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)

A comparative clinical study of the efficacy of Benzoral, Trasicor, Viskene, Aptene, Eraldine and Inderal was conducted in the ischaemic heart disease patients. Their antiarrhythmic and antianginal effect was determined, as well as their optimum therapeutic dosages, the activity of their specific beta-adrenolytic properties, the effect of the drugs on the bronchi and the peripheral venous tone. Apart from the clinical study, electro- and polycardiography, functional pulmonary tests and the Schellong orthostatic test were used. All the drugs in question were found to produce a distinct specific beta-blocking effect. They are effective in cases of atrial and ventricular extrasystole, paroxysmal tachycardia, sinus tachycardia and tachyarrhythmic fibrillation, as well as for the prevention of anginal attacks and arrhythmic fibrillation. All the drugs produce a negative inotropic effect, Inderal--the strongest, Viskene and Benzoral--the weakest. All beta-blockers can impair bronchial patency in patients with bronchial obstruction. This effect is least pronounced with Eraldine that may be used as the drug of choice in such cases. In most cases the beta-blockers do not affect the peripheral venous tone, but in some cases they may reduce it.
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PMID:[Comparative evaluation of the clinical action of a series of beta-adrenergic blockaders]. 1 Apr 63

46 patients with ischaemic heart disease were treated with Micristin (20-40 mg/kg) or a combination of Micristin and Propranolol (80-120 mg/die). The values of bleeding time, the platelet factor 4 in lysate of thrombocytes or in plasma of patients as well as the soluble fibrin monomer complexes were investigated. They showed no obvious correlation to the clinical findings.
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PMID:[Clinical aspects of control in therapy with platelet inhibitors]. 9 69

Effects of propranolol on ischemic segmental function were studied in anesthetized open-chest dogs. Two segment-length gauges were used for measuring the regional myocardial function: one was sutured on to the left ventricular surface perfused by the anterior descending coronary artery (ischemic zone) and the other was on to that perfused by the circumflex coronary artery (normal zone). A bolus of propranolol (0.5 mg/kg) was injected into the right femoral vein. Five min later, the left anterior descending coronary artery (LAD) was completely occluded for one mine and thereafter released. Then a second coronary occlusion for 20 min was performed; an interval of 20 min was allowed between two occlusions. Propranolol, in the ischemic segment, apparently decreased the extent of paradoxical lengthening in the late systole following one min LAD occlusion, and facilitated improvement of segmental function after release of the occlusion. Moreover, the extent of abnormal stretching induced by 20 min occlusion during early systole, was also reduced by propranolol pretreatment. In contrast, compensatory increase in shortening by the normal segment was disturbed by propranolol. These results suggest that propranolol might exert a favourable influence on the segmental myocardial function during either transient or maintained myocardial ischemia.
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PMID:Effect of propranolol on regional myocardial function in anesthetized open-chest dogs with myocardial ischemia. 15 88

Continuously recorded bipolar electrograms were obtained simultaneously from epi-, endo-, and mid-myocardial regions of the ischemic and normal zones of cat left ventricle in vivo after coronary occlusion, analyzed by computer, and compared to regional cyclic AMP levels. Regional cyclic AMP content was used as an index of the combined local effects of: (a) efferent sympathetic nerve discharge; (b) release of myocardial catecholamines due to ischemia; and (c) circulating catecholamines. Ischemia resulted in a progressive increase in pulse width and rise time and a decrease in rate of rise of voltage (dV/dt) of the local electrograms from ischemic zones reaching a maximum within 2.4+/-0.3 min (mean+/-SE) at the time of onset of severe ventricular dysrhythmias, all of which returned toward control before the cessation of the dysrhythmia (33.5+/-1.5 min after coronary occlusion). Increases in cyclic AMP in ischemic zones preceded corresponding increases in the frequency of premature ventricular complexes (PVCs). Propranolol inhibited the increases in cyclic AMP and reduced the frequency of PVCs in animals without ventricular fibrillation. In animals with ventricular fibrillation, cyclic AMP was significantly elevated in normal and ischemic zones compared to animals with PVCs only. Electrical induction of PVCs or ventricular fibrillation in ischemic and nonischemic hearts failed to increase cyclic AMP. The results suggest that the changes in regional adrenergic stimulation of the heart may contribute to perpetuation of ventricular dysrhythmia and the genesis of ventricular fibrillation early after the onset of myocardial ischemia.
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PMID:Mechanisms contributing to malignant dysrhythmias induced by ischemia in the cat. 20 67

Twelve patients with ischemic heart disease were investigated by right and left heart catheterisation. All patients were studied at rest and during exercise, both before and after administration of beta-blocker propranolol, Inderal (ICI). Left ventricular function decreased after administration of propranolol, but these changes were significant only during exercise. Contractility was depressed after administration of propranolol already at rest. On the other hand, left ventricular filling pressure decreased after administration of propranolol. Our results show the poor reliability of the evaluation of the left ventricular function based solely on the left ventricular filling pressure.
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PMID:The effect of propranolol on left ventricular function at rest and during exercise in patients with ischemic heart disease. 45 95

The effects of propranolol on periinfarction block, myocardial ischemic injury and left ventricular performance following anterior descending coronary artery occlusion were studied. Experiments were made in 14 dogs anesthetized with pentobarbital sodium. Two minutes of reversible myocardial ischemia was induced by occlusion of descending left coronary artery. The severity of myocardial ischemia estimated by summing S-T segment elevation (sigma ST) from epicardial ECG mapping, heart rate, femoral arterial pressure and left ventricular (LV) dp/dt was determined before, during coronary occlusion alone and following propranolol infusion (0.25 mg/Kg) and coronary occlusion. Periinfarction block aspects on epicardial ECG appeared in four dogs following five repeated coronary occlusions. Propranolol infusion before coronary occlusion prevented the periinfarction block in every animal. The decrease of myocardial ischemia (sigma ST elevation), heart rate, arterial blood pressure and LV dp/dt following propranolol and coronary occlusion might be partly due to the beneficial effect of this drug on periinfarction block.
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PMID:Effect of propranolol on experimental periinfarction block and myocardial ischemia. 59 24

To clarify the influence of propranolol-and particularly its heart-rate effects-on myocardial ischemia, coronary hemodynamics and metabolism were studied in 15 patients utilizing a protocol to control heart rate. Ten patients had significant coronary narrowing (CAD) and 5 were normal. Systemic pressure, coronary sinus blood flow (CSBF), left ventricular oxygen utilization (LVVO2), ST Segment depression, and myocardial lactate extraction were measured before and after propranolol (10 mg IV), at rest, during pacing-induced tachycardia stress. Propranolol-related reduction in CSBF and LVVO2 at rest was reversed when heart rate was controlled in both patient groups. Propranolol failed to alter heart-rate threshold, tension-time index (TTI), CSBF, or LVVO2 at angina in the CAD patients. Likewise, ischemic-type ST depression, decreases in lactate extraction, and coronary resistance were unchanged compared to values observed during tachycardia stress before propranolol. In normal coronary patients, propranolol also produced no significant change in LVVO2 or coronary resistance when its heart rate effects were controlled. These data imply that a major coronary and metabolic influence of propranolol relates to changes occurring secondary to its influence on heart rate. Furthermore, this agent's anti-ischemic effect is not prominent during tachycardia stress suggesting that this stress test may be clinically useful in patients taking propranolol.
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PMID:Effects of propranolol on coronary hemodynamic and metabolic responses to tachycardia stress in patients with and without coronary disease. 83 33

The effects of coronary occlusion and of subsequent propranolol administration were examined in 18 conscious dogs. Overall left ventricular (LV) function was assessed by measurements of LV pressure and dP/dt, and regional myocardial function was assessed by measurements of segment length (SL), velocity of SL shortening and regional myocardial "work", i.e., pressure-length loops in normal, moderately, and severely ischemic zones. Regional intra-myocardial electrograms were measured from the same sites along with regional myocardial blood flow as determined by the radioactive microsphere technique. Coronary occlusion resulted in graded loss of function from the normal to severely ischemic zones with graded flow reduction and graded elevation of the ST segment. Propranolol depressed overall LV function, function in the normal zone (work fell by 17+/-4%), and in the majority of moderately ischemic segments (work fell by 7+/-3%). In severely ischemic segments the extent of paradoxical motion and post-systolic shortening was reduced by propranolol. After propranolol regional myocardial blood flow fell in the normal zone (11+/-2%) and rose in the moderately (15+/-4%) and severely (63+/-10%) ischemic zones. Thus, in the conscious dog with regional myocardial ischemia, propranolol induces a redistribution of myocardial blood flow, with flow falling in normal zones and rising in moderately and severely ischemic zones. The improvement in perfusion of ischemic tissue was associated with slight but significant depression of shortening, velocity, and work in the moderately ischemic zones and of paradoxical bulging and post-systolic shortening in the severely ischemic zone.
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PMID:Effects of propranolol on regional myocardial function, electrograms, and blood flow in conscious dogs with myocardial ischemia. 87 96

Serum triiodothyronine (T3) and thyroxine (T4) levels were measured in twelve hyperthyroid patients before and after treatment with propranolol, 40 mg four times daily, for 2 weeks. There was a significant fall in serum T3 and a significant rise in serum T4 concentrations in the group as a whole and it was concluded that the clinical effectiveness of propranolol in hyperthyroidism may be mediated in part by its action on the peripheral metabolism of thyroid hormones. Propranolol treatment should be withdrawn gradually as removal of the suppressive action of the drug on thyroid hormone metabolism is potentially hazardous, particularly in patients with ischaemic heart disease.
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PMID:Thyroxine and triiodothyronine levels in hyperthyroid patients during treatment with propranolol. 88 Jul 33

Improvement of myocardial oxygenation is a major goal in the treatment of ischaemic heart disease. Propranolol, 0-1 mg/kg intravenously, was administered to 20 patients with acute myocardial infarction without clinical evidence of left ventricular failure. The most important haemodynamic response was a substantial decrease in myocardial contractility. This was reflected by a fall in cardiac index (average of 0-4 l/min/M2, P less than 0-001) and of arterial mean pressure (average of 16 mmHg, P less than 0-001) with little change in systemic vascular resistance. Heart rate, not strikingly increased at the control state in the majority of patients, decreased an average of 7 beats/minute (P less than 0-001). Pulmonary wedge pressure varied; it decreased in 6 patients with high values (greater than 15 mmHg) prior to propranolol. These changes in wedge pressure in the presence of decreased contractility are probably related to improved left ventricular compliance, produced by propranolol. Propranolol markedly improved myocardial metabolism. Arterial-coronary sinus oxygen difference decreased an average of 0-72 ml/100 ml (P less than 0-001). Myocardial lactate production shifted to extraction (average of -8% to 14%) or the rate of lactate extraction increased (average of 20% to 29%). Coronary blood flow decreased an average of 13 ml/100 g/min (P less than 0-001). The finding, that myocardial metabolism improved, suggests that decrease in coronary blood flow was mediated by reduced myocardial oxygen requirements. None of the 20 patients developed left ventricular failure or other complications related to beta-adrenergic blockade. Severe chest pain, unresponsive to conventional therapy in four patients, was relieved by propranolol. These findings demonstrate that acutely administered propranolol improves myocardila oxygenation in patients with uncomplicated acute infarction without endangering perfusion of other vital organs.
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PMID:Propranolol in acute myocardial infarction in man: effects of haemodynamics and myocardial oxygenation. 96 69


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