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)

Fourteen patients, 2 to 20 years old were investigated. Two had primary pulmonary hypertension, 11 had congenital heart disease and post-tricuspid shunts, and 1, a 20-year-old patient, was investigated after he had undergone surgical correction of truncus arteriosus I. Pulmonary arterial pressure, pulmonary flow index, peripheral systolic blood pressure and heart rate were measured before, and several times after intrapulmonary injection into the pulmonary artery of 0.5 microgram nifedipine/kg. Six patients were given an additional dose of 1 microgram nifedipine per kilogram into the pulmonary artery and hemodynamic measurements were repeated. In eight children, receiving 100% oxygen via a breathing mask, nifedipine effects were compared with oxygen effects. After 10 minutes under oxygen, the same hemodynamics were determined as after nifedipine. In addition, in four of these children aortic pressure and arterial oxygen saturation were also measured. Maximal effects occurred within 4 minutes. 0.5 micrograms nifedipine per kilogram caused a slight reduction in mean pulmonary arterial pressure (p less than 0.05), as well as increase in pulmonary flow index (p less than 0.005). However, no significant change in heart rate or in systolic blood pressure was observed. 1 microgram nifedipine per kilogram IP had almost the same effects. No adverse side effects occurred, besides mild headaches in one child. A comparison of nifedipine injected into the pulmonary artery with oxygen breathing in congenital heart disease combined with pulmonary hypertension, is reported for the first time. Nifedipine had a more pronounced and beneficial effect with a selective action on the pulmonary vascular bed.
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PMID:Hemodynamic effects of nifedipine and oxygen in children with pulmonary hypertension. 315 41

Nifedipine, the dihydropyridine calcium channel antagonist prototype, is characterized by wide variability of its hepatic first-pass metabolism and individual response. This could be due to a new genetic polymorphism of drug metabolism, and this hypothesis was investigated in a randomized and cross-over population study in normal volunteers (n = 80). The kinetics and effects of an oral dose of nifedipine (10 mg) and (+/-)-nicardipine (20 mg), a second generation derivative with presumed different biotransformation routes, were evaluated at 0, 1, 2 and 3 h. The two drugs displayed a similar pharmacodynamic profile in terms of heart rate and blood pressure. The observed frequency distributions showed no asymmetry or bimodality suggesting polymorphism. The frequency of headaches and flushes were 21/80 and 19/80 respectively for nifedipine and (+/-)-nicardipine. At the doses administered nifedipine and (+/-)-nicardipine show the same efficacy. This study does not confirm the presence of polymorphism in the response to these dihydropyridines.
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PMID:[Absence of polymorphism in individual response to the dihydropyridines nifedipine and (+/-)-nicardipine]. 322 86

Nifedipine, 30 mg/day for 4 weeks, was compared to placebo in a double-blind, randomized, crossover study, as an additional drug added to the usual treatment of 14 patients with bronchial asthma. Nifedipine did not significantly change peak expiratory flow rates or subjective symptoms like cough, sputum, wheezing, shortness of breath, or disturbed sleep. Nifedipine did not decrease the number of salbutamol rotacaps inhaled per day. Arterial blood pressure significantly decreased (p less than 0.01) after nifedipine treatment, and side effects (headache and flushing) were not uncommon. In this study, long-term treatment with nifedipine had essentially no effect on subjective symptoms at peak expiratory flow rates.
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PMID:Nifedipine treatment of patients with bronchial asthma. 329 78

Objective evidence of transient ischaemia can be obtained by ST-segment analysis of ambulatory ECG recordings. To compare the anti-ischaemic effects of isosorbide 5-mononitrate (IS 5-MN) and nifedipine in sustained-release formulations, we entered 16 patients with documented spontaneous ischaemic episodes in a double-blind cross-over study. The study consisted of four 1-week treatment periods with repeated 24-hour recordings at the end of each period. Nifedipine 3 X 20 mg/day was compared to IS 5-MN 3 X 20 mg/day and IS 5-MN 50 mg once daily for 1 week each. 12 patients completed the study protocol: 1 withdrew because of headache, 1 developed hyperthyroidism and in 2 patients the study was discontinued because the anginal symptoms became unstable. For the entire group both ways of treatment showed beneficial effects with significant reductions of the number of episodes (reduced by 65-68%, p less than 0.01), duration of episodes (reduced by 65-70%, p less than 0.05) and degree of ST deviation (reduced by 39-70%, p less than 0.05). With both IS 5-MN (7 of 12 and 6 of 12 patients) and nifedipine (5 of 12 and 8 of 12) a part of the group of patients became free of ischaemic episodes. In individual patients, however, different patterns of response were observed: 3/12 showed a complete response on both treatments, 1/12 was free on IS 5-MN only and 1/12 on nifedipine only.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of isosorbide 5-mononitrate 20 mg, sustained-release 50 mg and sustained-release nifedipine 20 mg on ischaemic ST-segment changes during Holter monitoring. A double-blind cross-over study in patients with spontaneous angina pectoris. 330 Sep 77

The effect of food on the bioavailability of nifedipine (Procardia), 10 mg capsules, was studied. Each of 15 male volunteers received a single oral 10 mg dose with 120 ml water under three conditions: fasting, after a low-fat (high-carbohydrate) meal, and after a high-fat meal. An open, three-way Latin-square design was employed with a 4-day washout period between administrations. Serial blood samples were collected just before the dose (0 hour) and from 0 to 8 hours after administration. Nifedipine assays were performed by GLC/electron capture detection. Diet did not appreciably alter the AUC from 0 to 8 hours, the AUC from 0 to infinity, or the elimination half-life. The time to peak (tmax) and peak concentrations (Cmax) were significantly altered by food. The mean Cmax values for fasting, low-fat, and high-fat meals were 78.9, 42.2, and 58.7 ng/ml, respectively. The mean tmax values for these three conditions were 0.97, 1.89, and 1.07 hours, respectively. The results indicate that food, in particular a low-fat (high-carbohydrate) meal, slows the rate but does not alter the extent of nifedipine absorption. Insofar as certain side effects (e.g., flushing and headache) may be related to the high peak plasma levels associated with rapid absorption, administration with meals might serve to reduce the incidence of such effects. Clinical trials would be necessary to confirm this possibility. For the majority of patients on routine maintenance therapeutic regimens, nifedipine capsules may be administered without regard to food intake.
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PMID:Effect of food on nifedipine pharmacokinetics. 359 68

In 93 patients with hypertension uncontrolled by bendrofluazide 5 mg plus atenolol 100 mg daily, the effects of adding nifedipine (up to 60 mg/day, n = 31), prazosin (up to 20 mg/day, n = 31), or hydralazine (up to 200 mg/day, n = 31) were compared in a 6 month open random parallel group study. The three drugs did not differ significantly as regards antihypertensive effect, withdrawal rate, total number of side effects, or effect on serum biochemical variables. The pattern of side-effects differed. Headache, flushing and oedema were common with nifedipine, tiredness and drowsiness with prazosin, and headache with hydralazine. Nifedipine is an acceptable third-line antihypertensive drug which may have some advantage over hydralazine and prazosin.
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PMID:Comparison of nifedipine, prazosin and hydralazine added to treatment of hypertensive patients uncontrolled by thiazide diuretic plus beta-blocker. 367 Dec 50

Four adolescents with achalasia were treated with nifedipine. All the patients' symptoms improved dramatically. On manometric evaluation, following oral nifedipine, the lower esophageal sphincter pressure decreased approximately 50%. No change in esophageal peristaltic activity was noted. Side effects were minimal; two patients had mild headache initially. Nifedipine, which is commonly used in adult patients with achalasia, may be beneficial for short-term symptomatic relief in children until more definitive therapy can be performed.
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PMID:The use of nifedipine for the treatment of achalasia in children. 379 5

A controlled multicentre trial was organised to compare the effects of 20 mg Nifedipine tablets (N) and 2,5 mg Indapamide tablets (I) during a 4 months' treatment period after a placebo period, in 59 patients with moderate essential hypertension (n = 59). The results of blood pressure measurements of 18 patients treated by nifedipine (1 tablet twice daily) and 22 patients treated by indapamide (1 tablet every morning) were compared. The systolic blood pressure, after 10 minutes recumbency, fell from 165 +/- 10 mmHg to 148 +/- 13 mmHg (p less than 0.01), and the diastolic pressure from 104 +/- 6 mmHg to 86 +/- 7 mmHg (p less than 0.01) in the patients treated with nifedipine. In the indapamide group, the SBP fell from 164 +/- 13 mmHg to 152 +/- 15 mmHg (p less than 0.01) and the DBP from 100 +/- 4 mmHg to 87 +/- 6 mmHg (p less than 0.01). There were no significant changes of heart rate with either drug; plasma creatinine, potassium and uric acid concentrations were also unchanged. There was a higher incidence of headaches and tiredness in the nifedipine group, whilst patients treated with indapamide complained more often of muscular cramps. Flushing was observed in nearly a quarter of the patients in both groups. These results confirm that both nifedipine and indapamide induce significant and persistant falls in systolic and diastolic blood pressure. Although the fall was greater with nifedipine than with indapamide, the difference was not statistically significant. The tolerance was satisfactory in both groups of patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Comparative effects of nifedipine and indapamide in the treatment of arterial hypertension]. 393 9

In migraine patients the effect of calcium antagonists (flunarizine, verapamil and nifedipine) on both venous and pupillary neuromuscular functions, as well as on blood pressure have been evaluated. A single oral dose of flunarizine (10 mg) and verapamil infusion (50 micrograms/ml/min) increased venous compliance. Verapamil also counteracted dose-dependent dopamine induced venoconstriction. Nifedipine (10 mg orally) reduced mean arterial pressure in upright position in migraineurs but not in controls. In addition, chronic treatment with flunarizine (10 mg for 2 weeks) induced a transient miotic effect and a reduction of tyramine induced mydriasis. These findings demonstrated that calcium antagonists affect vascular and extravascular structures. It is postulated that, in migraine, calcium entry blockers may prevent exaggerated responses to catecholaminergic stimulation.
Cephalalgia 1985 May
PMID:Pupillary and vascular effects of calcium antagonists in migraine. 401 32

Calcium channel blockers are assuming increasingly important roles in the practice of emergency medicine. Two cases and a review of the literature relating to treatment of hypertensive emergencies with nifedipine are presented. Nifedipine has a rapid onset of action (buccal, 10-15 minutes; oral, 30-45 minutes) and peak effect (buccal, 30 minutes, oral, 60 minutes). The duration of effects is four to six hours regardless of the route of administration, with a mean arterial pressure reduction of 21.6% (248/134 mm Hg to 165/87 mm Hg). In patients with severe hypertension and left ventricular failure, a consistent reduction in systemic vascular resistance (2,088 dynes/sec/cm-5 to 1242 dynes/sec/cm-5) and cardiac index (2.76 l/min/m2 to 3.77 l/min/m2) has been reported. The patients in this study had severe hypertension (systolic blood pressure greater than 180 mm Hg, diastolic blood pressure greater than 120 mm Hg) and end organ involvement (including heart failure, left ventricular strain, headache, confusion, dizziness, and shortness of breath). Nifedipine (10 mg) was administered buccally with prompt reduction of blood pressure and resolution of the patients' symptoms. Nifedipine appears to be a safe, effective agent for the management of hypertensive emergencies. Its pharmacokinetic profile and routes of administration make it particularly valuable in the practice of emergency medicine.
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PMID:Nifedipine in the management of hypertensive emergencies: report of two cases and review of the literature. 406 18


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