Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In our earlier experiments administration of the stable PGI2 analogue: 7-oxo-PGI2-ephedrine salt to dogs resulted in a late appearing and long-lasting protection from coronary ligation induced ischemia and subsequent postocclusion and reperfusion arrhythmias. Objective of the present study was to evaluate the extent and duration of antiischemic and antiarrhythmic action induced by a single dose 50 micrograms/kg i.m. 7-oxo-PGI2 in dogs subjected to myocardial ischemia evoked by left anterior descending coronary (LAD) ligation at different intervals (2, 6, 24, 48, 72 hours and 2 weeks) after treatment. In the 2 weeks prolonged treatment group treatment started with 50 micrograms/kg i.m. dose, followed every third day by administration of 25 micrograms/kg 7-oxo-PGI2. After anesthesia and thoracotomy the electrophysiological parameters (SCL, CSNRT, AFRP, VFRP and A-V ERP) were determined by means of computer controlled programmed electrical stimulation. Then the animals were subjected to LAD occlusion for 25 min and subsequent reperfusion. 7-oxo-PGI2 pretreatment considerably protected against myocardial ischemia, i.e. there was a marked reduction in ST-segment elevation, the number of ES and the incidence of VF. The maximal antiischemic action and the most striking reduction in ventricular arrhythmias could be observed 48 hours after a single dose of 7-oxo-PGI2 and also after prolonged treatment of two weeks. In this latter group CSNRT showed the most expressed prolongation, however, AFRP and to lesser degree VFRP was also prolonged.
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PMID:7-oxo-PGI2 induced late protective action from arrhythmias due to local myocardial ischemia. 202 55

Hypertension and serum cholesterol levels are strongly interrelated as cardiovascular risk factors. The Framingham study showed that the risk of both ischaemic heart disease and brain infarction doubles in presence of mild hypertensive status and triplicates in presence of a definitive hypertension. The systolic pressure showed to be the best predictor of both ischaemic heart disease and cerebral infarction particularly in persons aged more than 65 years. In terms of physiopathology we point out several mechanisms by which hypertension could interact with hypercholesterolemia on the arterial wall causing endothelial lesion, enhancing the penetration of arterial wall by lipoproteins, calcium accumulation on smooth subendothelial muscle and suppression of the relaxation factor produced by endothelial cells. In relation to the dietetic treatment, we must restrict more rigorously the ingestion of salt, saturated fatty acids, and total calories. In terms of anti-hypertensive drugs, we should: Avoid thiazide diuretics in case of cholesterol levels of moderate to high risk. Avoid beta blockers in patients with high levels of triglycerides, low HDL and low ratio total cholesterol/HDL. Consider to choose a calcium antagonist, a converting enzyme or an alpha blocker.
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PMID:[Arterial hypertension associated with hyperlipoproteinemia]. 218 49

Racial differences in the prevalence, course, and pathophysiologic characteristics of hypertension in black and white populations are reviewed. Accumulated epidemiologic data indicate that the prevalence of hypertension among blacks is greater than that among whites in almost all age- and sex-matched groups. Hypertensive blacks have a higher incidence of left ventricular dysfunction, stroke, and renal damage, but a lower incidence of ischemic heart disease, than do hypertensive whites. A significant pathophysiologic difference between blacks and whites is salt sensitivity; normotensive, as well as hypertensive, blacks tend to be salt sensitive. Blacks also tend to have lower renin levels than do whites, while dopamine response to a salt load is diminished among blacks as compared with whites. These differences and others lead to the recommendation that hypertension among blacks should be managed initially with salt restriction; if dietary control is insufficient, administration of an antihypertensive agent with 24-hour efficacy, which lowers vascular peripheral resistance, promotes sodium excretion, and potentially improves renal hemodynamics, is recommended. A calcium channel blocker may satisfy these requirements.
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PMID:Hypertension: racial differences. 222 Jul 99

The mortality from ischemic heart disease has increased steadily in most industrialized countries from the 19th century up to 1970. In some developed countries, such as the U.S.A. and Australia, it started to decrease in the nineteen seventies and accelerated recently. However, it has increased in some East European countries, such as Rumania, Poland and Hungary. The mortality had been extraordinarily low and the age standardized rate declined since the nineteen seventies in our country as in the U.S.A. These finding strongly suggests the possibility of prevention of ischemic heart disease worldwide. Among the risk factors, hypertension has gradually decreased due to treatment and lower intake salt in Japan. However, the compliance of antihypertensive treatment could be improved and the average intake of salt further decreased. The frequency of hypercholesterolemia was quite low for many years, but increased recently in Japan. However, the national average level of serum cholesterol is probably close to 200 mg/dl, and the new cholesterol level data will be revealed by the national survey in 1990. The world-famous high figure of smoking among Japanese men has been declining for these 20 years down to 61.2% in 1988, along with an exceptionally low rate for women in industrialized countries. The average figure of body weight by stature was in line with the desirable body weight for Japanese and the average intake of lipids has leveled off recently according to the National Nutrition Survey. After all it can be concluded that incidence of ischemic heart disease could be reduced further, even in Japan.
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PMID:[Trends, risk factors, and prevention of ischemic heart disease in Japan]. 223 8

The authors suggest that identification of high-risk individuals, modification of nutritional habit, preventing the smoking habit, increased physical activity, low salt intake, and early diagnosis and treatment of hypertension should be the most important methods used for atherosclerosis and IHD prevention in youths.
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PMID:[Methods of preventing atherosclerosis and ischemic heart disease in vocational school students]. 239 14

The aim of this study was to examine the electrophysiological effects of isoprenaline, phenylephrine, and noradrenaline on sheep Purkinje fibers in vitro, superfused either with a normal or with a modified physiological salt solution (PSS) designed to mimic some of the conditions occurring during mild myocardial ischemia (hyperkalemia, hypoxia, and acidosis). Intracellular microelectrode recording techniques were used to record resting and action potentials. Noradrenaline (10(-7) to 10(-5) M) and phenylephrine (10(-7) to 10(-5) M) prolonged the action potential of normal fibers in a concentration-dependent manner, the effect of phenylephrine being greater than that of noradrenaline. The only effect of isoprenaline (10(-7) to 10(-5) M) was a slight hyperpolarization. The modified PSS caused marked reductions in resting membrane potential, upstroke, and duration of the action potential. On these depressed fibers isoprenaline, noradrenaline, and phenylephrine all prolonged the action potential, and in the case of noradrenaline the duration of the abbreviated action potential was restored beyond control. This effect of noradrenaline and isoprenaline was more marked under ischemic than normal conditions, whereas the opposite was true of phenylephrine. In the presence of effective alpha- or beta-adrenoceptor blockade, the noradrenaline-induced prolongation of the "ischemia"-abbreviated action potential was attenuated. In some of the preparations exposed to simulated ischemia, noradrenaline caused inexcitability. In conclusion, isoprenaline, phenylephrine, and noradrenaline exhibited different electrophysiological effects on mildly "ischemic" sheep Purkinje fibers compared to their effects on normal fibers.
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PMID:Cardiac electrophysiological effects of isoprenaline, phenylephrine, and noradrenaline on normal and mildly "ischaemic" sheep Purkinje fibers. 246 60

We have previously observed a long-lasting antiischemic and antiarrhythmic effect induced by prostacyclin (PgI2) or its stable analogue, 7-oxo-PgI2-ephedrine salt in dogs subject to local myocardial ischemia. This protection appeared when the vasodilating and platelet aggregation inhibiting effect of PgI2 or its analogue was over and persisted even 72 h after treatment. We have also found that short incubation with 7-oxo-PgI2 may induce a long-lasting prolongation of the action potential duration and of the effective refractory period in the isolated rabbit papillary muscle preparation without affecting the membrane potential or the rate of rise of the action potential. Our present experiments have shown a 7-oxo-PgI2 induced, dose-dependent prolongation of the ventricular functional refractory period in conscious rabbits and anesthetized dogs, as well as an increase of the QT interval in the ECG in both species and also in conscious guinea-pigs. In all three species 50 micrograms/kg i.m. dose proved to be optimal, evoking maximal effect 48 h after treatment. In conscious rabbits this pre-treatment prevented the train of non-stimulated extra beats induced by premature stimuli. Furthermore it also prevented widening of the QRS complex appearing in non-treated controls after programmed stimulation. Pre-treatment significantly increased electrical fibrillo-flutter thresholds in the auricles and ventricles of anesthetized cats. These electrophysiological changes seem to be closely related to the 7-oxo-PgI2 induced, late appearing and long-lasting protection from ischemic and reperfusion arrhythmias.
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PMID:7-oxo-PgI2 induced late appearing and long-lasting electrophysiological changes in the heart in situ of the rabbit, guinea-pig, dog and cat. 267 53

The survey presents current knowledge on the role of nutrition in prevention of hypercholesterolemia and ischemic heart disease. From the standpoint of their role in atherogenesis, nutritional factors can be divided into protective and risk factors. The group of protective factors includes n-3 and n-6 polyunsaturated fatty acids, oleic acid, plant sterols, plant lecithins, some fiber components (e.g. pectin), plant proteins (e.g. soybean), vitamin C, vitamin E, magnesium, potassium, calcium, chromium, and selenium. The group of risk factors comprises saturated fatty acids, cholesterol, sucrose, sodium, vitamin D, and ethanol. After World War II the development of food consumption in Czechoslovakia resulted in an imbalanced state persisting for some decades now which is characterized by a high involvement of risk factors (high consumption of meat, sausages, animal fats, eggs, common salt, and alcoholic beverages) and by a low involvement of protective factors (low consumption of vegetables, fruit, potatoes, legumes, fish, and roughly milled grain). The imbalance of risk and protective factors in nutrition is conceivably one of the main causes of the extremely high mortality from cardiovascular diseases in Czechoslovakia. The current unfavorable trend in the rate of ischemic heart disease and in life expectancy of the population in Czechoslovakia can not be reversed without substantial changes in the composition of nutrition.
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PMID:[Nutrition in the prevention of ischemic heart disease]. 272 Apr 47

Significant differences in nutrition exist between the northern and the southern regions of Belgium. The most important differences are a lower saturated fat intake, a higher polyunsaturated fat intake and a higher P/S ratio in the north. Total protein, animal and vegetal protein, salt from processed foods and fiber intake are also higher in the north. The intake of butter is higher in the south and the intake of total and dietetic margarine and of fish are higher in the north. All causes, total cardiovascular, IHD (only in men), stroke and residual cardiovascular mortality are higher in the south, consistent with the regional distribution of fat intake. However, within each region there is no correlation between these mortality patterns and fat intake. This phenomenon can be explained by the presence of confounding factors: salt intake from processed foods, fish, alcohol intake and smoking habits, all of them having a different and sometimes inverse distribution among the counties. The geographical association of fat intake and cardiovascular mortality is strengthened by a similar association between trends in fat intake and trends in cardiovascular mortality. From 1968 onwards until about 1975 a decrease in saturated fat and a marked increase in polyunsaturated fat occurred together with a decreasing dietary cholesterol and salt intake. An important decrease in IHD occurred in Belgium, particularly between 1972 and 1979, and is still the highest in Europe (1968-1984). Belgium is ranked among the five top countries of Europe where stroke mortality (age 45-74 years) is declining most. The nutritional situation of Belgium and the level of mortality, though improving, are still far from ideal. The total fat, saturated fat and salt intake are much higher than recommended by W.H.O. Continued vigorous action will be necessary in order to achieve the W.H.O. goals. A comparison of what occurred in Belgium and in other countries with regard to cardiovascular mortality and nutrition underlines the role of nutrition as a key factor in public health.
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PMID:Nutrition and cardiovascular mortality in Belgium. For the B.I.R.N.H. Study Group. 275 Apr 16

Excessive cigarette smoking is recognized as a major risk factor for ischemic heart disease. Although the mechanism by which smoking enhances this risk is not known, multiple lines of indirect evidence suggest that an adverse effect of nicotine on the interaction between neutrophils and the myocardium may play a central pathogenic role. Accordingly, this study employed an isolated rabbit heart preparation perfused at a constant flow rate with physiologic salt solution containing autologous neutrophils to test the hypotheses that nicotine promotes myocardial neutrophil uptake and that an augmented myocardial neutrophil burden intensifies the actions of stimulated neutrophils on the coronary circulation. Addition of 10(-7) M nicotine to the perfusion medium caused an abrupt and sustained sequestration of 111In-labeled neutrophils by isolated rabbit hearts. In contrast, preincubation of neutrophils in 10(-7) M nicotine without inclusion of the alkaloid in the perfusion medium failed to promote neutrophil uptake. Nicotine neither enhanced myocardial neutrophil sequestration induced by perfusion with hypoxic medium nor potentiated neutrophil chemotactic responses evoked by leukotriene B4, the putative mediator of hypoxia-induced myocardial neutrophil uptake. In addition, nicotine failed to influence either baseline levels or the hypoxia-induced accumulation of immunoreactive leukotriene B4 detected in myocardial biopsies. The inflammatory cell stimulant, formylmethionyl-leucyl-phenylalanine (fMLP), increased coronary vascular resistance in neutrophil-perfused hearts but not in hearts perfused with neutrophil-free medium. The magnitude of the fMLP-induced coronary response was augmented when the myocardial neutrophil burden was increased by the addition of nicotine to the perfusion medium or by perfusion with hypoxic medium. These observations suggest that nicotine promotes myocardial neutrophil uptake by mechanisms that do not relate to enhanced release and/or effects of endogenous leukotriene B4 and that sequestration of neutrophils intensifies their actions on the coronary circulation.
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PMID:Impact of nicotine on myocardial neutrophil uptake. 282 89


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