Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a double-blind 3-month study in mild-to-moderate essential hypertensive patients over 50 years of age, ketanserin, a selective S2-serotoninergic antagonist with additional alpha 1-adrenergic blocking properties, has been compared with enalapril, an angiotensin-converting enzyme inhibitor. Supine and upright blood pressures and heart rates were recorded for placebo and during active treatment (-4, -2, 0, 2, 4, 6, 8, 10, and 12 weeks). Metabolic profile (plasma glucose, creatinine, sodium, potassium, total and HDL-cholesterol, triglycerides, uric acid) was monitored during treatment with placebo and at the end of the study. Mean blood pressure was equally and significantly (p less than 0.001) lowered by both drugs from 2 weeks of treatment, whereas no changes occurred in mean heart rate or in biochemical variables. Dizziness was observed in three patients on ketanserin and in one patient on enalapril, whereas headache occurred in only one patient on enalapril. These data indicate that ketanserin is as effective and well tolerated as enalapril in hypertensive patients over 50 years of age.
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PMID:Comparison of ketanserin and enalapril in the treatment of mild-to-moderate essential hypertension. 228 42

Seventeen subjects with essential hypertension (14 men, 3 women, 40-69 years of age), 13 of whom continued their previous antihypertensive therapy, completed a double-blind crossover trial of ketanserin 40 mg twice daily versus placebo tablets twice daily. Each treatment phase was 6 weeks in duration. For the group as a whole, blood pressure (BP) was reduced in the ketanserin phase compared with the placebo phase: supine mean BP decrease: 4 +/- 1 mm Hg (p less than 0.05); standing mean BP decrease: 7 +/- 1 mm Hg (p less than 0.001). Heart rate (HR) was also significantly decreased in the ketanserin phase (5 +/- 1 beats/min) (p less than 0.001). When individual subgroups were analysed, the reductions in BP and HR were greater in subjects already receiving antihypertensive therapy, diuretics, and/or beta-adrenergic blockers. Changes were observed in 24-h urine sodium and potassium excretion: Sodium (mmol/day): placebo 137 +/- 17, ketanserin 174 +/- 19 (p less than 0.05); potassium (mmol/day): placebo 74 +/- 8, ketanserin 57 +/- 5. For the group as a whole, there were no significant adverse effects during the ketanserin phase, although two subjects had a dose reduction of ketanserin because of drowsiness and dizziness. Two additional subjects withdrew from the study owing to adverse effects, one in the placebo phase. In conclusion, ketanserin in the dose administered has a modest hypotensive effect, which is best seen in subjects already receiving other antihypertensive agents.
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PMID:Effect of ketanserin on blood pressure and biochemical parameters in patients with essential hypertension. 241 43

The dihydropyridine calcium antagonist nitrendipine offers a pathophysiologically based antihypertensive treatment with a potent dilation of resistance vessels, increased arterial compliance, and an acute natriuretic/diuretic response. Prolonged nitrendipine treatment in essential hypertension is not associated with stimulation of the sympathetic nervous and the renin-angiotensin systems or accumulation of sodium and water. The antihypertensive effectiveness is similar to that of diuretics and beta-blockers, and the responsiveness appears to be greater in elderly and black patients. During long-term (approximately 1 year) nitrendipine treatment in mild to moderate hypertension, the blood pressure reduction is well sustained in "short-term" nitrendipine responders. In patients with severe hypertension, nitrendipine has a potent antihypertensive effect in combination with beta-blockers and/or diuretics. In mild-moderate hypertension, a single daily dose (10-40 mg) may be sufficient, whereas two daily doses (20-80 mg/day) seem necessary in severe hypertension. Common side effects are headache, flush, and palpitations (approximately 20-30%), but these are generally mild and transient. Dizziness and malaise occur in approximately 5%, often later during treatment. Peripheral edema in 5-20% of the patients is generally mild but persistent. Nitrendipine has no adverse effects on glucose and lipid metabolism or on plasma levels of electrolytes and urate. The ultimate aim of antihypertensive treatment is to prevent cardiovascular complications. As for other calcium antagonists, no study on primary prevention of cardiovascular complications in hypertension has been published. With regard to regression of left ventricular hypertrophy accompanying essential hypertension, conflicting results have been found with nitrendipine.
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PMID:Review of long-term trials with nitrendipine. 246 50

Urapidil has been approved as sustained-release capsules containing 30, 60 and 90 mg, respectively, and as ampules containing 25 and 50 mg for treatment of all grades of hypertension, in several countries in Europe, South America, as well as in Japan and other Asian regions. In general, the treatment should start with 60 mg twice daily, 1 capsule in the morning and 1 in the evening. This schedule may be adapted according to the therapeutic needs. During the last few years, urapidil has been investigated extensively in comparison with several types of established antihypertensive drugs. Urapidil given orally has been tested in comparative trials against placebo, acebutolol, metoprolol, captopril, nifedipine and nitrendipine with responder rates of 40 to 70%. These responder rates are to be expected for a variety of antihypertensive drugs in monotherapy. Further studies with clonidine, prazosin and alpha-methyldopa showed similar responder rates as established for the other antihypertensive drugs studied. Adverse reactions include dizziness, headache and nausea and occasionally tiredness, orthostatic dysregulation and gastric disorders. These symptoms were transient, mostly occurring during the early phases of therapy and disappearing as treatment continued. Adverse effects are considered to be mainly due to blood pressure reduction. Intravenous comparative trials have been performed with urapidil against placebo, diazoxide and sodium nitroprusside. Adverse effects of parenterally applied urapidil are similar to those observed during oral treatment. Specific contraindications for urapidil are unknown. However, as for other vasodilating drugs, intravenous urapidil should not be administered to patients with stenosis of the aortic isthmus or with aortic valve insufficiency.
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PMID:Overview of clinical trials with urapidil. 266 12

51 hypertensive outpatients, whose diastolic blood pressure exceeded 100 mmHg after a 2-week period on atenolol alone (100 mg once daily) participated in this long-term study. They received, in addition to atenolol, the vasodilator cadralazine (ISF 2469; 10 to 30 mg once daily) for a standard period of 24 weeks, according to an open design. Cadralazine caused a progressive and important decrease in both systolic and diastolic blood pressure, from 173/111 mmHg (end of atenolol alone) to 154/99 mmHg (12th week, p less than 0.01/p less than 0.01; mean dose, 24.5 mg/day). At this time a diuretic was added as a third-step drug in 15/51 initial patients (29%), and final blood pressure in all patients was 150/96 mmHg (p less than 0.01/p less than 0.01), with positive results in 88% of the cases. During cadralazine treatment, heart rate was always significantly lower than before atenolol alone; the most common side effects, many of which were already present during treatment with atenolol alone, included headache, asthenia, dizziness, palpitation and flushing, and tended to disappear spontaneously as therapy progressed. Routine laboratory tests did not show important changes; sodium excretion was not reduced. In conclusion, the therapeutic efficacy of cadralazine, its low or absent salt and water retention effects, its good tolerability, and the high compliance obtained with once daily administration allowed the use of this vasodilator as a second-step drug for long-term treatment of hypertension.
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PMID:Cadralazine, a new vasodilator, in addition to a beta-blocker for long-term treatment of hypertension. 285 65

The ferrihaemoglobin (HbFe3+) formation by amyl nitrite (AN) or sodium nitrite (NaNO2) was studied in different species including man, in vivo and in vitro. In in vivo studies AN was administered intravenously (i.v.), intramuscularly (i.m.), by inhalation, or orally. NaNO2 was injected i.v.. AN i.v. produced HbFe3+ much more rapidly than NaNO2 in dogs, cats, rabbits, and rats. In dogs, i.m. injection of AN was followed by a very slow linear increase in the HbFe3+ content. Inhalation of AN did not lead to HbFe3+ formation in dogs unless it was rebreathed in a closed (bag) or not completely open (gas mask) system. HbFe3+ was produced by oral AN in dogs, the effect being enhanced by addition of DMSO. Inhalation of AN by human volunteers in a gas mask and from ampoules crushed close to the nose did not induce haemoglobin oxidation to a practically significant extent, but it was associated with headache, tiredness, dizziness, and a fall in blood pressure. In in vitro studies, in contrast to NaNO2, AN produced HbFe3+ instantaneously in erythrocytes of various species and in purified human haemoglobin. AN 1 mol yielded 2 mol Fe3+. Only 20% of the oxygen released during the oxidation of haemoglobin by AN or NaNO2 was recovered. In 0.2 M phosphate buffer, pH 7.4, 0.01 mol O2/mol AN was consumed. CO2 was released in the presence of AN, but not of NaNO2, from blood, plasma, and 0.02 M NaHCO3 solution. The ratio (lactate)/(pyruvate) decreased when HbFe3+ was formed by AN or NaNO2.
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PMID:Ferrihaemoglobin formation by amyl nitrite and sodium nitrite in different species in vivo and in vitro. 290 49

Postoperative morbidity was assessed in 100 patients who underwent minor gynaecological procedures. Fifty patients received intra-operative crystalloid (1000 ml compound sodium lactate solution) and the remaining fifty none. Identical short-acting intravenous anaesthetic techniques were used in both groups. There was no statistically significant difference between the groups in symptoms of nausea, vomiting, headache and drowsiness within the first 6 hours after operation. Patients who received intra-operative fluids exhibited a decreased incidence of dizziness within the first 6 hours and a decreased incidence of nausea when questioned at 3 days compared with those who did not receive any fluid; the difference was statistically significant.
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PMID:Intravenous fluids in minor gynaecological surgery. Their effect on postoperative morbidity. 323 84

In patients with portal hypertension and tense ascites, large-volume paracentesis improves patient comfort and may improve systemic hemodynamics. However, it has been avoided in nonedematous patients because of concern for complications, including intravascular volume depletion. In this study, 12 nonedematous patients with chronic liver disease, portal hypertension and tense ascites underwent 14 large-volume (5-liter) paracenteses for the relief of discomfort and/or respiratory distress. Plasma volume was measured directly by a dilution method with 125I-labeled human serum albumin prior to and at 24 or 48 hr after 13 of the paracenteses. All patients felt better postparacentesis. No dizziness, hypotension, tachycardia, encephalopathy or change in mean serum sodium, creatinine or blood urea nitrogen occurred. Two patients experienced a decrease in hematocrit, which was not explained by blood loss or increase in plasma volume. Mean plasma volume was 3,713 +/- 129 ml (55.1 +/- 1.5 ml per kg ideal body weight) preparacentesis and 3,684 +/- 136 ml postparacentesis, the difference being -0.78% (p = 0.48, NS). Our results suggest that 5-liter paracentesis in nonedematous patients with tense portal hypertension-related ascites improves patient comfort and is not associated with a decrease in measured plasma volume.
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PMID:Large-volume paracentesis in nonedematous patients with tense ascites: its effect on intravascular volume. 335

The efficacy and tolerance of 1200 mg/day oxaprozin and 100 mg/day diclofenac sodium were compared in 40 patients with ankylosing spondylitis in a 6-week open study. Overall improvement was seen in the patients in both treatment groups. Oxaprozin-treated patients showed significant improvement in spontaneous pain of the vertebral spine and in morning stiffness after 6 weeks' treatment. There were no statistically significant differences between the treatment groups. Therapy was discontinued in 10 patients; five treated with oxaprozin (three because of intolerance and two because of worsening of symptoms) and five taking diclofenac sodium (four because of intolerance and one because of worsening of symptoms). Five (25%) oxaprozin-treated patients and six (30%) diclofenac sodium-treated patients had side-effects, with gastro-intestinal disturbances and dizziness reported most frequently. There were no statistically significant differences between the groups in the frequency of side-effects. These results indicate that oxaprozin is a promising therapeutic agent for ankylosing spondylitis.
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PMID:Oxaprozin versus diclofenac sodium in the treatment of ankylosing spondylitis. 337 61

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13


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