Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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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.
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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

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.
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PMID:Pain induces decrease of blood flow in the common carotid arteries in cluster headache attacks. 849 50

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.
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PMID:Effect of a nitric oxide donor (glyceryl trinitrate) on nociceptive thresholds in man. 873 68

The effects on the sphincter of Oddi of intravenous administration of dipyrone, 2.5 g; tramadol, 50 mg; indomethacin, 75 mg; N-butylscopolamine, 20 mg; and nitroglycerin, 1 mg, in comparison to physiological saline were assessed in a single-blind study in 36 patients hospitalized with upper abdominal pain. Basal sphincter pressure and sphincter motility were measured for a 5-min period after treatment by endoscopic manometry. Nitroglycerin and dipyrone both caused a significant fall in basal sphincter pressure, while N-butylscopolamine and nitroglycerin produced a significant decrease in contraction frequency. Therefore, dipyrone, in contrast to tramadol and indomethacin, exhibits spasmolytic activity in addition to analgesia in biliary pain.
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PMID:Influence of spasmolytic analgesics on motility of sphincter of Oddi. 879

Nine patients with chronic cluster headache were studied as to end-tidal PCO2, heart rate, blood pressure, common carotid artery blood flow, vascular resistance, and intensity and duration of pain before, during, and after breathing 6% CO2 in air for 6 minutes and before and after administration of 1 mg nitroglycerin sublingually. End-tidal PCO2 was low at rest without provocation indicating that chronic cluster headache patients hyperventilate. Carbon dioxide provocation induced an increase in common carotid artery blood flow. This provocation, previously shown to induce pain in episodic cluster headache patients, did not result in unilateral pain in chronic cluster headache patients. Nitroglycerin did not provoke any pain in 4 of 5 chronic cluster headache patients in contrast to the effects in episodic cluster headache patients in a cluster period. In one chronic cluster headache patient, a short-lasting attack of moderate pain intensity was provoked. The results agree with the hypothesis that chronic cluster headache patients have changed vascular reactivity due to permanent sympathicoplegia unilaterally in the middle fossa in contrast to episodic cluster headache patients who it has been suggested have a nonpermanent sympathicoplegia unilaterally in the same region.
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PMID:Chronic cluster headache: provocation with carbon dioxide breathing and nitroglycerin. 898 91

We performed a randomized, placebo-controlled, double-blind study to compare the efficacy of intravenous (I.V.) lidocaine and topical nitroglycerin ointment in preventing pain during propofol injection. Nitroglycerin or placebo ointments were applied to the back of the hand over the skin area overlying the I.V. catheter tip; lidocaine was or was not added to the propofol solution. One hundred twenty-four patients were randomly assigned to receive one of four treatments: placebo and plain propofol, propofol mixed with lidocaine, nitroglycerin ointment and plain propofol, and nitroglycerin ointment and propofol mixed with lidocaine. Hence, there were 31 patients in each treatment group. Patients receiving nitroglycerin ointment and plain propofol had the highest incidence of pain on propofol injection (23 of 31 patients, 74%), and the highest median pain score. Only when lidocaine was added to propofol did it effectively reduce the incidence and severity of pain. Patients aged 50 yr and older had a significantly lower incidence and less severe pain. We conclude that lidocaine and age, but not topical nitroglycerin ointment, are factors associated with a decreased incidence of propofol-induced pain.
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PMID:Effects of topical nitroglycerin and intravenous lidocaine on propofol-induced pain on injection. 908 72

Although vasodilator agents have been used to alleviate the pain of complex regional pain syndromes, the precise mechanism of pain relief is not well known. In this study the effects of various kinds of vasodilators on primary afferent nociceptors were investigated by measuring the thermal pain threshold. Evaluated in the study were the effects of guanethidine (2 mg/mL), nicardipine (0.2 mg/mL). Nitroglycerin (0.3 mg/mL), and prostaglandin E1 (1 microgram/mL) on the cutaneous pain threshold and blood flow at 7-day intervals in six healthy volunteers. Each aliquot of 0.5 mL of the test vasodilator or lidocaine (10 mg/mL) and saline (control) were intradermally injected at three sites each on both forearms. The pricking-pain threshold and skin tissue blood flow were determined using a radiant heat-stimulating system and a laser-Doppler tissue-blood flowmeter, respectively. The pain threshold increased with lidocaine, guanethidine, and nicardipine; remained unchanged with Nitroglycerin; but decreased with prostaglandin E1. In contrast, the skin tissue blood flow increased by four to nine times with all vasodilators. These results indicate that the effect of vasodilators on primary afferent nociceptors is not related to the vasodilating effect and may not involve a common mechanism of action for pain relief in complex regional pain syndromes.
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PMID:Effects of vasodilators guanethidine, nicardipine, nitroglycerin, and prostaglandin E1 on primary afferent nociceptors in humans. 911 59


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