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)

The contractile response to three different prostanoids of the isolated human myometrium and the different layers of the uterotubal junction (UTJ) was studied in vitro. The prostaglandin endoperoxide, PGH2, stimulated contractility of both the myometrium and the outer and inner muscle layers of the UTJ, whereas the intermediate layer of the UTJ was inhibited. Thromboxane A2 generated from PGH2 and a thromboxane synthase preparation caused a stimulation of both the myometrium and all three layers of the UTJ. The stimulatory response to TxA2 occurred at concentrations as low as 50-70 pg/ml. The sodium salt of PGi2 was found to relax both the myometrium and all the layers of the UTJ. Intravenous administration of PGI2 in repeated doses between 2-8 microgram induced facial flushing and headache but had little if any effect on in vivo uterine contractility. At least under in vitro conditions, these short-lived prostanoids and/or their metabolites apparently have a specific action on uterine contractility, an action which is manifested at comparatively low concentrations.
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PMID:PGH2, TxA2 and PGI2 have potent and differentiated actions on human uterine contractility. 701 35

Bumetanide was compared with furosemide in a total of 43 outpatients with edema due to renal disease, selected from three clinics following a uniform protocol. By random selection, 31 patients received 1 to 10 mg/day bumetanide, and 12 received 40 to 400 mg/day furosemide for at least six months. The patients were evaluated clinically, by standard laboratory tests, as well as by ECG, audiometry, eye examination, and mammary examination. Pooled statistical analysis of the results was done. Edema, body weight, and abdominal girth were reduced during both treatments. There was no significant difference in the mean response to the two diuretic agents by the two sided probability test in the other parameters studied, e.g., supine and standing blood pressure and pulse, serum electrolytes (sodium, potassium, chloride), and uric acid. There were no differences in liver function tests, hematology, or chest x-ray, and no remarkable effects on hearing. Gynecomastia improved in some patients while being treated with bumetanide after spironolactone was discontinued. Adverse reactions in patients on bumetanide which were considered possibly or probably related to the drug were muscle cramps (two patients); and vertigo, headache, muscle pain, urticaria, chest pain, arthritis, dehydration, postural hypotension, and leg cramps (one each). Laboratory abnormalities in both groups were generally those that could be attributed to the pharmacologic action of the diuretics or due to the patients' underlying disease states. No drug-related adverse effects were noted in ECG, ophthalmologic examinations, or chest x-rays. Two patients in the furosemide group had a probably or possibly drug-related loss of hearing sensitivity. In summary, bumetanide appeared to be as safe and as efficacious as furosemide in controlling edema and hypertension in patients with renal disease.
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PMID:Long-term bumetanide treatment of patients with edema due to renal disease. Cooperative studies. 704 Apr 92

A patient with disabling postural tachycardia without postural hypotension had symptoms that included palpitations, weakness, abdominal and leg pain, light-headedness, headache and diaphoresis that occurred only in the upright position. She was shown to have an enhanced sympathetic neural response to standing (exaggerated plasma nor epinephrine response), and her cardiovascular responsiveness to released catecholamines was clearly intact. However, she was unable to maintain normal sodium balance and had a measurably reduced plasma volume while consuming normal amounts (120 mmol daily) of dietary sodium. Sodium loading (240 mmol ingested daily plus administration of fluorohydrocortisone, 0.1 mg daily) largely corrected the hemodynamic abnormalities, prevented postural symptoms and caused the compensatory sympathetic response to revert to normal.
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PMID:Postural tachycardia syndrome. Reversal of sympathetic hyperresponsiveness and clinical improvement during sodium loading. 708 Dec 80

This study compares the frequency of dialysis disequilibrium symptoms (DDS), in 17 stable non-diabetic chronic hemodialysis patients, during a period using low glucose (200 mg/100 ml) dialyzate to a similar period using a glucose free dialyzate. There was a significant decrease in the total number of symptoms as well as the frequency of headache and post-dialysis fatigue during the low glucose period as compared to the glucose free period. The decrease in nausea or vomiting, and cramps was not significant while frequency of hypotension was unchanged. Evaluation of serum sodium, potassium, BUN, glucose and osmolarity did not reveal significant differences during the two periods. Dialysis with a low glucose bath produces less DDS than glucose free dialyzate.
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PMID:Improvement in disequilibrium symptoms during dialysis with low glucose dialyzate. 714 23

Although genuine gastro-intestinal allergy is sought as the cause of chronic urticaria or repeated vaso-motor headaches, a non-allergic intolerance of one or more ingested substances, additives to foodstuffs (colourants and conserving agents) are likely to be implicated. Dietary histories from such patients often reveal heavy consumption of charcuterie. Oral provocation tests, performed using additives and placebo, can reproduce symptoms reliably. The substance most frequently incriminated is sodium nitrite (E 250): out of 76 tests, 4 were positive and 4 doubtful. In these cases complete avoidance of E 250 led to significant improvement or cure. We discuss various hypotheses on the harmful effects of sodium nitrite, such as denaturation of histamine-binding SH-group rich mucoproteins, direct toxicity on microvilli or inhibition of intestinal histaminase.
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PMID:[Role of sodium nitrite in histamine urticaria of dietary origin]. 725 12

1. A randomised, placebo controlled, double-blind, parallel group study was conducted to assess the effect of tenidap sodium, a novel cytokine modulating drug, on the stable hypotensive response to the angiotension converting enzyme (ACE) inhibitor enalapril in subjects with mild to moderate, uncomplicated, essential hypertension. 2. Twenty-four male and female hypertensives, aged 33-77 years, received either 120 mg tenidap sodium or matched placebo daily for 22 days concomitantly with enalapril. 3. Mean endpoint supine and standing, systolic and diastolic pressures remained within 10% of baseline in each treatment group. However, the endpoint values were marginally above baseline during double-blind treatment with tenidap and marginally below baseline in the group receiving placebo. The increases in supine and standing systolic pressures in the tenidap group differed significantly from the changes in the placebo group. There were no significant differences between groups in changes in pulse rate. 4. Gastrointestinal side effects of mild to moderate severity attributed to treatment with tenidap were experienced by five subjects, one of whom was withdrawn during the third week of treatment. One subject receiving placebo was withdrawn because of a moderate headache attributed to study treatment. 5. The results of this study suggest that treatment with tenidap may interfere with the anti-hypertensive efficacy of ACE inhibitors. It is recommended that blood pressure should be monitored when tenidap is administered concomitantly with an ACE inhibitor.
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PMID:The effect of tenidap on the anti-hypertensive efficacy of ACE inhibitors in patients treated for mild to moderate hypertension. 754 97

The safety and efficacy of treatment of tension-type headache with either ketoprofen or ibuprofen and naproxen sodium were evaluated in a prospective, randomized, double-blind parallel-group-study in 345 subjects. All patients were valid for evaluation of efficacy and safety. Headache pain intensity and pain relief were measured on categorical verbal scales 30, 45, 60, 120, 180 and 240 min after ingestion of a single dose of 12.5 mg or 25 mg ketoprofen, 200 mg ibuprofen and 275 mg naproxen sodium. At no time in four hours observation the efficacy of the four treatments differed, neither in pain intensity difference nor in the pain relief scale. A statistical comparison test was performed only once analysing the primary efficacy variable, the sum of pain intensity differences. There was no statistically significant difference among all treatments in this respect. The results of this clearly indicate that ketoprofen in a dosage of 12.5 or 25 mg, compared to 200 mg ibuprofen and 275 mg naproxen sodium, is an effective and safe treatment in tension-type headache.
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PMID:Comparison ketoprofen, ibuprofen and naproxen sodium in the treatment of tension-type headache. 755 17

This multicenter, open-label trial was designed to study the safety of intravenous (IV) sodium valproate in patients with epilepsy. All 318 patients (previously treated with antiepileptic drugs) were hospitalized for seizure control or anticipated seizures. The protocol allowed physicians to set the number of infusions and treatment duration. Adverse events, laboratory studies performed, and seizure activity were documented on case report forms. The patients' mean age was 34.4 years (range, 2-87 years). The most common reason for admission was lack of seizure control (235 patients, 185 of whom were admitted for video-electroencephalographic monitoring). The median dosage of valproate was 375 mg infused over 1 hour. The median number of doses was four, given over 2 days. In 54 patients (17%), transient adverse events were reported. The most frequent were headache, reaction at the injection site, and nausea (2.2% each); somnolence (1.9%); vomiting (1.6%); and dizziness and taste perversion (1.3% each). No persistent or severe hematologic or serum chemistry abnormalities were found. Vital signs were not significantly affected by the IV infusion of valproate. At the dosages and rates of administration studied, intravenous valproate appears to be safe and well tolerated.
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PMID:Safety of intravenous valproate. 757 66

The use of psychotropic drugs has been associated with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in a number of case reports. SIADH is characterised by the sustained release of antidiuretic hormone (ADH) from the posterior pituitary. The patients have a reduced ability to excrete diluted urine, ingested fluid is retained, and the extracellular fluid expands and becomes hypo-osmolar. The cardinal signs are hyponatraemia, serum hypoosmolality and a less than maximally diluted urine. Common symptoms include weakness, lethargy, headache, anorexia and weight gain. These symptoms may be followed by confusion, convulsions, coma and death. The early symptoms are vague and nonspecific, and they may even mimic the symptoms of the psychiatric disorder itself. For antidepressants, the risk of SIADH seems to be highest during the first weeks of treatment. For antipsychotics, the risk seems to be more spread out in time. The causative role of the drug may sometimes be difficult to estimate, as even drug-free psychiatric patients, mostly those with schizophrenia, develop SIADH on the basis of psychogenic polydipsia. Smoking is another factor associated with the development of SIADH, and the risk may also increase with age. The acute treatment of SIADH induced by a psychotropic drug includes discontinuation of the drug as well as restriction of fluid intake. In cases with significant clinical symptoms, infusion of sodium chloride is recommended. After the acute management, it is useful to evaluate the causative role of the drug by performing a water loading test and/or drug rechallenge. If continued treatment with an antidepressant or antipsychotic is indicated, a drug with a different pharmacological profile should be chosen, and the serum sodium levels should be monitored closely. If treatment with the drug that caused SIADH must be continued, concomitant treatment with demeclocycline may reduce the tendency of hyponatraemia.
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PMID:Hyponatraemia and the syndrome of inappropriate antidiuretic hormone secretion (SIADH) induced by psychotropic drugs. 761 32

1. The role of nitric (NO) in the regulation of capillary and arteriovenous anastomotic blood flow was evaluated in the carotid circulation of the pig. For this purpose, the effect of intracarotid (i.c.) infusions of saline and two NO donors, nitroprusside sodium (NPR) and S-nitroso-N-acetylpenicillamine (SNAP) in concentrations of 3-100 micrograms min-1 was studied on systemic haemodynamics and carotid blood flow and its distribution in anaesthetized pigs with low arteriovenous anastomotic blood flow, by use of the radioactive microsphere method. 2. Apart from heart rate, which increased after both NPR and SNAP, no major changes in systemic haemodynamic variables were observed. In contrast to saline, both NPR and SNAP increased common carotid blood flow, vascular conductance and vascular pulsations dose-dependently. 3. The distribution of the carotid artery blood flow over capillary and arteriovenous anastomotic fraction remained stable after saline infusions. Both NPR and SNAP enhanced total capillary blood flow and conductance. In contrast to NPR, arteriovenous anastomotic blood flow and conductance were increased by SNAP. 4. At the tissue level, capillary blood flow increases following NPR or SNAP were reflected by an increase in both extracerebral and dural blood flow without changes in total brain blood flow. 5. These results indicate that both NO donors cause arteriolar dilatation together with enhanced vascular pulsations in the carotid circulation of the pig. Probably by way of a 'steal' phenomenon, this pronounced arteriolar dilatation limits the effect of NO donors on arteriovenous anastomoses. 6. The results of the present investigation support the contention that dilatation of intra- and extra cranial arteries and arteriovenous anastomoses leads to increased vascular pulsations, which (rather than increased blood flow) could, at least in part, be responsible for the headache caused by nitro vasodilators.
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PMID:The effect of nitric oxide donors on haemodynamics and blood flow distribution in the porcine carotid circulation. 762 Jul 22


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