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

Hemodynamic effects of isoproterenol, dopamine, and epinephrine were studied before and after acute beta-adrenergic blockade in 16 open-chest, anesthetized mongrel dogs. Beta blockade was induced with 1 mg. per kilogram of intravenous propranolol. Cardiac output measurements were obtained by thermal dilution, and pressure recordings were obtained in the right ventricle, pulmonary artery, left atrium, left ventricle, and aorta. Derived parameters included stroke volume, pulmonary and systemic vascular resistances, and peak left ventricular dP/dt. In the presence of propranolol, epinephrine became a lethal drug in large doses and did not increase cardiac output in standard doses. Dopamine, in 25 to 50 mcg. per kilogram per minute doses, increased arterial pressure and systemic resistance; cardiac output was diminished compared with dopamine, 10 mcg. per kilogram per minute, prior to propranolol, as a result of increased resistance and decreased LV contractility. Isoproterenol, 0.6 to 0.9 mcg. per kilogram per minute, 15 to 20 times standard dosages, had moderately positive inotropic effects and increased cardiac output. Left ventricular systolic pressure with isoproterenol after propranolol was reduced when compared with effects of smaller doses prior to propranolol. These observations suggest that none of the catecholamines studied would be optimal for circulatory support in heart failure in the presence of propranolol. The present results define a pharmacologic basis for design of appropriate drug combinations for circulatory support in beta-blocked animals.
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PMID:Pharmacologic antagonism of beta-adrenergic blockade in dogs. I. Hemodynamic effects of isoproterenol, dopamine, and epinephrine in acute propranolol administration. 3 98

Dobutamine was infused at a rate of 8 mcg/kg/min in 17 patients with or without congestive heart failure. Cardiac output increased from an average 2.92 to 4.45 1/min/m2(p less than 0.001) with no change in mean aortic pressure (93.4 to 97.8 mmHg) and only a slight increase in heart rate (78 to 87 beats/min). Left ventricular end-diastolic pressure decreased from an average 19 to 13.7 mmHg (p less than 0.01). Peak left ventricular dp/dt was doubled (1147 to 2370 mmHg/sec, p less than 0.001) and Vmax increased from 1.08 to 2.18 circ/sec (p less than 0.001). In 10 patients given equi-inotropic doses (100 per cent increase in peak dp/dt) Isoproterenol produced a greater increase in cardiac output (71 percent) than Dobutamine /51 percent). Isoproterenol caused mean aortic pressure to fall significantly (8 percent) while no change was noted with Dobutamine. Accordingly, peripheral vascular resistances were reduced to a greater extent with Isoproterenol than with Dobutamine (p less than 0.05). Mean pulmonary arterial pressure decreased significantly (25 +/- 5.9 to 22 +/- 5.7 mmHg, p less than 0.05) with Isoproterenol infusion and remained unchanged with Dobutamine infusion. Dobutamine increased both stroke work (57 percent) and minute work (83 percent). With Isoproterenol however, only minute work was significantly increased (90 percent). Dobutamine therefore is a potent inotropic drug, with mild chronotropic and peripheral vascular effect and may be valuable in the management of severe heart failure not associated with hypotension.
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PMID:Comparative haemodynamic effects of dobutamine and isoproterenol in man. 89 74

Right heart catheterisation was undertaken in six patients with accidental deep hypothermia. Studies were carried out before and after rapid blood volume expansion, with and without Isoproterenol infusion, and were repeated at normal body temperatures. The initial haemodynamic pattern indicated a marked hypovolemia with a simultaneous decrease of both cardiac output and ventricular filling pressures, and a decreased measured total blood volume. Rapid correction of the hypovolemia revealed cardiac insufficiency, in part due to the persisting bradycardia. Left ventricular function was depressed in patients with prolonged cold exposure and normal in patients with short exposure. These abnormalities disappeared after Isoproterenol infusion during hypothermia, and spontaneously after return to normothermia. No imbalance existed between the decreased cardiac output and oxygen uptake in hypothermia, arterio-venous oxygen difference being within normal limits.
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PMID:Haemodynamic study of prolonged deep accidental hypothermia. 118 54

A 21 month-old unvaccinated boy was admitted for an acute respiratory distress episode associated with major leukocytosis (maximum = 146 G/l). Transient heart failure and pneumomediastinum occurred but the outcome was favourable. Coughing attacks then occurred and the diagnosis of pertussis was serologically confirmed. This case report is reminiscent of the possible severity of pertussis pneumoniae, the mechanisms of haematologic abnormalities, and stresses to the benefit of pertussis vaccination.
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PMID:[Diffuse alveolar pertussis with major hyperleukocytosis with "pseudocentrocytic" contingent]. 131 26

To examine the cellular mechanisms of contractile dysfunction in postinfarction heart failure, we studied the effects of beta-adrenergic receptor stimulation on contractile function and Ca2+i handling of noninfarcted papillary muscles from sham-operated (n = 17) and infarcted (n = 17) rats. Ca2+i transients measured with the bioluminescent protein aequorin and parameters of isometric contraction were recorded during graded isoproterenol stimulation. Developed tension and peak rate of tension rise were depressed (p less than 0.05) in muscles from infarcted rats at physiological and maximally stimulating [Ca2+]oS. The time to peak tension was prolonged in the muscles from the infarcted rats, corresponding with prolongation of the time to peak Ca2+i. In muscles from sham-operated rats, isoproterenol increased both the amplitude of the Ca2+i transient and the peak rate of tension rise. In contrast, the inotropic response to isoproterenol was severely blunted in the muscles from infarcted rats despite a large increase in the amplitude of the Ca2+i transient. Isoproterenol abbreviated the time course of the isometric twitch and the Ca2+i transient in both groups. These findings suggest that postinfarction heart failure may be related in part to decreased force-generating capacity of the myofilaments. Treatment with captopril for 5 weeks, beginning 1 week after infarction (n = 14), resulted in reduction of left ventricular filling pressures and partial normalization of myocardial contractility and Ca2+i handling. In addition, compared with muscles from untreated infarcted rats, muscles from the captopril-treated rats exhibited improved contractile responses to increasing [Ca2+]o or isoproterenol. The inotropic response to isoproterenol in muscles from all three groups of rats had a significant negative correlation (r = -0.64, p less than 0.0001) with left ventricular end-diastolic pressure measured in vivo. Thus, the defect in excitation-contraction coupling in rats with postinfarction heart failure may be partially normalized by chronic load reduction with an angiotensin converting enzyme inhibitor.
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PMID:Captopril enhances intracellular calcium handling and beta-adrenergic responsiveness of myocardium from rats with postinfarction failure. 132 96

Acute rejection often leads to severe myocardial failure and death. The beneficial hemodynamic effects of isoproterenol in improving immediate postoperative heart failure have prompted its routine use after transplantation. However, because of the physiopathological alterations documented during rejection, an inappropriate response of the graft to isoproterenol administration could be expected. Six dogs received orthotopic transplants and were prepared with implantable devices for serial hemodynamic studies. The studies were performed on the resting unanesthetized subject 3 hours after operation when transient heart failure was present and repeated when myocardial failure secondary to rejection occurred. After basal state measurement, various doses of isoproterenol were infused and the hemodynamic responses during each period were compared. During rejection, the hemodynamic response to 0.05 and 0.10 micrograms.kg-1.min-1 was significantly lower when compared with the response in the postoperative period. To achieve similar postoperative chronotropic and inotropic effects, 0.35 microgram.kg-1.min-1 of isoproterenol was necessary. Isoproterenol is therefore effective in controlling myocardial failure during acute rejection despite a reduced sensitivity of the sinoatrial node and myocardial tissue.
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PMID:Efficacy of isoproterenol on the failing transplanted heart during early acute rejection. 159 30

The purpose of this study was to confirm that an agent, which increases diastolic [Ca2+]i, namely digoxin, depresses cardiac performance, mitochondrial activity, and glycolysis in chronic alcohol-treated and myopathic hearts, and that an agent, which lowers diastolic [Ca2+]i, namely isoproterenol, activates cardiac performance, mitochondrial activity, and glycolysis in these animals. Energy levels, glycolysis, mitochondrial activity, hemodynamics, and cAMP were studied in isolated hearts from three groups of animals, i.e., 9-month control hamsters, hamsters given 50% alcohol until 9 months of age, and 6-month-old cardiomyopathic hamsters in heart failure. Isolated hearts were perfused with either a control medium, a medium containing isoproterenol, digoxin, or digoxin + isoproterenol. Measurement of phosphomonoester sugars, and glucose-6-phosphate, were used to assess glycolytic activity. Oxygen consumption was used to analyze mitochondrial activity. All hearts perfused with either isoproterenol or isoproterenol + digoxin showed an increase in developed pressure, rate-pressure-product, and a decrease in end-diastolic pressure. Isoproterenol activated mitochondrial activity and glycolysis in hearts from myopathic and chronic alcohol hamsters. Based on 31P-NMR studies, isoproterenol or isoproterenol + digoxin improved the over-all energy state of hearts from cardiomyopathic hamsters, but not hearts from control and chronic alcohol hamsters. Digoxin alone augmented the rate-pressure-product and oxygen consumption in control hearts but not hearts from myopathic and chronic alcohol hamsters. Digoxin caused an increase in end-diastolic pressure in myopathic and chronic alcohol hearts but not control hearts. Digoxin depressed glycolysis and worsened the energy state in hearts from cardiomyopathic and chronic alcohol hamsters, but not hearts from control hamsters. In conclusion digoxin, but not isoproterenol nor isoproterenol + digoxin, depressed cardiac performance and glycolysis as well as high energy phosphates in cardiomyopathic and chronic alcohol hearts. Isoproterenol added to digoxin negated the adverse effects of digoxin in cardiomyopathic and chronic alcohol hearts.
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PMID:Activation of glycolysis with isoproterenol but not digoxin reverses chronic alcohol depression in hamster hearts. 162 50

Isoprenaline produced concentration-dependent contractions of the in vitro canine saphenous vein which were attenuated by phentolamine (10(-6) M) and pacing-induced heart failure. Both at control and peak heart failure, a biphasic response was seen in the dorsal pedal artery, consisting of an initial relaxation followed by a contraction; phentolamine and heart failure enhanced the relaxation component. In the presence of propranolol, the isoprenaline-induced contraction was sensitive to yohimbine, but resistant to prazosin. Therefore it is concluded that isoprenaline interacts not only with vascular beta-adrenoceptors, but also with alpha 2-adrenoceptors. Endothelial denudation resulted in a diminished response to isoprenaline in control saphenous vein and dorsal pedal artery but not in vessels from dogs with heart failure. The observation that the contractile response to isoprenaline diminishes in heart failure implies a specific down-regulation of peripheral vascular alpha 2-adrenoceptors.
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PMID:Novel vascular effects of isoprenaline following pacing-induced heart failure in the dog. 166 28

After a 16-h in vivo infusion period of isoproterenol (400 micrograms/kg/h) from a minipump implanted subcutaneously (s.c.) in rats, we observed an increase in heart weight due to tissue edema. In isolated perfused heart preparations, the EC50s of isoproterenol to induce positive inotropy and increase in coronary flow were increased approximately 7 and 4 times, respectively. Isoproterenol dose-response curves performed in trachea preparations, were shifted to the right by about fivefold as compared with the control group. In the presence of phentolamine, the isoproterenol induced maximal relaxation in the isolated aorta from isoproterenol-pretreated animals was reduced from 46.5 to 9.2% as compared with saline-pretreated rats. In the absence of phentolamine, the epinephrine (EPI) and norepinephrine (NE) cumulative dose-response curves in this preparation were not affected by isoproterenol pretreatment with respect to EC50 and maximal effect. However, in the presence of phentolamine, the contractile response to a supramaximal dose of NE (10 microM) amounted to 30 and 70% in the saline- and isoproterenol-pretreated rats, respectively. In the presence of both phentolamine and propranolol, a similar response of 70% was observed by this supramaximal dose of agonist in the saline-pretreated rats as well. In anesthetized rats, 120 min after removal of the minipumps, sodium nitroprusside induced increase in heart rate (HR) was reduced after isoproterenol pretreatment, whereas for salbutamol the decrease in diastolic blood pressure (DBP) was also reduced. As compared with salbutamol, a marked increase was observed in the ratio of mean arterial blood pressure (MAP) to HR for SNP after isoproterenol pretreatment. The phenylephrine-induced increase in MAP was increased after isoproterenol pretreatment. We conclude that in the pathogenesis of heart failure the beta-adrenoceptor-mediated effects of catecholamines are attenuated and alpha-adrenoceptor-mediated effects become progressively important.
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PMID:Modulation of adrenoceptor-mediated cardiovascular effects by short-term in vivo infusion of isoproterenol in rats. 170 99

A 21-month-old infant presented with simultaneous localized scleroderma and severe cardiomyopathy with heart failure. Cardiac abnormalities and serological changes (positive rheumatoid factor assay, elevated IgM and IgG levels, and elevated erythrocyte sedimentation rate) reverted to normal with prednisone therapy, and there was substantial, though incomplete, resolution of her skin changes during the same period. To our knowledge, this is the first patient with definite, clinically significant cardiac involvement associated with focal scleroderma. The possibility of internal organ involvement, including cardiac involvement, must be considered with focal scleroderma as well as with progressive systemic sclerosis.
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PMID:Focal scleroderma and severe cardiomyopathy. Patient report and brief review. 199 94


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