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)

Myocardon (1 tablet=0.5 mg Nitroglycerin, 100 mg Euphyllin, 29.7 mg Papaverin-hydrochlorid and 0.3 mg Atropinmethylnitrat, without phenobarbital) was given in a dosis of 3 and 6 tablets in patients with acute myocardial infarction. According to the initial value of left ventricular filling pressure (LVFP) the patients were divided into 2 groups: Group I with a LVFP below 20 mm Hg and group II with a LVFP above 20 mm Hg. In group II there was clinical evidence of left ventricular failure. In both groups a decrease in pulmonary artery pressure and especially in left ventricular filling pressure was observed (in group I from 13 +/- 4 to 8 +/- 3 mm Hg and in group II from 26 +/- 7 to 16 +/- 4 mm Hg). Heart rate and mean arterial pressure did not change. In group II cardiac output increased from 3.5 +/- 0.6 to 4.3 +/- 1.31/min, whereas in group I it decreased from 5.1 +/- 0.9 to 4.6 +/- 0.91/min. Like isosorbid dinitrate Myocardon is useful in the management of left ventricular failure in patients with acute myocardial infarction. Side effects were observed: in two patients vomiting and in one patient sickness. The main effect of Myocardon is probably due to nitroglycerin, which is part of the substance. In higher dosis Myocardon has to be given without phenobarbital. Myocardon is especially useful if in the case of headache after nitrates the drug has to be changed.
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PMID:[The effect of nitroglycerin in patients with acute myocardial infarction. IV. Myocardon in patients with and without left ventricular failure (author's transl)]. 81 16

Corneal sensitivity has been studied in cluster headache (n = 38) and controls (n = 16). The patients were studied either during remission (n = 20), interparoxysmally in a bout (n = 17), or during attacks (spontaneously occurring attacks (n = 5) and nitroglycerin-provoked attacks (n = 6). For the measurements, a Cochet-Bonnet esthesiometer was utilized. This esthesiometer has a 6 cm long, adjustable nylon monofilament, which can be reduced in length by 0.5 cm at a time, the length of the filament determining the pressure exerted onto the corneal surface. All controls sensed the pressure at 6.0 cm filament length. In 5 cluster headache patients (remission, n = 4; cluster period, n = 1) a slight reduction in corneal sensitivity was found. No statistical difference was, however, found between any of the groups tested, and there was no asymmetry as far as averages were concerned.
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PMID:Corneal sensitivity during and outside attacks of cluster headache. 129 58

Amlodipine, a potent long-acting dihydropyridine calcium antagonist, was compared with placebo in a parallel, randomized, double-blind study in 134 patients with chronic stable angina pectoris maintained on beta-adrenergic blocking agents. After a single-blind, two-week placebo period, patients were randomized to receive either amlodipine (2.5, 5, and 10 mg) or placebo once daily for four weeks. The effects of amlodipine on maximal exercise time, work, time to angina onset, and subjective indices including angina frequency, nitroglycerin tablet consumption, and patient and investigator ratings were assessed. Each dose of amlodipine produced increases in exercise time and calculated total work accomplished compared to baseline. Improvements at 5 and 10 mg were significantly greater than placebo which produced no significant change (p less than 0.05). Qualitative improvements in the severity of angina were produced by amlodipine at 5 and 10 mg daily assessed by patient-rating questionnaires (p less than 0.05). Reductions in angina frequency attacks per week and weekly nitroglycerin tablet consumption occurred but were not statistically significant when compared with placebo. Adverse effects observed during amlodipine treatment prompted discontinuation of treatment in only 2 out of 100 patients. Three patients discontinued treatment for reported lack of efficacy. No laboratory abnormalities prompted treatment discontinuation and minor side effects of dizziness, nausea, headache, and fatigue were observed infrequently. The results of this controlled, large-scale multicenter trial suggest that amlodipine significantly increased exercise capacity and was well tolerated when added to the antianginal regimen of patients remaining symptomatic while receiving beta-blocking agents.
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PMID:Amlodipine combined with beta blockade for chronic angina: results of a multicenter, placebo-controlled, randomized double-blind study. 135 85

Six patients with episodic cluster headache were investigated as to blood pressure, heart rate, cerebrospinal fluid pressure (Pcsf) and frontal vein pressure (Pvf) during five nitroglycerin (NG) provoked attacks and one spontaneous attack. In a seventh studied patient the NG failed to provoke an attack. The earlier reported decrease of systolic blood pressure and increase of diastolic blood pressure and heart rate after NG administration were also found in these patients. The "dynamite headache" was related to the start and duration of an increase of the cerebrospinal fluid pressure. There was no relationship between the start or the maximum pain of the cluster headache attack and changes in Pcsf or Pvf. On breathing oxygen during a cluster headache attack, there was a decrease of Pcsf but in some patients a temporary increase of Pvf was observed, which possibly indicates that oxygen simultaneously attains constriction of arteries and veins.
Headache 1992 Oct
PMID:Cerebrospinal fluid pressure and venous pressure in "dynamite headache" and cluster headache attacks. 144 86

In a double-blind, randomized, placebo cross-controlled trial the effectiveness and the adverse effects of two types of buccal tablets containing 5 mg nitroglycerin: Polnitrin produced by Warsaw Pharmaceutical Works POLFA and its analogue of foreign origin, were assessed. The third compared preparation was sublingual nitroglycerin in 0.5 mg tablets. The longest dissolution in the buccal cavity showed Polnitrin (mean 6.6 hours). Polnitrin significantly increased the resting heart rate during 3 hours, and during 6 hours at maximal effort. The foreign analogue decreased significantly the systolic pressure during 3 hours after application. No significant differences were noted in the effects on the basic haemodynamic parameters between the compared buccal tablets. Exercise tolerance and coronary reserve were assessed with repeated exercise tests on moving track (Marquette Case-12). Immediately after being stuck to the gum Polnitrin, its analogue and sublingual nitroglycerin significantly prolonged the marching time: total, till pain, and till ischaemia. After 6 hours the marching time till pain appearance was significantly longer after Polnitrin than after placebo or its analogue. Local adverse effects connected with the presence of the tablet in the oral vestibule may hamper the treatment with Polnitrin in some cases. The most frequent side effect were headaches which are known to occur usually after all nitrates.
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PMID:[Evaluation of clinical effectiveness and adverse effects of Polnitrin]. 145 53

Eight patients with episodic cluster headache, five in active episode, three out of episode, were investigated as to diameters of intracranial arteries before and after nitroglycerin (NG) administration. The diameter of all intracranial carotids were increased about 10 minutes after NG, although more in the patients in episode than in patients out of episode. The dilatation remained for the next 60 minutes in the patients who did not get a cluster headache attack. There was a normalization of the diameters of the internal carotid arteries compared to the initial values, at maximum pain in all patients who got a cluster headache attack. Similar changes were also found in the basilar arteries. The findings support the hypothesis of a constriction of intracranial arteries at maximum pain in cluster headache attacks to stop the pain.
Headache 1992 Nov
PMID:MRI of intracranial arteries in nitroglycerin induced cluster headache attacks. 146 5

Since the time of Liveing and Gowers in the nineteenth century, migraine has been thought to be inherited, although family history has been widely studied, nearly all the reports are not scientifically based and studies on twins have never shown 100% concordance in monozygotic (MZ) pairs, indicating that migraine cannot be inherited by a single gene. Furthermore, the criteria for a polygenic trait are not fulfilled by migraine patients. The only two syndromes with a strong genetic basis of inheritance are familial hemiplegic migraine and migraine occurring in Mitochondrial Encephalomyopathy with Lactic Acidosis and Stroke-like episodes (MELAS). It is the predisposition to headache that is likely to be inherited; this is supported by the induction of migraine-like headaches with either m-chlorophenyl-piperazine (m-CPP) or nitroglycerin in normal subjects with a positive family history for migraine.
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PMID:Migraine and heredity. 149 12

The effects of N-acetylcysteine, a sulfhydryl group donor, on nitroglycerin-induced headache and dilation of temporal and radial arteries were investigated in 11 healthy volunteers. Nitroglycerin, 0.06 microgram/kg/min, was infused for 20 minutes immediately after and 120 minutes after pretreatment with N-acetylcysteine (100 mg/kg) or placebo. Arterial diameters were measured with high frequency ultrasound, and pain was scored by use of a previously evaluated 10-point scale. Plasma levels of free (n = 2) and total (n = 11) N-acetylcysteine were determined. N-Acetylcysteine potentiated the headache response (median headache score, 3 versus 1), and the headache retained its vascular characteristics. Temporal artery dilation was also potentiated by N-acetylcysteine, 139% +/- 3% versus 127% +/- 3% of baseline, whereas the radial artery was unaffected. The potentiation was most pronounced after the first nitroglycerin infusion (12% versus 4.5% compared with placebo). A prolonged dilation of the temporal artery was observed only after the first nitroglycerin infusion, when high levels of N-acetylcysteine were present.
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PMID:N-acetylcysteine enhances nitroglycerin-induced headache and cranial arterial responses. 150 48

Nitroglycerin was administered to eight healthy volunteers in the form of sublingual tablets, oral sustained-release tablets, and an oral solution. Blood samples were collected for measurement of nitroglycerin and its two isomeric glyceryl dinitrate metabolites. Blood pressure and pulse rate were monitored; subjective evaluations of headache, dizziness, facial flushing, skin irritation, and gastrointestinal upset were made. Nitroglycerin itself was virtually undetectable after the solution and tablet preparations; the metabolites were consistently detectable from a few minutes after dosing to 24 h later. Mean total (nitroglycerin plus metabolite) concentrations were comparable in the 15 min following sublingual administration, and the 8 h following tablet administration. The relative bioavailability of the tablets in comparison with the oral solution was 70 per cent based on metabolite concentrations. Nitroglycerin sustained-release tablets appear to exert their beneficial effects in the prolonged prophylaxis of angina through active metabolites.
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PMID:Pharmacokinetics of nitroglycerin and its metabolites after administration of sustained-release tablets. 155 Sep 9

Twenty-eight cluster headache patients were examined either in remission (n = 10), in the interparoxysmal period ("cluster phase") (n = 12), or during spontaneously occurring (n = 7), or nitroglycerin provoked (n = 7) attacks. Fourteen healthy controls participated in the study. Oxygen saturation (SaO2), end-tidal CO2 (PCO2), and respiratory rate (R.R.) were recorded for the controls and the patients during the different phases of cluster headache. Both PCO2 and SaO2 tended to be lower during the interparoxysmal period of the cluster phase when compared to the control group or to the remission. During both nitroglycerin-provoked and spontaneous attacks, PCO2 and SaO2 tended to respectively decrease and increase, both when compared with the "cluster phase" and with the period immediately prior to attack ("pre-attack"). Hence the "pre-attack" state may, on an average, be characterized by a slight hypoxia and a slight hyperventilation. Marked, clinically observable hyperventilation was present only in the occasional cluster headache patient. There was no SaO2 decrease from the "cluster phase" (interparoxysmal period) to the period immediately preceding the attack ("pre-attack"), and SaO2 "dips" preceding an attack were only observed in one cluster headache patient. As demonstrated previously by our group, a considerable lowering of SaO2 (i.e. partly to less than or equal to 83%) does only exceptionally lead to attack (Zhao et al, 1990). This observation combined with the evidence presented herein may seem to indicate that the slight pre-attack oxygen desaturation probably is too small to be a symptom-producing factor in cluster headache--be it in the spontaneously occurring or in the induced attack.(ABSTRACT TRUNCATED AT 250 WORDS)
Headache 1992 Mar
PMID:Cluster headache: oxygen saturation and end-tidal CO2 during and without attack. 156 43


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