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 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

The interest in mountain tracking and climbing has increased and there is a need for knowledge of altitude-related diseases. About one million non-acclimatized individuals annually frequent areas around 2,000 to 3,000 m above sea level and incur unpleasant symptoms in the form of acute altitude sickness or potentially fatal conditions such as pulmonary and/or cerebral oedema. Headache is the most prominent sign of acute altitude sickness but fainting fits, loss of appetite, hesitant gait, euphoria, or confusion also occur. Dyspnoea, cyanosis at rest, and a dry cough are signs of pulmonary oedema. Cerebral oedema may be feared when inexperienced climbers are afflicted by severe headaches, vomiting, and hesitant gait. Coma ensues relatively soon. Treatment consisting in descent to lower altitude, administration of oxygen, and possible medicinal therapy is effective if immediately introduced.
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PMID:[Altitude sickness]. 291 57

Profound transient nocturnal hypoxemia is common during REM sleep in "blue bloaters" with chronic obstructive lung disease, these patients having hypoxemia and CO2 retention when awake, when breathing air. These hypoxemic episodes appear to be due to a combination of reduced ventilation in REM sleep with a possible increase in the maldistribution of ventilation to perfusion within the alveoli at that time, and a reduction in functional residual capacity. The episodes are associated with exacerbations of pulmonary vasoconstriction, which can be reversed by oxygen therapy throughout sleep. Cardiac arrhythmias and alterations in ST segments are also found in these patients during sleep when breathing air. It is probable that the severity of hypoxemia in REM sleep can be predicted from knowledge of the arterial PO2 when breathing air when awake in patients with COPD. If so, expensive sleep studies are not essential to indicate the presence of hypoxemia in sleep in these patients, but such studies may be required in obese patients, in those who snore, or those who complain of headache following nocturnal oxygen therapy to demonstrate the presence of the overlap syndrome, in which obstructive sleep apnea is combined with chronic obstructive lung disease in the same patient. Nocturnal oxygen therapy may be dangerous in such patients with the overlap syndrome but appears to cause little rise in PCO2, in patients with COPD and REM-associated hypoxemia alone. Hypoxemia and sleep quality can probably be improved by oxygen therapy in "blue bloaters," and this treatment can also reverse pulmonary hypertension in REM sleep. The new ventilatory stimulant almitrine can also correct hypoxemia, without disturbing sleep quality, but the effects of this drug on pulmonary vasoconstriction during REM sleep are as yet unknown.
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PMID:Sleep in chronic obstructive lung disease. 293 59

After 3 days of symptoms suggesting a viral illness, a 35-year-old man experienced three episodes of aphasia, right-sided sensory symptoms, and bifrontal headache. Each lasted several hours. CSF examination revealed a moderate lymphocytosis consisting of 80% OKT-8+ cells. Serum anti-cytomegalovirus (anti-CMV) antibody titer was elevated at 1:1,024 and subsequently fell to 1:64. Episodic symptoms recurred 5 months later, at which time the anti-CMV titer peaked at 1:8,192. A trial of inhaled oxygen aborted two episodes after several minutes each.
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PMID:Cytomegalovirus encephalitis associated with episodic neurologic deficits and OKT-8+ pleocytosis. 302 72

Nisoldipine is an orally administered calcium entry blocking drug structurally related to nifedipine. In limited clinical trials it has been shown to be effective and relatively well tolerated in the treatment of patients with chronic stable angina pectoris and mild to moderate essential hypertension. As for all dihydropyridine-calcium antagonists, its major properties include potent peripheral and coronary vasodilation and improvement in myocardial oxygen supply relative to demand. These actions occur without depression of cardiac conduction or left ventricular function. Short term clinical trials have shown nisoldipine to produce both symptomatic and objective improvements in patients with chronic angina of effort and have suggested a benefit in vasospastic angina. A small number of comparative trials indicate that nisoldipine is equally as effective as nifedipine. In addition, in combination with beta-adrenoceptor blockade nisoldipine appears to offer additional benefit compared with beta-blockade alone and is well tolerated. In patients with mild to moderate essential hypertension nisoldipine monotherapy, in 1 or 2 daily doses, has maintained blood pressure control and has also been a useful addition to diuretics and beta-adrenoceptor blocking drugs in patients with poorly controlled disease. Side effects appear to be dose related, generally mild and transient, and are primarily those resulting from potent peripheral vasodilation - headache, flushing and pretibial or ankle oedema. Although studies to date are promising, there are no published long term studies (greater than 1 year) of nisoldipine in comparison with other calcium entry blockers and other drugs currently in clinical use for the treatment of angina pectoris or hypertension. Until such studies are completed the exact place of nisoldipine in the treatment of these diseases remains to be established.
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PMID:Nisoldipine. A preliminary review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy in the treatment of angina pectoris, hypertension and related cardiovascular disorders. 306 58

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

A case of inadvertent intravascular injection of PGF2alpha during induction of labor by intraamniotic injection for fetal demise, involving alternating extreme hypotension and hypertension, is described. The woman was a 29-year old in late 2nd trimester with oligohydramnios, but no other related history. She was given epidural anesthesia, 7.5 mg midazolam and 5 mg morphine S04 for anxiety. Because of oligohydramnios, 300 ml Ringers lactate was instilled to dilute the PG. A test dose of 1 mg PGF2alpha was tolerated well. 80 g urea and 20 mg PGF2alpha were injected over 10 minutes. A few minutes later contractions began, followed by complaints of burning on face and chest and dyspnea. Oxygen was given by mask. Systolic pressure fell to 70 mm by cuff; peripheral pulses could not be palpated, but the patient remained alert and oriented. She was given 35 mg ephedrine and increased iv fluids. She remained dyspneic, her extremities became mottled, and she complained of chest pressure, severe headache and severe breast tenderness. Blood pressure rose to 220/135 mm Hg; pulse to 95, and respiratory rate to 44. Pulse oximetry, detectable at the earlobe only, was 94% saturation. After 50 mg labetalol, blood pressure fell to 134/77, but symptoms remained. For 2 hours blood pressure swung between 76/50 and 225/125, until delivery of the fetus. An arterial line could not be started because of extreme vasoconstriction. Central venous pressure was 13 cm H20. After artificial rupture of the membranes and removal of remaining PG, blood pressure stabilized. Delivery was accomplished without incident. The symptoms and labile blood pressure were considered to be due to intravascular injection of PGF2alpha, caused by repeated bolus injection at each uterine contraction. In case of PG induction for fetal demise, it is recommended that anesthesiologists be prepared to treat intravascular collapse, hypertension and bronchoconstriction.
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PMID:Life-threatening effects of intravascular absorption of PGF2 alpha during therapeutic termination of pregnancy. 318 4

Nicardipine is an antagonist of calcium influx through the slow channel of the cell membrane and has been shown to be an effective and relatively well-tolerated treatment for stable effort angina and rest angina due to coronary artery spasm, and mild to moderate hypertension. Although its exact mechanism of action in these disease states has not been precisely defined, the potent coronary and peripheral arterial dilator properties of nicardipine, with concomitant improvements in oxygen supply/demand and reductions in systemic vascular resistance, are of major importance. Clinical studies have shown that nicardipine appears to be effective in the treatment of chronic stable exercise-induced angina pectoris and possibly in angina at rest due to coronary artery spasm. In the treatment of stable angina, nicardipine has proved to be equally as effective as nifedipine. However, haemodynamic and clinical studies indicate that nicardipine may have a further advantage of not depressing cardiac conduction or left ventricular function, even in patients with compromised cardiac pumping ability. Nicardipine also appears to be useful as initial monotherapy or in combination with other antihypertensive drugs when used in the treatment of mild to moderate hypertension, and may have some advantages over other vasodilators in this regard in that it may not be as frequently associated with fluid retention or weight gain as other similar drugs. In the treatment of hypertension nicardipine has been shown to be as effective as drugs such as hydrochlorothiazide, cyclopenthiazide, propranolol and verapamil in short term studies although confirmation of its long term usefulness in well-designed clinical trials is still required. Similarly, although the use of nicardipine in other disorders such as congestive heart failure and cerebrovascular disease has provided encouraging preliminary results, more studies are needed to clarify its place in their treatment. Side effects appear to be dose related and more frequent within the first few weeks of therapy. Most of these effects are minor and transient in nature and include headache, flushing and peripheral oedema. Thus, there is no doubt that nicardipine provides a suitable alternative to other drugs available for the treatment of angina and hypertension. However, further well-designed comparative clinical trials are needed to clarify its relative place in the long term management of these disorders.
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PMID:Nicardipine. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy, in the treatment of angina pectoris, hypertension and related cardiovascular disorders. 329 16

Several calcium antagonists, each with significantly different chemical structures, have demonstrated variable attenuation of exercise-induced asthma. Quantitative comparisons have been hampered by differences in the intensity of challenge and the severity of the underlying disease between groups of patients. In 12 asthmatic adults with relatively severe exercise-induced asthma, we compared the effect of a new calcium antagonist, PY 108-068, in doses of 75 mg and 150 mg with nifedipine (30 mg) and placebo on resting flow rates and flow rates after exercise. Over a three-week period, each patient completed a four-day, randomized, double-blind Latin-square study. After receiving one of four oral drugs, spirometry was repeated every 30 minutes for two hours, followed by a six-minute treadmill exercise test breathing dry air. The exercise tests were well matched for work rate, ventilation, heart rate, and oxygen uptake. Spirometry was then repeated seven times over the next 30 minutes after exercise. Though both 150 mg of PY 108-068 and nifedipine were associated with mild bronchodilation before exercise, only the latter was significant (p less than 0.05). Exercise-induced asthma (expressed as maximal percent fall in the forced expiratory volume in one second from before baseline) was significantly attenuated only by 150 mg of PY 108-068 compared to placebo (24 +/- 13 vs 40 +/- 16; p less than 0.05). Headache, which occurred in six subjects after nifedipine, five after 150 mg of PY 108-068, one after 75 mg of PY 108-068, and none after placebo, was subjectively more severe after nifedipine. We conclude that in these patients, there was a tendency for mild bronchodilation before exercise with both 150 mg of PY 108-068 and nifedipine, but only the 150-mg dose provided significant protection against exercise-induced asthma two hours after the drug.
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PMID:Comparison of PY 108-068, a new calcium antagonist, with nifedipine in exercise-induced asthma. 352 23

Cluster headache is a rare headache entity that predominantly occurs in younger males. The clinical features are characterized by sudden attacks of unilateral excruciating pain localized periorbitally, associated with ipsilateral autonomic symptoms. The attacks occur in periods: clusters. The pathophysiology is still unknown. Such vasodilating substances as histamine, nitroglycerin and alcohol may provoke attacks. These substances may be used as diagnostic tests, but the interpretation of a negative result must be careful, as the attacks can not be induced in a refractory period after spontaneous occurrence, or at the beginning and end of cluster periods. As symptomatic treatment, ergotamine is the drug of first choice. High attack frequency may lead to overconsumption with ergotisme and further increased frequency. In such cases and for nocturnal attacks, oxygen inhalations represent an alternative. As prophylactic treatment ergotamine, methysergide, lithium and prednisone have proved efficacious. Most patients benefit from such treatment and may become virtually free from attacks. It is, therefore, important to differentiate this headache entity from classical migraine, common migraine and trigeminal neuralgia.
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PMID:Cluster headache: a review. 353 83


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