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

A linear three-pool model of rhythm-inotropic phenomena in the cardiac muscle is proposed. Dynamics of accumulation and liberation of calcium from intracellular pools is described by differential equations. It has been shown by numerical experiments that rhythm-inotropic phenomena in the normal cardiac muscle and under cardiac insufficiency can be described qualitatively in terms of the concept on calcium recirculation in intracellular pools.
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PMID:[Modeling the effect of rhythm on the strength of myocardial contraction]. 67 76

A syndrome on four dairy farms in which calves up to two months of age died suddenly during a period of excitement usually precipitated by feeding was investigated. The description given by owners was that during, or shortly after milk feeding, the calves grunted, fell and died within one minute. Post mortem examinations revealed patchy myocardial pallor but no other lesions or evidence of infectious disease. Histopathological studies revealed peracute myocardial degeneration. Biochemical examinations have shown a selenium deficiency in in-contact calves and since this was corrected, no further cases have occurred. It is suggested that this is an additional manifestation of the selenium deficiency syndrome and that in certain circumstances, a deficiency of available selenium renders cardiac muscle vulnerable to stresses which induce severe peracute damage and leads to cardiac failure and sudden death.
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PMID:Sudden death in calves associated with acute myocardial degeneration and selenium deficiency. 71 69

Although an inotropic effect of digitalis on skeletal muscle has been demonstrated in animals, it has not been shown in man. Digitalis, in previous studies, has failed to improve voluntary exercise performance. In this investigation the strength of nerve-stimulated involuntary thumb adduction was measured before, during and after infusion of ouabain into the brachial artery. With this experimental design, the many uncontrolled factors that govern ordinary exercise tolerance were avoided. Large doses of ouabain (0.5 mg) produced significant augmentation of peak strength of thumb adduction whereas smaller doses (75 mug) more likely to reach the thumb during systemic digitalization produced only suggestive increases in peak contraction strength. In patients previously digitalized for heart failure, the large doses of ouabain did not significantly change contractility. The findings suggest that skeletal muscle is less sensitive than cardiac muscle to ouabain, and that systemic digitalization has a minor effect on skeletal muscle. When the differences between skeletal and cardiac muscle in excitation-contraction coupling are considered, the reduced effect of ouabain on skeletal muscle contraction is compatible with cell membrane locus of action in both tissues.
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PMID:Effect of digitalis on skeletal muscle in man. 77 59

In vitro experiments employing the polarographic technique of in-rush currents have demonstrated that adrenalin and noradrenaline in concentrations approaching those found in blood of myocardial infarction patients during the early days of the disease inhibit the tissue respiration of the cardiac muscle by 10--50%. A 10-minute intensive pain stimulation was found to inhibit the aerobic processes in the myocardium by 20--24%. Hypercatecholaminemia observed in the acute period of myocardial infarction is suggested to play an important role in the pathogenesis of cardiac insufficiency during myocardial infarction, since it causes histotoxic hypoxia of the intact portions of the cardiac muscle. The importance of eliminating the pain syndrome in patients with myocardial infarction and angina pectoris is emphasized.
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PMID:[Effect of exogenous catecholamines and pain action on the tissue respiration of the myocardium]. 85 43

Left ventricular failure was produced in dogs by inducing mitral insufficiency and the cardiac muscle was examined for ultrastructural changes in thsese failing hearts after 5-10 months of mitral insufficiency. The left ventricular failure was established by haemodynamic measurements, chest X-ray and examination of the heart. In the failing heart, the increased number of mitochondria showed close approximation with the sarcolemmal membrane in the T-tubules as well as in the intercalated discs (ID); this is in contrast to what is seen in normal hearts, where T-tubules were mostly coupled with sarcoplasmic reticulum. It is possible that in the heart failing on account of mitral insufficiency mitochondria may be taking over the function of the sarcoplasmic reticulum. Although ID were jumbled up in the failing heart, the intercellular gap and specialized membrane junctions (gap and tight junctions, desmosomes) were quite comparable to normal, indicating that intercellular communication at ID in this type of heart failure is probably maintained. Nuclear chromatin in the failing heart was condensed and lined the inner nuclear membrane. Microbodies with a single limiting membrane were frequent and so were lipofuscin granules. The latter could be an end product of degenerative mitochondria. Golgi bodies in the failing heart were also present in locations away from the nucleus.
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PMID:Ultrastructure of failing myocardium due to induced chronic mitral insufficiency in dogs. 87 78

The cardiomyoplasty is a new surgical procedure that uses a skeletal muscle electrostimulated in order to reinforce or even substitute partially the cardiac muscle. We present the electrophysiology aspects in a patient with dilated cardiomyopathy that underwent cardiomyoplasty. First the latissimus dorsi muscle was prepared with a neurostimulant ITREL II. During the surgical procedure a dual-chamber pacemaker mode DDD brand CPI was placed. After three months, ablation radiofrequency of the AV node was performed in order to control the atrial fibrillation that caused heart failure. By means of the AV block we obtained synchrony between the ventricular stimulation and the latissimus dorsi muscle, and by this the patient improved. Using the modern pacemakers and radiofrequency we can control the bradyarrhythmias as well as the tachyarrhythmias frequent in patients with dilated cardiomyopathy, increasing the success rate of cardiomyoplasty.
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PMID:[The usefulness of electrophysiology in a patient undergoing cardiomyoplasty]. 128 59

Cytoplasmic free calcium ions (Ca2+) play a central role in excitation-contraction coupling of cardiac muscle. Abnormal Ca2+ handling has been implicated in systolic and diastolic dysfunction in patients with end-stage heart failure. The current study tests the hypothesis that expression of genes encoding proteins regulating myocardial Ca2+ homeostasis is altered in human heart failure. We analyzed RNA isolated from the left ventricular (LV) myocardium of 30 cardiac transplant recipients with end-stage heart failure (HF) and five organ donors (normal control), using cDNA probes specific for the cardiac dihydropyridine (DHP) receptor (the alpha 1 subunit of the DHP-sensitive Ca2+ channel) and cardiac calsequestrin of sarcoplasmic reticulum (SR). In addition, abundance of DHP binding sites was assessed by ligand binding techniques (n = 6 each for the patients and normal controls). There was no difference in the level of cardiac calsequestrin mRNA between the HF patients and normal controls. In contrast, the level of mRNA encoding the DHP receptor was decreased by 47% (P less than 0.001) in the LV myocardium from the patients with HF compared to the normal controls. The number of DHP binding sites was decreased by 35-48%. As reported previously, expression of the SR Ca(2+)-ATPase mRNA was also diminished by 50% (P less than 0.001) in the HF group. These data suggest that expression of the genes encoding the cardiac DHP receptor and SR Ca(2+)-ATPase is reduced in the LV myocardium from patients with HF. Altered expression of these genes may be related to abnormal Ca2+ handling in the failing myocardium, contributing to LV systolic and diastolic dysfunction in patients with end-stage heart failure.
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PMID:Expression of dihydropyridine receptor (Ca2+ channel) and calsequestrin genes in the myocardium of patients with end-stage heart failure. 132 1

The authors investigated the effect of intravenous nitroglycerin and trimepranol on the haemodynamics of patients with acute myocardial infarction. They found that nitroglycerin has a favourable effect on haemodynamics as it leads to a reduction of the pressure in the wedged pulmonary artery and to a reduction of oxygen requirement of the cardiac muscle, while the changes of the minute volume and pulse rate are insignificant. Trimepranol leads to a rise of pressure in the wedged pulmonary artery, sometimes to critical values, and to a decline of the cardiac minute output. The authors conclude that trimepranol is suitable for a selected group of patients with sinus tachycardia and without signs of cardiac failure while the pulmonary pressure is carefully monitored. Nitroglycerin can be administered to the majority of patients with acute myocardial infarction. To ensure safe administration it is sufficient to monitor the heart rate and in particular the systemic pressure. It is best to administer it to patients with extensive myocardial infarctions with a high filling pressure of the left ventricle.
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PMID:[Hemodynamic effects of nitroglycerin and trimepranol in acute myocardial infarct]. 135 22

Since the use of cardiac glycosides for heart failure therapy is limited by their narrow margin of safety, numerous efforts have been made to find and develop novel cardiotonic agents that are superior to the cardiotonic glycosides. Positive inotropic drugs acting on beta-adrenoceptors and inhibitors of cAMP phosphodiesterase have been extensively studied for the treatment of patients with heart failure. The main mechanism of these agents is elevation of cAMP tissue levels. Furthermore, Ca sensitizers such as sulmazol, pimobendan, MCI-154, END 53998 and DPI 201-106 are of interest, since such a mechanism of action may be beneficial for the failing heart. Recently, cardiotonic substances with a novel mechanism of action such as gingerol and xestoquinone have been isolated from natural sources. Natural products, purealin, goniodomin and okadaic acid, have proven to be valuable pharmacological tools for studies on cardiac muscle contraction.
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PMID:[Novel types of cardiotonic drugs]. 139 36

Cardiomyoplasty, a new therapy for heart failure, uses autologous skeletal muscle to mechanically assist the heart. The success of dynamic cardiomyoplasty is critically dependent on the contraction strength of the assisting skeletal muscle. Unlike cardiac muscle, skeletal muscle contracts in a graded response to electrical stimulation. However, in current cardiomyoplasty practice, no systematic technique exists to set the stimulating voltage effecting skeletal muscle contraction. The stimulating voltage is simply set to some multiple of the "threshold" voltage. Furthermore, researchers do not consider the role of stimulating voltage when they determine the amount of assistance afforded during cardiomyoplasty. To more accurately assess the value of this heuristic voltage-setting technique, we investigated the role of stimulating voltage on the strength of contraction of the latissimus dorsi muscle. Six New Zealand white rabbits had isovolumic hydraulic pouches constructed from the latissimus dorsi muscle. The muscles were wrapped around a compliant balloon in which isovolumic pressure development was measured during tetany-inducing burst (pulse-train) stimulation. The tetanic plateau of the pouch pressure record was used to measure the effects of stimulating voltage on skeletal muscle contraction. Results indicated that (1) increasing stimulating voltage from two to four times the "threshold" voltage increased normalized pouch pressure from 0.38 +/- 0.21 to 0.78 +/- 0.12 (mean +/- SD) (p < 0.05); (2) the threshold-normalized voltage necessary to cause maximal muscle contraction varied widely (5.7 +/- 2.0, mean +/- SD; range, 3.1 to 9.3); and (3) the current achieving maximal pressure development varied from 5.6 to 31.4 mA (19.9 +/- 10.4 mA).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Voltage-dependent performance of skeletal muscle pouches: implications for cardiomyoplasty. 142 Feb 24


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