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

Urinary levels of free adrenaline and noradrenaline were measured in two groups of healthy male industrial workers exposed to alternate four-day periods of working conditions with and without time stress, to test the hypothesis that the sympathetic nervous system is overactivated by occupational stress. Thirty confectionary workers alternated piece-work (payment by results) and work with a fixed daily wage while 30 metal workers alternated work on an assembly line with work off it. Under time stress urinary free adrenaline was 450 per cent and noradrenaline 230 per cent of the levels for similar work without time stress but involving equal oxygen consumption. These differences were statistically highly significant and they persisted on retesting after six months of alternating work regimens. They support the concept that occupational stress in industrial workers influences the adrenosympathetic system and they indicate a possible method for assessing the effects of high levels of sympathetic activity on the aetiology of ischaemic heart disease.
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PMID:Free adrenaline and noradrenaline excretion related to occupational stress. 50 78

Verapamil, at a dose of 1 mg/kg, was given intravenously to anesthetized cats one hour after coronary artery occlusion. Verapamil significantly reduced mean arterial blood pressure, but produced an increase in heart rate, partially offsetting the reduction in myocardial oxygen demand resulting from the reduction in pressure. Verapamil failed to prevent the elevations in the S-T segment of the electrocardiogram observed in cats subjected to myocardial ischemia (MI) and given only the vehicle for verapamil (i.e., 0.9% NaCl). Moreover, verapamil also did not prevent the accumulation of creatine phosphokinase (CPK) activity in the circulating blood after MI. Nevertheless, verapamil significantly prevented the loss in CPK and in amino-nitrogen observed in the ischemic region of the myocardium, indicating some protective effect on myocardial integrity. The major effects of verapamil on electrolyte content of ischemic myocardial tissue were a decrease in sodium and an increase in potassium. However, calcium gain by the heart was not prevented by verapamil. Verapamil, therefore, exerts a partial degree of protection of the ischemic myocardium but exerts some other effects which do not help prevent the spread of ischemic damage in the myocardium.
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PMID:Influence of verapamil on cellular integrity and electrolyte concentrations of ischemic myocardial tissue in the cat. 52 60

Intact anesthetized dogs were exposed for 75 min to either 5.75, 9.0, or 12.0% oxygen in nitrogen. Although pulmonary artery pressures were significantly elevated in all hypoxic exposures, systemic hypertension occurred only at the onset of severe hypoxia(5.75% O2). Coronary blood flow increased from an average of 130 during normoxia to a peak of 400 ml/100 g per min during inhalation of 5.75% O2, and coronary sinus oxygen tensions of 8 Torr and oxygen contents of 1.1 ml/100 ml were sustained for 75 min without biochemical, functional, or electrophysiological evidence of myocardial ischemia. Cardiac index (CI) increased significantly only during severe hypoxia (5.75% O2) with the greatest elevation after 30 min. Subsequently, CI decreased concomitantly with a 27% elevation in arterial hemoglobin concentration and oxygen-carrying capacity. It is concluded that the hypoxic threshold for significant elevations of cardiac output is between 6.0 and 9.0% O2.
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PMID:Effects of acute prolonged hypoxia on cardiovascular dynamics in dogs. 59 70

An in vitro model of myocardial ischemia has been established with primary monolayer cultures of neonatal rat heart cells. Ischemic conditions were simulated in vitro by subjecting the heart cell cultures to various levels of oxygen and glucose deprivation. After the ischemic treatments, cultures of beating muscle (M) cells were evaluated for functional and morphological changes. The experimental protocol consisted of treatment with 20% or 0% O2 and 1000, 500 or 0 mg glucose per 1 of medium for 4, 12 or 24 hr. Control cultures were treated with 20% O2 and 1000 mg glucose. The morphological alterations induced by the deficiency of O2 and glucose in the medium were the formation of pseudopodia and cytoplasmic vacuoles; increased cytoplasmic granulation; and the formation of abnormal cell shapes, such as long, spindly shaped M cells. There was a time-dependent decrease in beating activity as the M cells were exposed to longer durations of ischemic conditions. However, if the cultures were replenished with complete medium (1000 mg glucose) and 20% O2, the cells regained their ability to beat.
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PMID:Ischemic myocardial injury in cultured heart cells: preliminary observations on morphology and beating activity. 59 50

The effect of KoQ4 on the energetics, contractility, and electrogram of the ischemized myocardium was studied in acute experiments on dogs with induced myocardial ischemia. Intracornoary administration of KoQ4, 1.3 mg/kg, directly into the focus of ischemia for 15 min promoted a decrease in the lactate level in blood draining from the ischemic zone as compared to the control data in the absence of a difference in the dynamics of the pyruvic acid content. In distinction to the control experimental series, there was no decrease in the concentration of glucose in samples of venous blood draining from the focus of ischemia. Under the effect of KoQ4 the amplitude of left ventricular pressure and the maximum rate of its growth (dp/dt) increased moderately and the ST segment and ST/R coefficient of the epicardial electrogram from the border zone of ischemia decreased. It was shown in the rat experiments that preliminary intravenous administration of KoQ4 (14 mg/kg) increased myocardial resistance to oxygen deficiency under conditions of diacetylcholine-induced apnoe.
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PMID:[Effect of hexahydroubiquinone-4 (KoQ4) on the bioenergetics and functional activity of the myocardium in ischemia]. 59 31

The effects of intravenous dopamine were evaluated in 10 patients with severe but stable coronary artery disease, 17 consecutive patients with primary cardiogenic shock and 3 with severe congestive heart failure and oliguria. Dopamine infusion at 10 mug/kg.min in the 10 patients increased cardiac output by 35%, left ventricular peak dP/dt by 38%, left ventricular minute work index by 44% and mean systolic ejection rate by 7% (P < 0.01); heart rate, aortic pressure, left ventricular end-diastolic pressure and tension-time index were unchanged. For oxygen, potassium and lactate, arterial and coronary sinus values, coronary arteriovenous oxygen differences and myocardial extraction were unchanged. Hemodynamically 13 of the 17 patients in shock responded favourably to dopamine infusion (0.5 to 15 mug/kg.min), with decrease in heart rate, increase in systolic arterial pressure from 75 to 100 mm Hg (P <0.001), decrease in ventricular filling pressure from 20 to 16 mm Hg (P < 0.01) and increase in urine output from 10 to 100 ml/h (P < 0.01). Eleven of those patients survived the shock episode. A close relation was observed between the hemodynamic response to dopamine, survival from the shock episode and the time between onset of shock and initiation of therapy. Low rates of dopamine infusion induced diuresis in the three patients with severe cardiac failure.Dopamine thus seems to improve the mechanical efficiency of the heart in coronary artery disease. Cardiac output is selectively increased and myocardial ischemia does not appear to be induced; those beneficial effects as well as presumably specific action on renal flow and natriuresis, improve immediate survival from cardiogenic shock and severe heart failure.
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PMID:Hemodynamic and therapeutic effects of intravenous dopamine. 60 65

Twenty patients with fixed coronary artery obstruction were studied during rapid atrial pacing and methoxamine infusion. During pacing to heart rates of 142 +/- 4 (mean +/- SEM) beats per minute coronary sinus flow increased from 108 +/- 8 to 187 +/- 15 cc/min and myocardial oxygen consumption increased by + 80 +/- 11%. During methoxamine infusion that raised arterial systolic pressure to 196 +/- 5 mm Hg, similar increases in coronary sinus flow (to 179 +/- 13 cc/min) and myocardial oxygen consumption (+ 77 +/- 12%) occurred. Chest pain and ischemic ST segment changes developed in 17 and 14 patients respectively during atrial pacing, an incidence significantly greater (P less than 0.05) than during infusion of methoxamine (6 and 3 patients). Myocardial lactate extraction which averaged 26 +/- 4% during control was decreased to 10 +/- 8% during pacing and to 24 +/- 7% during methoxamine; the difference between decreases was not significant. The data show that at similar increases in myocardial oxygen consumption stress of increased heart rate results in more myocardial ischemia than stress of increased afterload.
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PMID:Effects of pharmacologically-induced hypertension on myocardial ischemia and coronary hemodynamics in patients with fixed coronary obstruction. 61 96

In order to evaluate hemodynamic predictors of myocardial oxygen consumption (MVO2), 27 normotensive men with angina pectoris were studied at rest and during a steady state at sympton-tolerated maximal exercise (STME). Myocardial blood flow (MBF) was measured by the nitrous oxide method using gas chromatography. MBF increased by 71% from a resting value of 57.4 +/- 10.2 to 98.3 +/- 15.6 ml/100 g LV/min (P less than 0.001) during STME while MVO2 increased by 81% from a resting value of 6.7 +/- 1.3 to 12.1 +/- 2.8 ml O2/100 g LV/min (P less than 0.001). MVO2 correlated well with heart rate (HR) (r = 0.79), with HR x blood pressure (BP) (r = 0.83), and, adding end-diastolic pressure and peak LV dp/dt as independent variables, slightly improved this correlation (r = .86). Including the ejection period (tension-time index) did not improve the correlation (r = 0.80). Thus, HR and HR x BP, both easily measured hemodynamic variables, are good predictors of MVO2 during exercise in normotensive patients with ischemic heart disease. Including variables reflecting the contractile state of the heart and ventricular volume may further improve the predictability.
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PMID:The rate-pressure product as an index of myocardial oxygen consumption during exercise in patients with angina pectoris. 62 64

Myocardial ischemia at rest occurs only late in the course of coronary artery disease, but transient ischemia can often be induced by increasing myocardial oxygen demand with exercise or atrial pacing. Myocardial ischemia causes a series of physiologic abnormalities that can be detected by assessment of myocardial perfusion, regional mechanical function, electrophysiology, and metabolism. Methods of assessment vary widely in sensitivity, specificity, cost, and ease of application. Although the appropriate choice of diagnostic test may be difficult, the morbidity and mortality that result from myocardial ischemia and infarction and the demonstrated potential of coronary artery bypass surgery to reverse myocardial ischemia before the development of permanent sequellae make the detection of ischemia an important clinical problem. Present methods for quantitating myocardial ischemia are imprecise and difficult to apply but have been used successfully to evaluate the efficacy of therapies designed to reduce the size of myocardial infarction.
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PMID:Myocardial ischemia: detection and quantitation. 62 55

The indices of pulmonary ventilation and gas exchange, oxygen consumption per 1 kgm of work, the restoration coefficient, the effectiveness of work, etc. were studied at rest, during dosaged physical exertion on a bicycle ergoraph, and in the restoration period in 50 healthy individuals and in 175 patients with ischemic heart disease. Selective coronary angiography was conducted in all of the patients. Spiro-bicycle-ergometry is an informative method in the diagnosis of ischemic heart disease, enabling the physician to presume the presence of coronary sclerosis and judge the degree and extent of involvement of the coronary arteries before performing coronarography. With the gradual increase in the number of involved arteries, there were noted a gradual decrease of the restoration coefficient, diminution of the effectiveness of work, and an increase in oxygen consumption per 1 kgm of load. Changes in spiro-bicycle-ergometric indices in patients with ischemic heart disease and normal coronary arteries had the same trend as those in patients with coronary atherosclerosis.
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PMID:[Bicycle spiroergometric studies in the diagnosis of ischemic heart disease]. 63 24


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