Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent advances in development of immunoassay methods for marijuana constituents in body fluids provide a rapid means of detection for forensic purposes and a useful research tool for accurate quantitation of dose-response relation. Therapeutic possibilities of cannabis, such as reduction in intraocular pressure and bronchodilatation, may stimulate development of synthetic cannabinoid derivatives that meet acceptable standards of safety and effiicacy for treatment of glaucoma and asthma. Cannabis use may have harmful short- and long-term impacts on health. Potentially serious short-term effects include predisposition to angina during exercise in patients with coronary artery disease. Even in healthy subjects, marijuana smoking decreases peak exercise performance, possibly because of its chronotropic effect with achievement of maximum heart rate at reduced work loads. Although no conclusive evidence exists for long-term biologic consequences of chronic cannabis use, preliminary evidence, suggesting impairment in pulmonary function and immune responses, requires further investigation with large-scale epidemiologic studies.
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PMID:Cannabis, 1977. 35 85

Vasospasms in the eye are often combined with digital vasospasms, as can be diagnosed with a nailfold capillaroscopic local cooling test. In 16 patients with a history of cold hands and feet the presence of peripheral vasospasms without any underlying disease was demonstrated by means of nailfold video-capillaroscopy. These patients showed the phenomenologic diagnosis of low-tension glaucoma with visual field defects characteristic of glaucoma even though intraocular pressure above 21 mmHg was excluded. The visual field defects were not homonymous, indicating a prechiasmal location of the vascular disturbance. Ocular vasospasms cause visual field damage that can be aggravated or provoked by cooling one hand in cold water and that often improves after treatment with the calcium channel blocker nifedipine. The results suggest that vasospasms not only are present in Raynaud's disease, migraine, and Prinzmetal's variant angina but also may be an important factor in the genesis of low-tension glaucoma. This is a new finding and may be related to a general vasospastic syndrome.
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PMID:Do vasospasms provoke ocular diseases? 231 50

Clinical uses of calcium channel blockers are expanding. In addition to the established uses in patients with arrhythmias, angina pectoris or hypertension, newer and to some extent investigational uses indicate widespread application. For instance, their use has been reported in hypertrophic cardiomyopathy and cold cardioplegia, as well as in pulmonary hypertension, antiplatelet therapy, asthma, achalasia and oesophageal spasm, increased intraocular pressure and in cerebral vasospasm. Their use in obstetrical practice has been proposed. Thus, the presentation of a patient who is treated with calcium channel blockers and who requires anaesthesia will become more common. Calcium channel blockers may, under certain circumstances, potentiate haemodynamic and MAC depressive effects of inhalation agents. There is also evidence that the effects of neuromuscular blocking agents may be potentiated. The anaesthetist should be aware that the potential for interactions exists with digoxin, propranolol, quinidine, theophylline or dantrolene. Of interest and some significance are the anaesthetic implications of pathophysiological alterations that can be induced by calcium channel blockers, by affecting lower oesophageal tone, intracranial hypertension, bronchomotor tone (asthma), muscular dystrophy, neuromuscular function, hypoxic pulmonary vasoconstriction, malignant hyperthermia, inhibition of platelet aggregation and hyperkalemia. Despite these significant potential anaesthetic implications and because, at this time, in some instances withdrawal has clearly demonstrated increase in the signs of myocardial ischaemia, it would not seem necessary to recommend preoperative discontinuation of calcium channel blocker medication in patients presenting for anaesthesia. It is, however, appropriate that there is a high index of awareness of potential problems, unless there is some modification in inhalation anaesthetic concentrations and neuromuscular blocker dosage. Monitoring of cardiovascular and neuromuscular functions is essential. Calcium channel blockers would appear to be currently the drugs of choice for angina pectoris, arrhythmias or hypertension in patients with associated chronic obstructive pulmonary disease.
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PMID:Anaesthetic implications of calcium channel blockers. 286 80

Timolol, a nonselective beta-adrenoreceptor blocking agent without intrinsic sympathomimetic or membrane stabilizing activity, has been shown effective in the treatment of angina and hypertension. It is particularly useful in patients with stable angina pectoris and patients with mild to moderate hypertension. In both of these conditions, timolol appears to be comparable to propranolol. A recent study has suggested that timolol reduces mortality and reinfarction rate in patients who have recently had a myocardial infarction. When given topically timolol reduces intraocular pressure in patients with open-angle glaucoma; the drug may be used as the primary agent or as an adjunct to standard therapy. Careful selection of patients will reduce the frequency of adverse effects due to beta-receptor inhibition. Thus, timolol should not be used in patients who are predisposed to asthmatic bronchitis or cardiac failure, and it should be used with caution in patients with peripheral vascular disease or diabetes mellitus.
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PMID:Pharmacokinetics, mechanisms of action, indications, and adverse effects of timolol maleate, a nonselective beta-adrenoreceptor blocking agent. 676 88

Trimetazidine is an anti-ischemic agent which is frequently prescribed as a prophylactic treatment of episodes of angina pectoris and as a symptomatic treatment of vertigo and tinnitus. It has also shown beneficial effects in models of visual dysfunction, but the mechanism(s) by which this occurs is as yet undefined. The present study was intended to evaluate the influence of trimetazidine on retinal damage induced by ischemia-reperfusion in a rat model. Retinal ischemia was induced by increasing intraocular pressure to 160 mm Hg for 60 min. Trimetazidine or buffer controls were administered 3 days before the ischemia or in the postischemic period. The degree of retinal damage was assessed after 15 and 30 days of reperfusion after the ischemic insult by histopathologic study according to Hughes' quantification of ischemic damage. Retinal ischemia led to significant reductions in thickness and cell number, mainly in the inner retinal layers. The results from the study demonstrate that treatment with intraperitoneally injected trimetazidine conferred significant protection against retinal ischemic damage. Better results were obtained in the pretreatment group after 15 days of reperfusion. Trimetazidine protects the rat retina from pressure-induced ischemic injury and might be considered a potential therapeutic modality for combating retinal ischemia.
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PMID:Protective effect of trimetazidine in a model of ischemia-reperfusion in the rat retina. 1238 91

Calcium channel blockers (CCBs), which alter the intracellular calcium concentration by modifying calcium flux across cell membranes and affect various intracellular signaling processes, have been long and widely used to treat essential hypertension and certain types of cardiac diseases such as angina pectoris. Among five subtypes of calcium channels, only specific agents for L-type calcium channels have been used as therapeutics. Animal experiments have indicated that topical application of CCBs, especially verapamil, caused significant intraocular pressure (IOP) reductions, while ocular hypotensive effects in humans were not substantial. Although the results obtained for nifedipine and nimodipine were not always consistent, CCBs generally dilate isolated ocular vessels and increase ocular blood flow in experimental animals, normal humans, and patients with open-angle glaucoma (OAG). Several single-centered, hospital-based, prospective studies have suggested that nimodipine, brovincamine, and nilvadipine had beneficial effects on visual function not only in normal humans but also in patients with OAG, while the results of population-based and case-controlled studies were not always consistent with those obtained in hospital-based studies. In vitro studies showed that CCBs exerted neuroprotective effects on neurons undergoing apoptosis and necrosis. Although the neuroprotective effects of CCBs have been well documented in experimental cerebral ischemia models, no controlled studies have shown the clinical efficacy of CCBs in stroke or cerebral ischemia. Neuroprotective effects also were documented in retinal ganglion cells and photoreceptors in experimental animals. Some ophthalmic beta-adrenoceptor antagonists, especially betaxolol, interact with L-type calcium channels and show calcium channel-blocking activity, which may be partly responsible for the neuroprotective effects of these drugs reported in experimental animals. Based on the reported findings of CCBs and that the results of clinical studies in acute cerebral ischemia may not be directly applicable to a chronic neurodegenerative ocular disorder, such as OAG, CCBs deserve future study to investigate strategies that are additive or synergetic to ocular hypotensive therapy for OAG, especially in patients with lower IOP.
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PMID:Use of calcium channel blockers for glaucoma. 2093 4