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)

Nitrates are effective in the management of exertional angina pectoris primarily due to their peripheral effects i.e. venodilation and arterial dilation, and thereby reduction in myocardial oxygen demand. These drugs also improve collateral blood flow in ischemic areas and in some patients may increase coronary blood flow by modifying tonus in the conductive or conduit coronary vessels. Sublingual nitroglycerin is the most effective antianginal agent but its prophylactic use is limited by its short duration of action. Until recently, the efficacy of long-acting oral nitrates was seriously questioned. However, recent data suggests that when given acutely in adequate doses, oral nitrates, transcutaneous and buccal preparations of nitroglycerin all exert prolonged hemodynamic and antianginal effects. Development of tolerance to the circulatory and antianginal effects during chronic therapy, however, remains a concern. Published literature suggests that tolerance to the circulatory effects and to headaches develops rapidly during sustained therapy with long-acting nitrates. However, reports regarding the development of tolerance to the antianginal effects and reduction of ST segment depression remain conflicting. Partial tolerance to the antianginal effects has been well-documented during chronic therapy with isosorbide dinitrate. Duration of improvement in exercise tolerance during four times daily therapy with isosorbide dinitrate has been shown to be shortened compared to prolonged effects following acute therapy. Recent data suggests that given in high doses, beneficial effects of ST segment depression during exercise may also diminish during chronic therapy with long acting nitrates. Tolerance to antianginal and circulatory effects can be reversed by withholding long-acting nitrates for 24 to 36 hours. Furthermore, initial studies suggest that tolerance to antianginal effects during sustained therapy can be avoided by giving smaller but effective doses of ISDN (20 to 40 mg) twice a day rather than prescribing larger doses more frequently.
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PMID:Nitrates for angina pectoris. A critical review of therapeutic efficacy and tolerance. 643 Jul 66

Eleven patients were examined thermographically during spontaneous cluster headaches and 22 during attacks induced by nitroglycerin or alcohol. In cluster headache, heat loss increased from the affected orbital region, and in some patients, this spread above and below the eye, down the nose, and to the affected temple. Inhalation of 100% oxygen reduced or abolished cluster pain in 22 of 25 instances, and asymmetry of heat loss then disappeared. Since the unilateral increase in blood flow usually followed the onset of pain in affected areas, the vascular changes of cluster headache are probably secondary phenomena, initiated by a vasodilator pathway, with the trigeminal nerve as the afferent and the greater superficial petrosal nerve as the efferent limb.
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PMID:Thermographic changes in cluster headache. 654 1

Almitrine bismesylate was administered to young, healthy, non-smoking male subjects as single oral doses, multiple oral doses and multiple oral doses with food. A variety of physiological parameters and blood parameters were tested at specified times in relationship to drug ingestion, and multiple blood samples for plasma almitrine bismesylate levels were obtained. Evaluation of the data revealed almitrine bismesylate to be safe at all doses tested, up to 400 mg per day, with symptoms of mild nausea and headache occurring most frequently when the drug was administered in the fasting state. A striking complaint of shortness of breath on exertion was reported by subjects, with increased frequency and severity related to total amount of drug ingested and level of physical activity. Increased oxygen uptake and tidal volume were found after multiple oral dosing. Plasma almitrine bismesylate levels were highly variable, and marked individual differences in peak levels and terminal phase rate constants and half lives were found. Multiple oral dosing, either fasting or with food, significantly prolonged the terminal phase half life when compared to single oral dosing.
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PMID:Effects and handling of almitrine bismesylate in healthy subjects. 658 42

An hypothesis regarding the possible role of the carotid body in the pathogenesis of cluster headache is presented. It states: 1. The pathways concerned with cyclic cluster periods may begin centrally involving specific areas in the hypothalamus. The major influence of this physiological change is proposed to be an inhibition of the sympathetic and disinhibition of parasympathetic supplies to the carotid body. The result, whether due to increased vasomotor tonus or interruption of intrinsic sympathetic stimulation, is suggested to cause diminished peripheral chemoreceptor activity. 2. The pathway concerned with onset of spontaneous or induced attacks begins, as proposed, with oxygen desaturation--which, upon reaching threshold levels may induce a hyperactive chemoreceptor response, and stimulate through afferent pathways the nuclei of the 7th and 10th cranial nerves and respiratory centers, via the nucleus solitarius. 3. The consequence of this excitation may involve the third suggested pathway resulting in stimulation of peripheral secretory and other receptors innervated by the cranial nerves.
Cephalalgia 1983 Dec
PMID:A possible role of the carotid body in the pathogenesis of cluster headache. 664 Jun 58

Hemoglobin Chemilly (alpha 2 beta 2 99(G1)Asp leads to Val), a high oxygen affinity variant, was uncovered in the red blood cells of a polycythemic patient who reported to the hospital concerning periodic headaches. We describe the molecular abnormality and functional studies of this new abnormal Hb. beta 99(G1)Asp, an invariant residue of hemoglobin, is considered a key amino acid for conformational changes between the R in equilibrium T quaternary structures responsible for the allosteric behavior of hemoglobin. Hb Chemilly exhibits a high O2 affinity, very low cooperativity and reduced Bohr effect. Its functional abnormalities are compared to the 5 other Hb variants at site beta 99(G1) described up to now of the 7 single base substitutions predictable from the genetic code.
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PMID:A new hemoglobin variant altering the alpha 1 beta 2 contact: Hb Chemilly alpha 2 beta 2 99(G1)Asp leads to Val. 669 25

The impetus to study sleep changes in a cluster population arose from a recent hypothesis that predicted the finding of sleep apnea in this disorder. It holds that cluster attacks may occur in response to oxygen desaturation. Proposed mechanisms involve impairment of carotid body activity secondary to hypothalamic-vasomotor regulatory dysfunction. Five chronic and five episodic cluster patients underwent nocturnal polysomnography, utilizing standard equipment for monitoring sleep status, cardiac activity, nasal and buccal air flow change, chest and abdominal breathing, muscle activity and oxygen saturation. All episodic patients and one of five chronic patients were found to have sleep apnea (60%). Mean apneas per hour during NREM sleep were similar to that of REM sleep; 26.7 and 28.2, respectively. Six patients with sleep apnea experienced 14 cluster headache attacks during the study period. Eight attacks (57%) followed episodes of oxygen desaturation ranging from 65% to 85%. In the sleep apnea group, 8 out of 14 attacks (57%) were associated with REM; three without, and five following oxygen desaturation. Of the non-apnea group, all of whom had chronic cluster headache, none of 5 attacks were associated with oxygen desaturation, and only 2/5 attacks occurred in relation to REM. Thus, our study showed that sleep apnea was a common finding in a randomly selected group of episodic cluster patients; and most nocturnal attacks were preceded by oxyhemoglobin desaturation and REM-related. These findings were uncommon in the chronic cluster group.
Cephalalgia 1984 Mar
PMID:Sleep apnea in cluster headache. 671 22

The hypothesis postulates that a brief episode of focal cerebral hypoxia occurs in every attack of migraine. Clinical biochemical and technical (EEG and CT scans) evidence is summarized suggesting that cerebral hypoxia is seen as the turning-point in the pathogenesis of the attack. It may be provoked by different mechanisms in different patients; the potential role of decreased oxygen supply and of increased oxygen need are reviewed and excess sympathetic drive is considered a potential key mechanism in a majority of patients. Whether or not focal hypoxia leads to a genuine migraine attack, depends largely upon the quality of the whirlpool of biochemical, vascular and hematological changes that follow the hypoxic episode. These changes are discussed and it is concluded that those which have been reported to occur during migraine attacks could be due to a preceding hypoxic event. Finally, the hypoxia viewpoint is confronted with some popular theories about the pathogenesis of migraine. It is found that the other points of view are compatible with the hypoxia hypothesis.
Cephalalgia 1982 Jun
PMID:Brain hypoxia: the turning-point in the genesis of the migraine attack? 675 54

Blood viscosity, cerebral blood flow (CBF) and cerebral oxygen carriage (CBF X arterial oxygen content) were measured in 12 patients with polycythaemia secondary to hypoxic lung disease. CBF and cerebral oxygen carriage were both significantly higher than in a comparative group of 20 patients with raised packed cell volumes and normal lung function. The patients with secondary polycythaemia then underwent venesection and their mean packed cell volume fell from 0.613 to 0.495. This led to a consistent reduction in blood viscosity, which fell by 44% at a low shear rate (0.67/s) and 33% at a high shear rate (0.91/s). CBF rose by 21% (p less than 0.01), but cerebral oxygen carriage did not significantly increase in the group as a whole. Four of the patients with secondary polycythaemia had complained of episodes of confusion before venesection, which improved considerably once the packed cell volume had been lowered. Headache was relieved in a further two patients and none of the subjects was adversely affected by venesection. It was not possible, however, to show a correlation between symptomatic improvement and an increase in cerebral oxygen carriage.
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PMID:Cerebral blood flow and blood viscosity in patients with polycythaemia secondary to hypoxic lung disease. 679 27

Prostaglandin E1 (PgE1) was administered intravenously to 26 patients with decompensated chronic obstructive pulmonary disease (COPD) in order to investigate the effects on hemodynamics and blood gases of a reduction in pulmonary hypertension in this condition. In the first 10 patients, PgE1 at 0.02 microgram/kg/min decreased pulmonary and systemic pressures, respectively, by 20 and 7%, increased cardiac index (CI) and oxygen delivery to the tissues (TO2), and did not affect blood gases. In the next 9 patients, PgE1 at 0.04 microgram/kg/min decreased pulmonary and systemic pressures, respectively, by 24 and 14%, increased CI and TO2, slightly decreased arterial oxygenation, and did not affect mixed venous blood gases. Side effects, consisting in facial flush, headache, and malaise occurred in 4 of these patients. In the last 7 patients who were artificially ventilated, PgE1 at 0.02 microgram/kg/min increased CI and TO2 but had no effect on vascular pressures and blood gases. Prostaglandin E1 was also given intravenously to 7 healthy subjects breathing 12.5% O2 in N2 for 10 min. Hypoxic pulmonary vasoconstriction was not inhibited by PgE1, even at the highest dosage of 0.04 microgram/kg/min, which caused a flush of the skin, headache, and malaise in all the subjects. Infusion of PgE1 reduces the pulmonary hypertension secondary to decompensated COPD. At adequate dosage, this effect can be obtained with minimal systemic vasodilation and no alteration in the gas exchange function of the lungs, which may be due to preservation of pulmonary vascular tone adaptation to hypoxia. The vasodilating activity fo PgE1 appears to be blunted during artificial ventilation.
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PMID:Reduction in pulmonary hypertension by prostaglandin E1 in decompensated chronic obstructive pulmonary disease. 680 45

Sublingual glyceryl trinitrate (nitroglycerin) is the most widely used drug in the treatment of angina pectoris, but its use is limited due to its short acting effect. Recent investigations have shown that some longer acting nitrates administered orally or topically have a long acting antianginal effect. The mechanism of the antianginal effect of nitrates is multifactorial. Nitrates increase oxygen supply to the myocardium by causing redistribution of coronary blood flow. In addition, nitrates decrease myocardial oxygen demand by reducing left ventricular volume, intramyocardial tension, and left ventricular afterload. The use of nitrates for the treatment of congestive heart failure has also been established in recent years. Nitrates have a predominant venodilatory effect resulting in peripheral blood pooling and decreased venous return to the heart, thereby decreasing left ventricular filling pressure. The effect of nitrates on the arteriolar circulation is small, and there is usually little or no change in cardiac output. Some reduction in systemic blood pressure can be seen, while there is usually no change in heart rate. In a small number of patients with myocardial infarction complicated by congestive heart failure, the use of long acting nitrates has resulted in haemodynamic and symptomatic improvement. Nitrates has also bee shown to improve variant angina. Nitrates are usually well tolerated in most patients. However, some troublesome side effects can occur, including headache, postural hypotension, and methaemoglobinaemia.
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PMID:Glyceryl trinitrate (nitroglycerin) ointment and isosorbide dinitrate: a review of their pharmacological properties and therapeutic use. 680 2


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