females and two males) with hypertonicity of the UAS (> 70 mm Hg); age was 49.5 +/- 15.6 years. Group 2 consisted of 10 patients (nine females and one male) without hypertonicity; age was 40.1 +/- 14.1 years. Group 3 consisted of eight asymptomatic controls (four females and four males); age was 51.7 +/- 6.9 years. After a 10-minute resting pressure recording of the UAS with a water-filled balloon, the probe was pulled through the outside and the UAS was assessed after spreading 5 mg of placebo and then 5 mg of NTG on the balloon. Resting pressure (RP), delay of the pressure decrease (DP), pressure after five minutes either during the NTG (PN5) or placebo (PP5) period, and mean duration of the pressure decrease (MD) were measured. None of the subjects experienced a decrease of PP5 vs. RP. All patients in Group 1 (106.2 vs. 38.4 mm Hg), Group 2 (57.9 vs. 31.4 mm Hg), and controls (62.2 vs. 33.7 mm Hg) experienced a significant decrease of pressure of the UAS (P < 0.005). Delay of the pressure decrease was less than two minutes, with wide interindividual variability of duration of the pressure decrease. Mild side effects--anal pain and transient headache--were reported in five patients. In situ NTG significantly reduced UAS Pressure in all groups. NTG has to be evaluated in anal pathology, especially in patients with hypertonic sphincter terminal constipation or acute hypertonicity of the sphincter due to a fissure.
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PMID:Action of in situ nitroglycerin on upper anal canal pressure of patients with terminal constipation. A pilot study. 845 65

Eighteen cluster headache patients and five controls were studied using ultrasound duplex techniques to measure blood flow in the common carotid arteries after nitroglycerin and placebo administration. Vessel diameter and blood flow tended to be greater before nitroglycerin in patients in the cluster headache period than in patients out of period and controls. Nitroglycerin tended to increase blood flow only in patients not in the cluster period and in controls. There was a significant decrease in common carotid blood flow and increase in vascular resistance related to maximum pain in both nitroglycerin-induced and spontaneous cluster headache attacks. Blood flow did not reach the initial flow values after the attack was over. In one patient a hyperventilation attack only temporarily decreased the pain. We suggest that the decrease in blood flow and increase in vascular resistance may be due to constriction of intracranial arteries by reflex activation of sympathetic efferents, rather than to decrease of arterial CO2 tension.
Cephalalgia 1993 Apr
PMID:Pain induces decrease of blood flow in the common carotid arteries in cluster headache attacks. 849 50

Nitroglycerin and the long-acting nitrates are effective antianginal agents that have been used in clinical medicine for over 100 years. These drugs are reliable, safe, familiar to clinicians, inexpensive, and easy to use. Side effects are limited to headache and postural hypotensive symptoms. Nitrate tolerance or attenuation, -ie, loss of, or decrease in, nitrate efficacy with repeated dosing-is common and represents the major drawback to chronic therapy. Carefully designed dosing regimens and/or appropriate use of nitrate formulations (to include a nitrate-free period each day) will decrease or eliminate the problem of nitrate tolerance. In head-on comparative studies, nitrates appear to be as effective as beta-blockers or calcium channel blockers in the monotherapy of chronic angina. Ideal patient characteristics for nitrate therapy include: predictably favourable response of chest pain to sublingual nitroglycerin; angina episodes suggestive of coronary vaso-constriction or spasm; left ventricular systolic dysfunction; symptoms of congestive heart failure (systolic or diastolic dysfunction).
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PMID:Therapy of angina pectoris with long-acting nitrates: which agent and when? 863 22

The aetiology of anal fissure is unclear, but there is an association with high maximum resting pressure (MRP). Internal sphincterotomy reduces MRP and heals fissure through an increase in local blood supply. Glyceryl trinitrate (GTN) is a nitric oxide donor which contributes to internal anal sphincter relaxation via a non-adrenergic non-cholinergic pathway. GTN ointment was applied topically in different concentration to the anal margin in patients with chronic anal fissure to monitor its effect primarily on MRP and secondarily on fissure healing. Nineteen patients with chronic anal fissure were treated with ointment containing increasing concentrations of GTN (0.2-0.8 per cent) to produce a reduction in MRP of greater than 25 per cent. The actual dose of GTN varied as no standard delivery system has been developed, but a 'typical amount' of GTN ointment weighed about 200 mg. In 15 of 19 patients, a concentration greater than 0.2 per cent was required to lower the MRP by at least 25 per cent. The minimum concentration of GTN that reduced the resting pressure by at least 25 per cent was prescribed and local application was carried out by the patient twice daily for 6 weeks. At 6 weeks, nine patients had healed, six required sphincterotomy and four were lost to follow-up. Eight of the nine patients with healed fistula required a GTN concentration of 0.3 per cent or more. Sixteen patients were resistant to the usually effective does of 0.2 per cent GTN. In three there was tachyphylaxis and the duration of action of GTN was less than the 12 h described previously in control patients. Two patients did not fulfil the study because of headache.
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PMID:Topical glyceryl trinitrate in the treatment of chronic anal fissure. 869 36

Several animal studies suggest that nitric oxide (NO) plays a role in central and peripheral modulation of nociception. Glyceryl trinitrate (GTN) exerts its physiological actions via donation of NO. The purpose of the present study was to examine the effect of this NO donor on nociceptive thresholds in man. On two different study days separated by at least a week 12 healthy subjects received a staircase infusion of GTN (0.015, 0.25, 1.0, 2.0 micrograms/kg/min, 20 min each dose) or placebo in a randomized double-blind crossover design. Before the infusion and after 15 min of infusion on each dose, pressure pain detection and tolerance thresholds were determined by pressure algometry (Somomedic AB, Sweden) in three different anatomic regions (finger, a temporal region with interposed myofascial tissue and a temporal region without interposed myofascial tissue). Relative to placebo, the three higher GTN doses induced a decrease in both detection and tolerance thresholds in the temporal region with interposed myofascial tissue (p = 0.003 detection and p = 0.002 tolerance thresholds, Friedman). No such changes were observed in the other two stimulated regions. These results could reflect central facilitation of nociception by NO. However, we regard convergence of nociceptive input from pericranial myofascial tissue and from cephalic blood vessels dilated by NO as a more likely explanation of our findings.
Cephalalgia 1996 May
PMID:Effect of a nitric oxide donor (glyceryl trinitrate) on nociceptive thresholds in man. 873 68


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