Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 47 year old man with episodes of attacks of pain, redness and mild blurring of vision was investigated for narrow angle glaucoma in view of shallow anterior chambers and a cupped optic disc. The history was reviewed following a spontaneous attack in hospital, which had features other than acute glaucoma. A diagnosis of cluster headache was made on the basis of tests. Cluster headache has been defined as unilateral intense pain, involving the eye and head on one side, usually associated with flushing, nasal congestion and lacrimation; the attacks recurring one or more times daily and lasting 20 - 120 minutes. Such attacks commonly continue for weeks or months and are separated by an asymptomatic period of months to years. This episodic nature, together with unilaterality and tendency to occur at night, closely mimics narrow angle glaucoma. Further, if patients have shallow anterior chambers and disc cupping, the differentiation becomes more difficult yet critical. Resource to provocative tests is often the only answer as the following case report demonstrates.
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PMID:Cluster headache or narrow angle glaucoma? 181 Aug 83

A double-blind, placebo-controlled trial was carried out in 40 patients affected by multi-infarct dementia to see if a daily intravenous infusion of 3 mg co-dergocrine mesylate ('Hydergine') over 14 days would improve severely deteriorated elderly patients and shorten the latent period (3 months) which is observed when the drug is given orally. All the patients had severe mental impairment, psychological deficit or altered consciousness. A Hachinski score of 7 or more, and a cumulative score of at least 12 points on SCAG scale Items 1, 2 and 4 (anxiety/depression) and/or Items 5, 6 and 8 (alertness/confusion) were required for admission. After 1 week of intravenous infusion of placebo, patients were randomly allocated to treatment with co-dergocrine mesylate or placebo, from Day 1 to Day 14. The solutions were infused over a period of 2 hours. During the follow-up period from Day 15 to Day 21, the patients did not receive any treatment. Thirty-six patients (17 on co-dergocrine mesylate, 19 on placebo) completed the study. The results, as rated on the SCAG scale, indicated significant improvements, in favour of co-dergocrine mesylate, in cognitive dysfunction, mood depression, withdrawal and overall impression. Furthermore, the factor fatigue on the Nowlis scale and clinical global assessments by physicians also showed significant advantages of the co-dergocrine mesylate group over placebo. Nine out of 17 co-dergocrine mesylate patients complained of side-effects, usually experienced during infusion; they consisted mainly of nausea (6 patients), gastric discomfort (2 patients), and tremor, nasal congestion, flushing, hypotension and hypertension (1 patient each). Despite the appearance of side-effects, general tolerability was rated as 'good' by both physicians and patients. It is concluded, therefore, that intravenous high dose co-dergocrine mesylate treatment has a fast and clinically relevant effect on the key clinical symptoms of multi-infarct dementia.
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PMID:Effects of intravenous high dose co-dergocrine mesylate ('Hydergine') in elderly patients with severe multi-infarct dementia: a double-blind, placebo-controlled trial. 268 Feb 86

Fenoldopam, a dopaminergic agonist, was administered intravenously to 18 healthy male subjects in doses ranging from 0.025 to 1.0 microgram/kg/min for 2 hours. Three subjects were studied in a three-way crossover of fenoldopam at doses of 0.025, 0.10, and 0.50 microgram/kg/min. Fenoldopam decreased diastolic blood pressure and increased pulse rate without changing systolic blood pressure. Fenoldopam produced dose-related increases in para-aminohippuric acid clearance up to 75% at the 0.50 microgram/kg/min dose. This increase in renal blood flow was accompanied by increases in urine volume, water, and solute excretion; glomerular filtration rate was unchanged. Doses greater than 0.25 microgram/kg/min caused flushing and nasal congestion. The dopamine receptor antagonist metoclopramide (0.1 mg/kg/hr) did not block the systemic hemodynamic effects of fenoldopam but attenuated the increase in para-aminohippuric acid clearance. Fenoldopam plasma levels achieved steady state between 30 and 120 minutes after the start of the infusion and were linear with respect to infusion rate. Our findings show that intravenous fenoldopam causes systemic arteriolar vasodilation, accompanied by renal vasodilation and increased sodium excretion.
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PMID:The effect of fenoldopam, a dopaminergic agonist, on renal hemodynamics. 288 Jun 88

The effects of 9 beta-methyl carbacyclin, a chemically stable analogue of epoprostenol (prostacyclin, PGI2) were studied, in comparison with epoprostenol, both in vitro and in vivo in man. In vitro 9 beta-methyl carbacyclin and epoprostenol inhibited platelet aggregation induced by ADP, collagen, the endoperoxide analogue U46619 and arachidonic acid. The potency of 9 beta-methyl carbacyclin relative to epoprostenol was comparable in ADP and collagen-aggregated platelet rich plasma (PRP), 9 beta-methyl carbacyclin being 0.01 times as active as epoprostenol. The anti-aggregatory potencies of the two compounds were comparable in PRP and whole blood. The phosphodiesterase inhibitor isobutyl methyl xanthine enhanced the anti-aggregatory activity of both compounds in vitro. 9 beta-methyl carbacyclin and epoprostenol elevated platelet cyclic AMP, 9 beta-methyl carbacyclin being 0.04 times as active as epoprostenol. In a placebo controlled trial both drugs produces significant headache and facial flushing when compared with placebo. Nasal stuffiness, abdominal discomfort and nausea were reported on all three treatments. Both drugs caused significant and comparable increase in heart rate and decrease in pre-ejection (PEP) and PEP/left ventricular ejection time (LVET) ratio compared with placebo. Systolic and diastolic blood pressure, LVET and QS2 index were unchanged. Platelet aggregation responses to ADP were significantly inhibited by all three doses of both drugs compared with placebo. Bleeding time was significantly longer during epoprostenol infusion than either placebo or 9 beta-methyl carbacyclin infusion. Neither drug had significant effect, compared with placebo, on kaolin activated clotting time in PPP, PRP or in PRP in the presence of heparin, prothrombin time, partial thromboplastin time, thrombin clotting time, fibrinogen, fibrinogen degradation products or euglobulin clot lysis time. The pharmacodynamic effects and duration of action of 9 beta-methyl carbacyclin and of epoprostenol are similar; 9 beta-methyl carbacyclin is approximately 100 times less potent than epoprostenol in man.
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PMID:A chemically stable analogue, 9 beta-methyl carbacyclin, with similar effects to epoprostenol (prostacyclin, PGI2) in man. 608 4

Prostaglandin D2 (PGD2) was infused intravenously into normal male volunteers. Seven subjects received infusions of 16, 32, 64 ng/kg/min and six of these a further dose of 128 ng/kg/min. Each individual's maximum dose was limited by discomfort caused by intense facial flushing and nasal congestion. At these doses there was no significant effect on systolic or diastolic blood pressure nor on spirometric measurements. There was a small but statistically significant tachycardia at 64 and 128 ng/kg/min. Collagen- and adenosine diphosphate (ADP)-induced platelet aggregation ex vivo was not affected at any of the infusion rates. Infused PGD2 is unlikely to be a useful antithrombotic agent.
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PMID:Effects of intravenous infusions of prostaglandin D2 in man. 659 53

Following an open pilot study, BW 245C , a hydantoin prostaglandin analogue, was given by mouth in an aqueous solution to six healthy volunteers. The subjects received BW 245C 50 and 150 micrograms and placebo on separate occasions according to a double blind randomised design. Heart rate, blood pressure and, using visual analogue scales, facial flushing, abdominal discomfort and headache, were measured before dosing, at 15 minute intervals after dosing for 2 hours and at 30 minute intervals for a further 2 hours. Platelet aggregation responses to ADP and to collagen were measured before dosing and at 15 minutes, 45 minutes, 2 hours and 4 hours after dosing. Cutaneous bleeding time was measured before and 45 minutes after dosing. 150 micrograms BW 245C produced significant (p less than 0.05) facial flushing over the period from 15 to 120 minutes after dosing. Heart rate increased slightly but significantly (p less than 0.05) in response to both doses of 245C only at 75 minutes after dosing. Systolic and diastolic blood pressures were unchanged by either dose of BW 245C . Platelet aggregation responses to ADP were significantly (p less than 0.05) inhibited only at 120 minutes after 150 micrograms BW 245C . Aggregation responses to collagen were significantly (p less than 0.05) inhibited 45 and 120 minutes after 150 micrograms BW 245C and also at 120 minutes after 50 micrograms BW 245C . Bleeding time was unchanged in response to either dose of BW 245C . There was no change in headache or abdominal discomfort scores following either dose of BW 245C . Nausea was reported after 7 out of 12 administrations of BW245C but not after placebo. Nasal congestion was experienced by two subjects receiving 150 micrograms BW 245C and muscle tension and stiffness, especially of the jaw muscles, was also reported following administration of BW 245C but not of placebo. BW 245C is active when given by mouth and has similar pharmacodynamic effects to prostacyclin in man.
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PMID:Effects of single oral dose administration of a hydantoin prostaglandin analogue BW 245C in man. 672 64

A 23-year-old Asian with histamine-reactive asthma complained of recurrent chest tightness, nasal congestion and flushing immediately after drinking minimal amounts of alcoholic beverages. He was extensively studied to determine the possible mechanism of his alcohol-induced respiratory symptoms. Drinking of either beer or 95 percent ethanol in apple juice immediately provoked vasomotor signs and moderately severe bronchospasm (54 percent and 73 percent decreases in specific airway conductance, respectively), which spontaneously improved over 30 minutes and two hours, respectively. Intravenous and inhaled ethanol caused less bronchospasm than observed with oral ethanol, and recovery was rapid. Pretreatment with cromolyn sodium (inhaled or oral) and isoproterenol had no inhibitory effect on the alcohol-induced bronchoconstriction, whereas atropine, acetylsalicylic acid, cyproheptadine, and chlorpheniramine appeared to have a partial inhibitory effect. Approximately 70 percent inhibition was observed after chlorpheniramine. Observations in this patient suggest that the bronchoconstriction induced by alcoholic beverages is related to their ethanol content and may be related to formation or release of one or more bronchoconstrictor and vasoactive compounds, including a stimulant of histamine1-receptors. The route of ethanol administration may also influence the bronchospastic response.
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PMID:Alcohol-induced bronchospasm in an asthmatic patient: pharmacologic evaluation of the mechanism. 724 61

Autonomic dysreflexia (AD) is a syndrome that consists of facial flushing, excessive sweating, nasal congestion, throbbing headache and paroxysmal hypertension which may occur in response to bladder distension in patients with spinal cord lesions above the T6 level. We report the case of a C2 quadriplegic patient who developed clinical features of AD along with cortical blindness and seizures after administration of meglumine (Hypaque) for diagnostic cystogram.
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PMID:Seizures and cortical blindness after meglumine (hypaque) administration: a variant of autonomic dysreflexia. 812 Mar 39

Sildenafil citrate, an oral therapy for erectile dysfunction, is a selective inhibitor of cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase type 5 (PDE5), the predominant isozyme metabolizing cGMP in the corpus cavernosum. Chemically, it is a compound of the pyrazolo-pyrimidinyl-methylpiperazine class. Sildenafil has no direct relaxant effect on human corpus cavernosum but enhances the relaxant effect of nitric oxide (NO) on the corpus cavernosum by inhibiting PDE5, which is responsible for degradation of cGMP in this tissue. When sexual stimulation causes local release of NO, inhibition of PDE5 by sildenafil increases concentrations of cGMP in the corpus cavernosum, causing smooth muscle relaxation and blood flow into the penis, resulting in an erection. Sildenafil at recommended doses has no effect in the absence of sexual stimulation. The drug is rapidly absorbed after oral administration, with absolute bioavailability of 40%. Its pharmacokinetics are dose proportional over the recommended dosage range. Maximum plasma concentrations are reached within 30 to 120 minutes after oral dosing in the fasting state. Sildenafil is cleared predominantly by the hepatic microsomal isoenzymes CYP3A4 (major route) and CYP2C9 (minor route). Clinical studies assessed the effect of sildenafil on the ability of men with erectile dysfunction to engage in sexual activity and, specifically, to achieve and maintain an erection sufficient for satisfactory sexual intercourse. Sildenafil was evaluated at doses of 25, 50, and 100 mg in randomized, double-masked, placebo-controlled clinical trials of up to 6 months' duration. The drug was administered to hundreds of patients aged 19 to 87 years having erectile dysfunction of various etiologies for a mean duration of 5 years. Sildenafil was associated with statistically significant improvement in erectile function compared with placebo. Adverse effects reported at a rate of >2% were headache, flushing, dyspepsia, nasal congestion, urinary tract infection, abnormal vision, diarrhea, dizziness, and rash. No cases of priapism were reported. The use of sildenafil is contraindicated in men who are taking organic nitrates, because of the potential for a precipitous decrease in blood pressure. Postmarketing reports and surveillance have revealed at least 39 deaths with sildenafil use in men having a history of heart disease, men taking nitrate medications, and men in poor physical health due to lack of exercise. Many of the men who experienced serious adverse effects or death had a variety of concomitant diseases and were taking multiple medications.
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PMID:Safety and efficacy of sildenafil citrate in the treatment of male erectile dysfunction. 991 1

Sildenafil is a selective and by oral administration potent type-5 phosphodiesterase (PDE 5) inhibitor, which increases the erection by corpus cavernosum smooth muscle relaxation. In a non-placebo controlled study, 134 patients with erectile dysfunction were treated with oral sildenafil. The aim of the study was to estimate the efficacy and adverse effects of this treatment. 51 patients (38%) had psychogenic, and 83 (62%) organic origin of the erectile dysfunction. 73 of them have already had some treatment for this problem before. The effective dose was 50 mg for 84 patients (63%), 100 mg for 32 (24%) and 25 mg for 4 patients. The treatment was effective for 120 patients (90%). The most common adverse effect was flushing in 18 (13%) and headache in 9 (7%) cases, two patients had headache and flushing together. Nasal congestion and visual disturbances were complained by two patients. Two patients reported prolonged (max. 2h) erections. Cardiological investigation was performed for cardiovascular patients and for patients with risk factors. Exact criteria of the cardiological opinion of sildenafil treatment are reviewed. Cardial or other serious adverse effects were not observed. It was not necessary to stop the treatment because of the adverse effects. The authors found, that sildenafil is an effective and safe treatment for the erectile dysfunction.
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PMID:[Effectiveness and adverse effects of sildenafil in erectile dysfunction]. 1069 32


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