Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Skeletal muscle possesses inherent plasticity of gene expression. Low frequency pulse-train stimulation can remodel the biochemical machinery that confers physiological expression and fatigue resistance approaching that of the myocardium. This fatigue-resistant muscle can generate sufficient force to meet the power requirements for useful cardiac work. This ultimate goal is currently being pursued in models of cardiomyoplasty and muscle-powered cardiac assist devices. In this article, we review the three major subcellular systems subserving canine skeletal muscle transformation and compare them to those of cardiac muscle. The magnitude of the problem of clinical heart failure and the feasibility of fatigue-resistant skeletal muscle joining the therapeutic armamentarium are addressed. The adaptation and transformation of fast-twitch skeletal muscle in response to chronic electrical stimulation augers therapeutic potential as an endogenous, readily available power source for myocardial assistance. The basis mechanisms of skeletal muscle fatigue require elucidation to gain a complete and thorough understanding of how to manipulate this property to provide continuous hemodynamic work.
 ...
PMID:The remodelling of skeletal muscle for indefatigable hemodynamic work. 205 39

210 patients with ischemic heart disease and heart failure, stage I, HA, IIB, aged 60 to 74 years, have been examined. The effect of HBO on central hemodynamics, gas composition and acid-base balance has been assessed. It has been established that HBO is associated with a definite tendency towards cardiac output normalization, as well as hemodynamic economization associated with accelerated heart rate and more adequate correlation between cardiac output and peripheral vascular resistance. The analysis of gas exchange and acid-base balance parameters indicates HBO-induced acidotic shifts. The data of polarographic studies demonstrate that increased metabolic activity is typical not only of the cardiac muscle but of other tissues as well. A favourable effect of HBO on oxygen tissue supply in patients with ischemic heart disease and heart failure is to a certain extent due to stimulation of peripheral circulation and its capillary compartment.
 ...
PMID:[The effect of hyperbaric oxygenation on central hemodynamics, blood gas composition and acid-base status in elderly patients with ischemic heart disease and circulatory insufficiency]. 207 32

Exposure of human body to high altitude environment initiate reaction which could be result whether of adaptation or of exhaustion. The purpose is to establish the human body environment which enables regeneration of own cells. Therefore, mechanism of reestablishment of prevention and recognition of symptoms and signs of insufficient adaptability on high altitude are of great interest for clinical and other medical investigators. Special position in research refers on cardiovascular system. Results show, according to effect of only one factor-catecholamines, that in course of physical training on high altitude, could be expected, cardiac muscle hypertrophy. It is proved, that under special circumstances catecholamines stimulate synthesis of proteins what enables faster regeneration of the cells. However, under conditions of myocardial ischemia, uncontrolled loading of these patients could lead to deterioration of heart function appearance of cardiac insufficiency.
 ...
PMID:[Aspects of acclimatization of the human body to acute and chronic high-altitude hypoxia]. 209 85

Cardiac transplantation is theoretically the optimal final treatment of terminal cardiac failure but the indications, especially in the emergency situation, should be carefully considered. Sympathomimetic agents are of limited use in patients with severe cardiac failure partly because of the down regulation of the myocardial beta-receptors. The phosphodiesterase inhibitors, represented by enoximone, are valuable because of their action on the cardiac muscle (inotropic and lusitropic) and their direct systemic vasodilator effect. Enoximone can be administered by intravenous bolus resulting in a rapid onset of action (peak at 30 minutes) with a prolonged effect due to its hepatic metabolites. The authors' experience in this indication dates over 5 years and over 50 patients were included. A preliminary study in 34 patients with cardiac failure resistant to betamimetic drugs, referred to the intensive care unit for urgent cardiac transplantation, or, in the absence of a donor, circulatory assistance is reported. A Swan Ganz catheter and radial artery canula were inserted for haemodynamic monitoring and enoximone was administered in an intravenous bolus over 15 minutes every 8 hours in addition to sympathomimetic agents. A haemodynamic improvement was observed after the 30th minute in 30 patients. The cardiac index increased from 1.82 to 2.67 l/mn/m2 and the pulmonary capillary pressures decreased from 30.8 to 18.9 mmHg. Systemic arterial resistances fell from 2,170 to 1,520 dynes.s.cm-5. No haemodynamic improvement was observed in 4 patients who were treated by mechanical ventricular assistance. After investigations to detect contra-indications to cardiac transplantation, 12 of the 30 patients remained candidates for cardiac transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Medical strategy in patients awaiting emergency heart transplantation]. 214 25

Development and growth of cardiac muscle tissue is controlled by a variety of intrinsic and extrinsic factors. Fetal growth is by hyperplasia, is strongly governed by inherent factors and is only slightly modified by external environmental factors. The number of cell divisions is species-dependent and normally stops shortly after birth. Developing blood volume and pressure dictate the hypertrophic stage of normal growth, and this may be further modified by abnormal hemodynamic and humoral factors. Connective tissue, neural and vascular components of the myocardium mature along with the myocyte, and alterations in these structures profoundly affect myocyte function. Hypertrophy beyond normal growth is the response of the myocyte by increased protein synthesis to various stimuli including hemodynamic, humoral and ischemic factors. Injury to normal and hypertrophied myocardium may vary due to structural and metabolic adaptations of hypertrophied tissue, such as connective tissue proliferation, vascular supply alterations and glycolytic metabolic potential. Ischemic effects influence not only cell necrosis, but also hypertrophy and congestive myocardial failure.
 ...
PMID:The myocardial cell: normal growth, cardiac hypertrophy and response to injury. 215 Oct 58

Ventricular dysfunction due to an abnormality of the heart which is associated with typical hemodynamic, renal and hormonal reactions, characterizes the clinical syndrome heart failure. The traditional definition of heart failure as the inability to pump an amount of blood sufficient to cover the metabolic needs of the body in the presence of adequate venous return, emphasizes mainly the reduction in cardiac output but not the increase in intracardiac pressures. Pressure or volume overload, decreased contractility, loss of muscle mass or restricted filling represent the most important pathological processes leading to heart failure. The disturbance of systolic ventricular function due to pressure or volume overload or diminished contractility is characterized by a decrease in the ejection fraction, the disturbance in diastolic ventricular function associated with restricted filling is characterized by elevated chamber stiffness. Decreased contractility is most commonly responsible for the development of heart failure. Impairment of diastolic ventricular function can only be regarded as the dominant mechanism leading to heart failure in the presence of a small noncompliant ventricle. Impairment of diastolic ventricular function in an enlarged heart is always associated with an impairment of systolic ventricular function and is, then, relegated to a subordinate role. Common causes of heart failure are coronary artery disease, hypertension, cardiomyopathies, valvular heart diseases and congenital heart diseases, for the incidence of which coronary artery disease is most frequently responsible. Most of these diseases lead to heart failure not via a single, but rather several of the specified pathophysiological processes. Possible mechanisms for loss of contractility include structural changes as well as alterations in excitation-contraction coupling. Possible mechanisms responsible for impaired diastolic ventricular function encompass, in addition to altered calcium flux, structural changes such as fibrosis and hypertrophy and factors such as asynchrony and abnormal loading conditions. With increasing derangement of cardiac function, there is recruitment of the compensatory mechanisms: hypertrophy of the cardiac muscle, Frank-Starling mechanism, activation of the sympathetic nervous system, the renin-angiotensin-aldosterone system and the arginine-vasopressin system. The goal is maintenance of adequate blood pressure and cardiac output whereby blood flow is redistributed in favor of the heart and brain and away from the skin, musculature and visceral organs. Activation of the neurohumoral system can lead to excessive vasoconstriction as well as sodium and water retention resulting in an undesired elevation of preload and afterload which, in turn, leads to further worsening of the heart failure.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:[Pathophysiologic and diagnostic aspects of heart failure]. 219 15

The direct effects of angiotensin II (Ang II) on human cardiac muscle were investigated using isolated trabecular muscles from failing and functionally normal hearts. Atrial and ventricular trabeculae were studied. Results demonstrated a positive inotropic effect of Ang II on human cardiac muscle. Comparison of the effects of Ang II among groups indicated that the responsiveness tended to be greater in atrial and normal muscle compared with failing muscle. Results of this study also demonstrated heterogeneity in the responsiveness to Ang II among human muscles, which was not correlated with patient age, sex, diagnosis, prior treatment with angiotensin converting enzyme inhibitor, or heart function. A significant correlation between response to Ang II and response to isoproterenol was demonstrated in failing ventricular trabeculae, which may suggest that defects in beta-adrenergic responsiveness in the failing human ventricle are accompanied by a loss of responsiveness to Ang II. Studies were extended to the Syrian cardiomyopathic hamster and its control. A dose-dependent inotropic response occurred in normal hamster ventricular muscle but was significantly diminished in cardiomyopathic muscle. Ang II did not shorten the timing of contraction, and pretreatment with adrenergic-blocking agents did not shift the dose-response curve, indicating that the response was not cyclic AMP mediated. This study demonstrates for the first time that Ang II can exert an inotropic effect directly on human cardiac muscle and confirms that there is a direct effect of Ang II on hamster cardiac muscle. The study further suggests, however, that the inotropic response to Ang II in cardiac muscle is heterogeneous and may be diminished by heart failure.
 ...
PMID:Inotropic effects of angiotensin II on human cardiac muscle in vitro. 224 22

The effects of emestrin (EMS), a secondary metabolite of the Emericella species, on male ICR mice were examined. The intraperitoneal LD50 values of EMS were 17.7 and 13.0 mg/kg at 24 and 48 hr, respectively. The target organs of EMS were the heart, liver and thymus. In doses over 30 mg/kg the experimental animals died from cardiac failure shortly after the injections. Several survivors that were given EMS in doses under 20 mg/kg showed severe centrilobular necrosis in the liver at 24 hr. Marked degeneration of mitochondria was seen in electron micrographs of both cardiac muscle cells and hepatocytes. In the degenerated hepatocytes, prominent proliferation of RER, membrane-limited inclusions containing both ribosome-like granules and RER, and fenestrated lamella-like structures were observed. Massive necrosis of lymphocytes was always observed in the cortical layer of the thymus of the survivors within 24 hr, while bilateral adrenalectomized mice showed no discernible pathomorphological changes in the lymphoid tissues. Pretreatment of mice with diethyl maleate increased the incidence and severity of hepatic necrosis, whereas that with either cysteine or CoCl2 reduced the severity of centrilobular necrosis of the liver. Pretreatment with phenobarbital had no significant effect on EMS-induced hepatic lesions.
 ...
PMID:Experimental acute poisoning in mice induced by emestrin, a new mycotoxin isolated from Emericella species. 229 35

The discovery of insulin in 1922 aroused immediate clinical interest in its use in heart disease. In severe heart failure, insulin release is suppressed by the combined effect of poor pancreatic perfusion and by increased sympathetic activity. In these circumstances, myocardial metabolism of glucose may break down through the deficiency of insulin. Because of this, glucose, insulin and potassium solution (GIK solution) has been used in cardiopulmonary resuscitation. However, its mechanism is not yet fully known. This study was designed to determine the effect of insulin on cardiac muscle at various temperatures. The mechanical response of papillary muscle isolated from guinea pig ventricle was observed under various thermal conditions (23-37 degrees C). Twitch tension was increased by the administration of 0.2 I.U./ml insulin under each thermal condition. In all circumstances, the increase in contractile force was noted about 2 min after the administration of insulin. The effect of insulin on 20 preparations demonstrated the mean maximum contractile force was 226% ( +/- 34 S.D., n = 5) in 37 degrees C, 194% ( +/- 36 S.D., n = 5) in 30 degrees C, 190% ( +/- 30 S.D., n = 5) in 27 degrees C and 200% ( +/- 36 S.D., n = 5) in in 23 degrees C. The differences between different temperatures was not significant. The effect of insulin during depression Na-K pump by high concentration of ouabain (g-strophanthin, 10(-5) M) was also observed. Insulin (0.2 I.U./ml) was administered when the papillary muscle showed no response to electrical stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Response of isolated guinea pig myocardium to insulin therapy during normothermia and graded hypothermia. 242 78

The myocardium consists of three compartments: cardiac muscle cells; a nutritive microcirculation; and an extracellular matrix composed largely of fibrillar collagen. The hypertrophic remodeling of the myocardium, which involves each of these compartments, can be adaptive or pathologic. This article reviews the remodeling process and the current state of our knowledge regarding the pathogenetic features of pathologic hypertrophy with heart failure.
 ...
PMID:Pathogenesis of heart failure. 252 40


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>