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

The influence of alpha-adrenoblocking drug tropaphen on cardio- and haemodynamics under experimental lung-heart failure was studied in dogs. The findings suggest effectiveness of tropaphen administration in such pathology shown by a decrease of lung hypertension and heart overload, significant increase of the contractile activity and relaxation properties of myocardium of both ventricles and in cardiac pump function optimization.
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PMID:[Tropaphen in experimental drug therapy of cor pulmonale]. 136 91

Experimental myocardial infarction is a model of cardiac overload due to amputation of part of the cardiac muscle. The development of cardiac failure depends on the size of the infarct and the time factor. This model of overload is associated with changes of the phenotype of the remaining healthy muscle and with peripheral vascular modifications partially dependent of the activation of pressor and/or deactivation of dilator systems. These changes are proportional to the size of the infarction at a given time after induction of the model. The degree of right ventricular hypertrophy and the decrease in blood pressure reflect the severity of infarction and the deterioration of the remaining myocardial function, affecting the haemodynamics both before and after the left ventricle. The increases in the 1/3 forms of isomyosins, the amount of subendocardial collagen, the biosynthesis, stocking and secretion of ANF are related to the infarct size and degree of overload. Similarly, the concentration of cyclic GMP is proportional to the infarct size. These parameters reflect ventricular overload, the increase of stress and energy deprivation of the remaining healthy muscle. The activation of peripheral pressor systems is also dependent on the infarct size reflects the effect of cardiac pump dysfunction on the kidney, liver, brain and endothelium. Large infarcts are associated with increased circulating renin and renal concentrations, with a decrease in angiotensinogen levels related to its consumption by the renin and to reduced hepatic synthesis and also with increased secretion and biosynthesis of vasopressin by the hypothalamus. In this model, Perindopril is beneficial by decreasing the cardiac load. It reduces the blood pressure, causes regression of bi-auricular and right ventricular hypertrophy. Changes in myosin isoenzyme configuration regress and subendocardial fibrosis and ANF concentrations are normalised. The effects of ACE inhibitors in this context, though very beneficial, are limited by the impossibility of normalising cardiac load and stress when the initial amputation of cardiac contractile mass exceeds 40%.
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PMID:[Experimental myocardial infarction in the rat. Effect of perindopril]. 166 27

The sympathetic activity in cardiac failure is elevated by excitatory afferents from underperfused muscle and from chemoreceptors, and by attenuated inhibitory control via arterial and cardiopulmonary baroreceptors. Together with renal hypotension, the sympathetic activity activates the renin-angiotensin-system, which in turn enhances sympathetic activity. Together, both systems induce a vicious cycle of further cardiac overload by vasoconstriction, volume retention, and formation of edemas, while beta-adrenergic responsiveness of the heart is depressed. The glomerular filtration rate in the kidney is preserved by efferent arteriolar constriction in the face of reduced renal perfusion. Since circulating angiotensins are preferentially formed by angiotensin-forming systems in the tissues, one has to assume strong local effects of angiotensin II at the site of its synthesis. These local effects cannot exactly be quantified from parameters of the circulating RAS. In the heart, myocardial stretch and neuroendocrine activity (via myocardial angiotensin- and alpha 1-receptors) induce a dedifferentiating growth of cardiocytes. This results in an improved economy of myocardial contraction, but also in delayed relaxation with the risk of Ca(++)-overload and generation of arrhythmias by late after-depolarizations. Probably, enhanced intracardiac formation of angiotensin contributes to these dangerous changes.
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PMID:[Pathophysiology of cardiorenal regulatory mechanisms in heart failure]. 202 37

After inducing haemodynamic cardiac overload in rabbits, the authors studied in several stages (1-14 months) the calcium transport activity of the mitochondrial and sarcoplasmic myocardial fractions using labelled 45CaCl2. A coincidence was found between changes in myocardial contractility and changes in calcium transport activity of intracellular organelles. A possible important role of mitochondria in this adaptive process was also documented. Since the calcium transport capacity of the sarcoplasmic reticulum progressively decreases (with the exception of the earliest stages following overload induction), it seems that increased myocardial contractility ensures enhanced Ca transport activity of the mitochondria. Myocardial contractility drops only at the time when the Ca transport activity of the mitochondria decreases. Since these changes occur already at the time of regression of myocardial hypertrophy, which precedes heart failure, it can be assumed that they are causally connected with the reduced contractility of a failing heart.
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PMID:Calcium transport by intracellular membrane structures in the myocardium of hypertrophied and failing hearts. 294 79

The effect of long-term treatment with the calcium antagonist nisoldipine on development of hypertension, cardiac hypertrophy, and plasma levels of atrial natriuretic peptides (ANP) was determined in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) of the same age. Measurement of immunoreactive ANP in plasma provided a sensitive marker for the severity of hypertension and the associated cardiac overload. Long-term treatment with nisoldipine prevented the development of hypertension, the associated heart failure, and the increase of plasma levels of ANP in SHR but had no effect on systolic blood pressure, heart weight, and plasma levels of ANP in WKY. In addition, nisoldipine had a therapeutic effect in old SHR with manifest cardiac failure in end-stage hypertension, as evidenced not only by the reduction of blood pressure but also by the reduction of cardiac hypertrophy, of elevated immunoreactive ANP in plasma, and of increased plasma renin activity.
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PMID:Role of nisoldipine on blood pressure, cardiac hypertrophy, and atrial natriuretic peptides in spontaneously hypertensive rats. 295 22

According to Meerson, the adaptation to cardiac overload can be divided into three periods: the first stage, immediately after the initiation of the defect during which hypertrophy develops, followed by the stable hypertrophy phase (SHP), and a third phase of myocardial failure. Ventricular muscle contraction during SHP has been extensively studied both in vivo and in vitro with conflicting results. In isolated papillary muscles, most studies showed a normal or depressed contractility during chronic volume overload and a depressed inotropic state in pressure overload with a reduced maximal velocity of shortening which has been related to a myosin isozyme shift. In contrast, in conscious animals, haemodynamic status is usually described as preserved during SHP with a ventricular hyperfunction and a normal contractile function per unit of muscle. This was the basis of the concept of preload reserve and afterload mismatch described by Ross. However, mechanisms other than preload reserve may play a role during cardiac adaptation to pressure or volume overload. For instance, we recently showed in the early phase of pressure overload an increased inotropic state of the in situ heart with a change of the excitation contraction coupling evidenced by a modification of the force-frequency relations. Changes in the adrenergic receptors (density and/or affinity) may also contribute to the adaptation of the in situ heart to cardiac overload. They represent an important research area because they may explain, along with species and model differences, the discrepancies between in vivo and in vitro studies.
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PMID:Mechanical adaptation to chronic pressure overload. 296 12

Experimental results obtained from studies on Goldblatt rats and spontaneously hypertensive rats as well as theoretical considerations render possible an approximate analysis and evaluation of the relative significance of specific factors at different levels of the heart for the manifestation of cardiac failure under chronic pressure overload. In our experimental models congestive failure was never observed independently of structural dilatation. Thus, as a rule dilatation had already set in before symptoms of heart failure became manifest. However, at moderate dilatation of the ventricle, e.g., at double the end-diastolic volume, the geometrical state per se cannot be the cause of hydropic decompensation whereas extreme dilatation would, in principle, cause cardiac pumping failure even in the absence of any impairment of myocardial "contractility". Generally, a more or less marked impairment of myocardial contractile capability was found, which exceeded the effects due to the altered isoenzyme pattern of myosin. As a rule, a reduction in myocardial "contractility" could be ascertained before a marked degree of dilatation was reached. Diffuse fibrosis impairs the contractile capability of the myocardium and certainly contributes to the manifestation of heart insufficiency; although, as a rule, it should not be the main cause. The adaptive transformation of myocardium towards a slower muscle (isoenzyme pattern of myosin; sarcoplasmatic reticulum) as such does not lead to resting insufficiency, not even under persisting pressure load. Further investigations on processes of excitation-mechanical coupling in the advanced stage of cardiac overload are indicated. The absence of sympathetic support to the heart, e.g., following blockade of beta-adrenergic receptors can, in the advanced stage, elicit a transition from the stage of pre-insufficiency to manifest failure. However, this was only observed when dilatation had already occurred. A network of factors are responsible for cardiac insufficiency due to pressure overloading, whereby the respective significance of each component varies, depending on the experimental model used.
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PMID:Pathophysiological mechanisms in cardiac insufficiency induced by chronic pressure overload--an attempt to analyze specific factors in animal experiment. 379 41

Chronic mechanical cardiac overload induces several adaptational processes, such as that provided by the Starling's law, which, allow the heart to function normally during a given period of time. Compensatory hypertrophy is, from a myocardial point of view, characterized by two main adaptational factors: hypertrophy due to a stimulation of protein synthesis and the slowing of the shortening velocity. This drop in contractility has undoubtedly been demonstrated in some experimental models, it is due to an isoenzymatic shift of myosin which is responsible for a depressed myosin ATPase activity. It has been clearly shown that this improves the efficiency of contraction, since for a given tension, the hypertrophied fiber produces less heat. Such a change does in fact exist in human heart but seems to have a limited physiological significance and in, any case, cannot explained the striking decrease in contractility which characterizes the final step of heart failure.
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PMID:[Biology of myocardial adaptation to mechanical overload]. 622 Jul 49

Presently we favor heparinless femorofemoral venoarterial bypass for all descending thoracic aneurysm resections. The advantages are minimal blood loss due to the absence of heparin, ease of insertion, especially in large aneurysms where it would be difficult to insert a temporary shunt, distal aortic perfusion, possibly a safety factor in preventing spinal cord and visceral ischemia, and prevention of left heart overload and myocardial failure. In acute traumatic ruptures, simple aortic cross clamping is a suitable alternative. It is safe and can be carried out expeditiously in any community hospital where bypass facilities may not be available. Proximal hypertension can be controlled pharmacologically. We have also used this successfully in ruptured atherosclerotic aneurysms. We have no experience with temporary tridodecylmethylamonium (TDMAC) shunts; several groups have used them successfully. We believe they may be difficult to insert in the proximal aorta with a large mediastinal hematoma or extensive aneurysm. Cannulation of the left ventricular apex necessitates cardiac manipulation and may produce effective aortic valve insufficiency. In patients with aortoesophageal and bronchoesophageal fistula, permanent extrathoracic bypass is preferable to a prosthetic graft in a contaminated field. We propose using a permanent bypass with a no. 10 or 12 right axillofemoral bypass. Our experience is limited to only two patients. This is also a method of treating a mycotic aneurysm or infected thoracic aortic graft.
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PMID:Descending thoracic aortic aneurysm: a 10 year surgical experience. 697 87

Hypertrophy of the overloaded heart, characterized by an increased number of sarcomeres, provides an adaptive, short-term response. However, when cardiac overload is long-standing, the hypertrophic response appears to cause shortened myocyte survival. The mechanisms responsible for the deleterious effects of chronic myocardial hypertrophy may include a maladaptive growth response of the mature heart. Because terminally differentiated adult cardiac myocytes have little or no capacity to divide, stimuli that promote growth in the overloaded adult heart cannot lead to normal cell division. Instead, overload initiates an unnatural growth response that appears to shorten cardiac myocyte survival, possibly because the same growth factors that mediate the hypertrophic response of the adult heart can also induce programmed cell death (apoptosis). The converting enzyme inhibitors and nitrates, which have growth-inhibitory as well as vasodilator effects, may improve prognosis in heart failure by inhibiting the production of transcription factors. These transcription factors stimulate both the unnatural growth response to overload and stimuli that lead to apoptosis. Since both beta-adrenergic agonists and cytokines, such as tumor necrosis factor-alpha, can stimulate production of similar transcription factors, evidence suggests that beta blockers and vesnarinone improve the prognosis in patients with heart failure possibly because of their ability to inhibit maladaptive growth.
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PMID:Cell death in the failing heart: role of an unnatural growth response to overload. 748 19


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