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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 21 day old infant, diagnosed as ASD, VSD, and PDA, was scheduled for an emergency radical operation. After admission, she fell into cardiac failure and was treated with artificial ventilation and infusion of inotropic agents. Anesthesia was induced with fentanyl and maintained with continuous fentanyl infusion and chlorpromazine. Dopamine and dobutamine were administered before she underwent a cor-pulmonary by-pass. At the time of release of aortic clamping, her blood pressure went down and dopamine, dobutamine and isoproterenol were administered. After completion of the cor-pulmonary by-pass, tachy-arrhythmia and hypotension occurred. Digitalis and calcium did not reverse the condition. The thorax was reopened and BP rose. After 15 min, ventricular fibrillation occurred. Defibrillation was carried out, but the heart was arrested. Even with pacing and cardiac massage, cardiac contraction did not resume. However immediately on intravenous administration of PGE1, 40 ng.kg-1.min-1, the heart started to beat. The cause of recovery from cardiac arrest was speculated to be due to reuptake of intracellular Ca2+ by PGE1. We stress therefore, that during and after cor-pulmonary by-pass procedures, PGE1 infusion may be beneficial.
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PMID:[Recovery from cardiac arrest by prostaglandin E1 infusion during emergency open heart surgery]. 227 47

We measured force of contraction and cAMP content in human isolated electrically driven right ventricular trabeculae carneae with and without the addition of isoprenaline (0.2 microM). Basal cAMP content was approximately 200% higher in preparations from nonfailing hearts than from hearts with end-stage myocardial failure. Isoprenaline was less effective in increasing force of contraction in failing (by approximately 100%) than in nonfailing cardiac preparations (by approximately 500%). With isoprenaline, cAMP content was approximately 50% lower in failing than in nonfailing preparations. We conclude that the reduced increase in force of contraction of failing human cardiac preparations with isoprenaline added may be causally related to an inadequately increased cAMP content.
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PMID:Basal and isoprenaline-stimulated cAMP content in failing versus nonfailing human cardiac preparations. 247 9

To investigate whether heart failure alters beta-adrenergic receptors on skeletal muscle and its associated vasculature, the density of beta-adrenergic receptors, isoproterenol-stimulated adenylate cyclase activity, and coupling of the guanine nucleotide-binding regulatory protein were compared in 18 control dogs and 16 dogs with heart failure induced by 5-8 wk of ventricular pacing at 260 beats/min. Hindlimb vascular responses to isoproterenol were compared in eight controls and eight of the dogs with heart failure. In dogs with heart failure, the density of beta-receptors on skeletal muscle was reduced in both gastrocnemius (control: 50 +/- 5; heart failure: 33 +/- 8 fmol/mg of protein) and semitendinosus muscle (control: 43 +/- 9; heart failure: 27 +/- 9 fmol/mg of protein, both P less than 0.05). Receptor coupling to the ternary complex, as determined by isoproterenol competition curves with and without guanosine 5'-triphosphate (GTP), was unchanged. Isoproterenol-stimulated adenylate cyclase activity was significantly decreased in semitendinosus muscle (control: 52.4 +/- 4.6; heart failure: 36.5 +/- 9.5 pmol.mg-1.min-1; P less than 0.05) and tended to be decreased in gastrocnemius muscle (control: 40.1 +/- 8.5; heart failure: 33.5 +/- 4.5 pmol.mg-1.min-1; P = NS). Isoproterenol-induced hindlimb vasodilation was not significantly different in controls and in dogs with heart failure. These findings suggest that heart failure causes downregulation of skeletal muscle beta-adrenergic receptors, probably due to receptor exposure to elevated catecholamine levels, but does not reduce beta-receptor-mediated vasodilation in muscle.
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PMID:Skeletal muscle beta-receptors and isoproterenol-stimulated vasodilation in canine heart failure. 255 23

Previously, we reported that amrinone increases isometric twitch force but relaxes K+-induced contracture in muscles from normal cat right ventricle. This study evaluated its effects on diseased cardiac tissue. Right-ventricular papillary muscles were obtained from cats with subacute right-ventricular failure (3-14 days after partial pulmonary-artery ligation) and studied in vitro during stimulation (0.5 Hz) and exposure to high-K+ Tyrode solution. Active isometric twitch force and rate of force development (dP/dt) were significantly lower in muscles from hearts with right-ventricular failure compared to control muscles. In addition, while time to peak force was not different, duration of the twitch was significantly longer. In contrast to its positive inotropic actions in control muscles, amrinone (5.3 X 10(-4) M) had no significant effects on twitch force and dP/dt in muscles from failed ventricles. Time to peak force was not changed by amrinone in either group, but unlike its action in control muscle, duration of the twitch was reduced in failed muscle. Amrinone reduced K+-contracture force similarly in both control and failed muscles. Isoproterenol (10(-6) M) significantly increased twitch force and dP/dt and reduced K+-contracture force in both muscle groups. Since amrinone appears to be a phosphodiesterase inhibitor, our data indicate that cyclic AMP (cAMP)-related relaxation processes, but not cAMP-related contractile processes, can be enhanced by phosphodiesterase inhibitors in experimental heart failure. Furthermore, amrinone's reduced positive inotropic effect in failed myocardium suggests that its improvement of ventricular function in patients reflects, in part, enhancement of relaxation.
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PMID:Enhanced relaxation and reduced positive inotropic effects of amrinone in ventricular muscle from cats with subacute heart failure. Implications for drug therapy. 298 64

The persistence of myocardial sinusoids in both ventricles as an isolated anomaly is described. A 21-year-old patient had progressive heart failure considered as cardiomyopathy of obscure etiology. Two-dimensional echocardiography demonstrated channel-like structures in the thickened myocardium of both hypokinetic ventricles. Angiography showed a honeycomblike inner contour in both ventricles. Autopsy proved the diagnosis of persistent sinusoids in a thickened myocardium.
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PMID:Persisting myocardial sinusoids of both ventricles as an isolated anomaly: echocardiographic, angiographic, and pathologic anatomical findings. 308 18

The haemodynamic and metabolic effects on the heart due to high doses of isoproterenol were compared in spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. In baseline conditions, the hypertrophied SHR heart displayed perfectly constant haemodynamics but had fewer energy reserves than the WKY heart. Isoproterenol (2 X 25 mg/kg, s.c.) caused high mortality, myocardial ischaemia, and heart failure in the SHR. These effects were accompanied by anaerobic metabolism. In the WKY rats, on the other hand, isoproterenol caused no changes in ST-segment elevation and no cardiac insufficiency; in addition, aerobic metabolism was maintained. A marked drop in coronary perfusion pressure and excessive accumulation of calcium in the myocardium account, in part, for the effects seen in the SHR. The results indicate that isoproterenol-induced heart failure in the SHR might be a useful model for selecting compounds designed to treat this disease.
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PMID:Cardiotoxicity of high doses of isoproterenol on cardiac haemodynamics and metabolism in SHR and WKY rats. 315 65

Sympathomimetic agents: isoproterenol (novodrin), dopamine, noradrenalin, adrenalin were used in 137 patients with acute circulatory insufficiency. Their hemodynamic effects were assessed, using catheterization of heart chambers and radiocardiography, and studies of circulating blood oxygen transport, acid-base state and metabolic product levels. A differential approach to sympathomimetic treatment has been developed. Isoproterenol is primarily indicated in those cases where myocardial failure is combined with decreased heart rate, conductivity disorders and markedly increased total peripheral resistance. Dopamine is more justified in cases where increasing the heart rate is more desirable, and there are signs of renal failure and heart rhythm disorders. The possibility of dopamine-induced pulmonary hypertension and pO2 fall should not be dismissed. Correct choice of an agent or a combination of agents makes it possible to control the patient's condition through action on various hemodynamic mechanisms that determine the magnitude of cardiac output.
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PMID:[Use of sympathomimetic agents in the treatment of acute circulatory insufficiency in the immediate postoperative period of heart surgery patients]. 356 Jun 16

Pulmonary mechanics were evaluated in 30 patients with acute myocardial infarction by measuring forced expiratory flow rates and total pulmonary resistance (R(T)) with the oscillometric method at the resonant frequency of the chest (6-8) cycle/s). During the first 3 days after infarction, forced expiratory volume (FEV) and forced mid-expiratory flow rate (FEF(25-75%)) were 69% and 60% of predicted values, respectively. 10 or more wk later these values were 95% and 91%. Initially, R(T) was 52% greater than predicted, but was only 4% greater 10 or more wk later. In 11 patients R(T) was measured at both resonant frequency and at 3 cycle/s. Five of these patients had no clinical signs of heart failure, but nine had abnormally high values of pulmonary artery pressure, "wedge" pressure and pulmonary extravascular water volume. All of these patients recovered. Initially, R(T) at resonance was 50% and R(T) at 3 cycle/s was 130% greater than predicted values. 2-3 wk later these figures were -3% and +6% of those predicted, respectively. At 10 wk or more, significant frequency dependence of R(T) had disappeared (R(T) at 3 cycle/s was 7% greater than R(T) at resonance). Isoproterenol inhalation in six patients caused no change in flow rates, R(T) at resonance, or R(T) at 3 cycle/s. R(T) at resonance and at 3 cycle/s, FEV, and FEF(25-75%) correlated significantly with the pulmonary vascular pressures. Patients with more marked arterial hypoxia and larger values for extravascular water volume had greater elevations of R(T) and depression of FEF(25-75%), but linear correlations were not significant. Clinical signs of congestive heart failure significantly correlated with a fall in FEV and FEF(25-75%), the development of frequency dependence of R(T), and elevation of the pulmonary wedge pressure. The initial elevation of R(T) and low flow rates indicate a modest degree of airway obstruction in acute myocardial infarction. Lack of response to isoproterenol suggests that bronchial muscular constriction is not a major factor. Frequency dependence of R(T) accompanied by elevated pulmonary vascular pressures and extravascular water volume indicates that pulmonary congestion causes the development of uneven time constants in the airways. Vascular engorgement and interstitial edema from elevated vascular pressures causing narrowing of the peripheral airways and closure of collateral airways could account for the above findings.
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PMID:Interrelation between alterations in pulmonary mechanics and hemodynamics in acute myocardial infarction. 471 74

Intravenous isoprenaline was given to 10 patients in septic shock, of which occult myocardial failure was the main indication. Isoprenaline expedited recovery in cases of "benign hypotension," where kidney function paradoxically remained satisfactory at low systolic pressures, and was useful in cases of "cold hypotension" which were complicated by renal failure alone. No significant improvement occurred in cases which were complicated by both massive pulmonary oedema and acute renal failure.
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PMID:Intravenous isoprenaline in treatment of septic shock in man. 544 79

Myocardial function and peripheral hemodynamic alterations were measured through the late stages of canine endotoxin shock. 60 min postendotoxin paired animals were given infusions of either 5 ml/kg per hr of 5% dextrose or dextrose plus isoproterenol (0.25 mug/kg per min). Comparable blood lactic and pyruvic acid levels were determined, the excess lactic acid calculated, and pH values were obtained. During the initial stages the classic pattern of hemodynamic alterations was observed; an excess of lactic acid appeared and the pH decreased. Outstanding was evidence of markedly reduced myocardial function in the late stages of shock with progressive rise in left ventricular end diastolic pressure (LVEDP), low cardiac index, rise of central venous pressure, increased central blood volume, tachycardia, and declining arterial pressure. Analyses of left ventricular function curves also indicated myocardial failure. Infusion of dextrose alone failed to decrease mortality rate (10 of 18 dying), whereas the rate was significantly decreased with isoproterenol (2 of 18). Dextrose infusion did not benefit myocardial function. Isoproterenol resulted in a marked improvement in myocardial action with a significant increase in heart work associated with, yet very minor, increments of LVEDP. In addition, tachycardia subsided, peripheral resistance decreased, and the blood pressure stabilized. The prognostic value of excess lactic acid was doubtful but a progressive fall in later stages was associated with survival.
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PMID:Hemodynamic effects of isoproterenol in canine endotoxin shock. 567 17


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