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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

However great the success in the therapy of hypertension, atherosclerosis and ischemic heart disease has been gained today by recent efficient drugs, the definite healing of patients is not yet attained. The late discovery of reserpine, such an efficient drug of plant origin against hypertension, convinced so far reluctant scientists to consider the chemical compounds of the plant world. With respect to this traditional medical knowledge, it seems necessary to define more accurately the specificity of these healings-sometimes recommended unspecifically for a whole branch of medicine. This experimental verification should not use inconsiderately the present-day classification of diseases; there should be an awareness that conventional experimental methods in pharmacology are often unsuitable for revealing the real biological activity of one or another medicinal plant. The interest in the millennial empirical field of health care is acknowledged by the World Health Organization which promotes research and development of traditional medicine, along with investigations into its psychosocial and ethnographic aspects. These studies cover a number of plants growing in Bulgaria that have a healing effect in hypertension, atherosclerosis and ischemic heart disease according to the data of traditional medicine. Using screening methods, extracts and chemically pure substances were investigated; extraction was done with solvents such as water, ether, chloroform, dichloretan, ethanol, methanol, and acetone. Most of the experiments were carried out on anesthetized cats, rabbits and dogs. The substances tested were applied mainly intravenously, and in some experiments orally. Chronic experiments were also carried out on wakeful dogs with induced hypertension, on animals fed on an atherogenic diet, and on animals with induced arrhythmia and coronary spasm. Data are presented of clinical examination of some plants or of active substances isolated from them. Major results of these studies are presented for the following plants: Garlic, Geranium; Hellebore; Mistletoe; Olive; Valerian; Hawthorn; Pseucedanum arenarium; Periwinkle; Fumitory. For another 50 plants growing in Bulgaria and in other countries the author presents his and other investigators' experimental and clinical data about hypotensive, antiatheromatous and coronarodilatating action.
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PMID:Plants and hypotensive, antiatheromatous and coronarodilatating action. 57 53

Suggesting endogenous digoxin-like factor (EDLF) to display arrhythmogenic activities in myocardial ischemia (MI), we studied the effect of anti-digoxin antiserum (ADS) on the ventricular fibrillation threshold (VFT) after the coronary ligation in cats and ventricular arrhythmias caused by MI in rats and chloroform-induced hypoxia in mice. Intravenous administration of ADS (5 mg/kg) enhanced VFT in cats with MI from 11.3 +/- 1.6 to 53.3 +/- 8.1 V (M +/- m; p less than 0.01) and significantly reduced ventricular arrhythmias in rats and mice. Our experiments on the isolated electro-stimulated rat atria demonstrated that EDLF is likely not to be an adrenergic cotransmitter in the heart. Possible mechanisms of the arrhythmogenic action of EDLF are discussed.
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PMID:[Anti-arrhythmia effect of digoxin antibodies in experimental myocardial infarct (arrhythmogenic action of endogenous digoxin-like factor)]. 166 57

The following discourse addresses the pharmacologic profile of KT-362, its clinical potential as an anti-arrhythmic agent with associated hypotensive effects, as well as its additional related potential in myocardial ischemia and related sequellae, and the specific cellular actions that may be responsible for these potential therapeutic effects. Although these include specific actions on both sodium and calcium entry, the focus is on the relevance of independent effects on calcium release. KT-362 relaxes arterial smooth muscle, concomitantly reducing the total peripheral resistance and mean arterial blood pressure. Vascular relaxing actions are attributed primarily to inhibitory effects on calcium release and secondarily to inhibitory effects on calcium entry via both potential-gated and receptor-linked channels. The "intracellular calcium antagonist" properties are correlated with a decrease in the production of the major second messenger, inositol 1,4,5-trisphosphate, which is responsible for calcium release and a concurrent ryanodine-like action that further decreases the amount of calcium released. Ventricular arrhythmias associated with coronary occlusion, cardiac glycosides, catecholamines, and chloroform are prevented by KT-362. General antiarrhythmic properties are associated with a use-dependent block of the "fast" sodium channel, primarily in the activated state, with ancillary effects on the "slow" calcium current. More selective effects on arrhythmias specifically associated with delayed after-depolarizations are attributed to effects on calcium release. In myocardial ischemia, KT-362 primarily reduces myocardial oxygen consumption rather than increases oxygen supply. The former is accomplished by depressing myocardial contractility and reducing afterload, while the latter is associated with a limited effect on coronary collateral blood flow. The negative inotropic effect is fundamentally related to its effects on calcium release, with additional contributions from its effects on calcium entry. Thus, the one intrinsic property of KT-362 that consistently emerges as significant and relevant in cardiovascular disease is the capacity to diminish calcium release.
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PMID:KT-362 related effects on intracellular calcium release and associated clinical potential: arrhythmias, myocardial ischemia, and hypertension. 227 70

Nicardipine has high affinity for the dihydropyridine-binding site and has been shown to inhibit the influx of extracellular calcium through membrane slow channels. The calcium antagonist activity of nicardipine is greater in vascular smooth muscle than in cardiac muscle. Nicardipine has also been shown to possess greater activity in coronary than in peripheral vascular smooth muscle. This in vitro profile accounts for the decreased blood pressure and increased coronary blood flow in animal models in vivo. These pharmacologic properties are the basis for nicardipine's clinical utility in essential hypertension and acute myocardial ischemia. Nicardipine has been shown to be more vascular selective than other calcium antagonists and, therefore, possibly less inclined to produce negative inotropicity. This latter property has been confirmed in human hemodynamic studies. Nicardipine is effective in models of acute myocardial ischemia and hypertension. These results have been confirmed in antianginal and antihypertensive studies in humans. This new calcium antagonist has been shown to limit myocardial infarct size in both dogs and baboons subject to left anterior descending coronary artery ligation and to reduce the extent of ischemia-induced cerebral neuronal death in rats. Other protective effects of nicardipine have been demonstrated in paracetamol overdose in mice, chloroform-induced hepatotoxicity in rats and cerebral ischemia in gerbils and baboons. The mechanism of this cell protection of nicardipine may be related to physicochemical effects.
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PMID:Animal pharmacology of nicardipine and its clinical relevance. 244 Feb 94

In the present study, the effect of DG chloroform root extract was assessed on isolated rat heart and in-vitro antioxidant models. Ischemia reperfusion injury was experimentally induced by using Langendroff apparatus. The free radical scavenging potential was studied in vitro by using different antioxidant models such as DPPH, super oxide scavenging activity, hydroxide scavenging activity and nitric oxide scavenging activity. Both experimental approaches not only substantiate its antioxidant potential but also the cardio-protection imparted by the extract. The cardio-stimulatory effects were investigated for the extract by treating it as a pre-conditioning agent against myocardial ischemia reperfusion injury. The improved antioxidant status of the myocardium indirectly predicts reduced oxidative stress mediated by ischemic reperfusion with evident reduction of infarct size determined by cardiac marker protein. These findings indicate that DG chloroform root extract may possess therapeutic potential against ischemia reperfusion injury.
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PMID:An in vivo and in vitro analysis of free radical scavenging potential possessed by Desmodium gangeticum chloroform root extract: interpretation by gsms. 2218 6

Clopidogrel is an antiplatelet drug. It is used for the treatment as well as for the prophylaxis of coronary artery disease. Clopidogrel resistance is an emerging problem in clinical settings. The aim of the present study was to evaluate the effect of CYP3A5*3 genetic polymorphism on clopidogrel resistance. One hundred and forty-seven patients from outpatient Department of Cardiology on 75 mg/day of clopidogrel as maintenance dose were recruited from April 2010 to July 2011. All subjects gave written informed consent to participate in the study. DNA extraction was performed using phenol chloroform extraction procedure and genotyping by standard Taqman based RT-PCR method. Platelet aggregation was done at the end of 7th and 14th day by using chronolog lumi Aggregometer which is expressed as impedance in ohms. Impedance values of >5 ohms at the end of 6 min were considered as clopidogrel resistance. Subjects (N = 147) were analysed for CYP3A5*3 polymorphism, of which 49 (33%) were found to be clopidogrel resistant. Homomutants of CYP3A5*3 gene had 2.78 (0.97-7.98; p < 0.05) fold risk and heteromutants had 2.4 (0.93-6.46; p < 0.05) fold risk of developing clopidogrel resistance. Carriers of defective allele G of CYP3A5*3 had higher propensity to cause clopidogrel resistance with an odds ratio of 1.63. Variant alleles and genotypes of CYP3A5*3 polymorphism contributed significantly to clopidogrel resistance with a higher odds ratio. Thus, pharmacogenomics paves way for the emergence of stratified medicine in clopidogrel therapy and personalised pharmacotherapy in ischaemic heart disease.
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PMID:Single nucleotide polymorphism of CYP3A5*3 contributes to clopidogrel resistance in coronary artery disease patients among Tamilian population. 2511 1