Search PubMed⌕ Search

Biomedical subjects

F Simko

Publications and source records attributed to F Simko.

53 records · Page 3Linked to original sources
PubMed1994

Pathophysiological aspects of the protective effect of magnesium in myocardial infarction (review).

Intravenous administration of magnesium has proved to have beneficial effect in acute myocardial infarction. Magnesium seems to act at different levels of the cardiovascular system. Of the greatest importance is the direct influence of Mg2+ on the cardiomyocyte which includes: reduction of cytoplasmatic calcium overload, protection of mitochondria against calcium influx, and diminution of cellular potassium, magnesium and ATP depletion. By means of these effects, or by its direct action on myocardium, Mg2+ inhibits the origin of postinfarctional dysrhythmias. Furthermore, magnesium reduces afterload by decrease in vascular resistance, and improves coronary flow. The mechanism underlying the protective effect of magnesium remains complex and poorly understood. Nevertheless, Mg2+ therapy is effective, undemanding, and easy to procure. Expectably, intravenous administration of Mg2+ may become a routine part of myocardial protection in acute myocardial infarction.

Coronary Circulation↗
PubMed1994

Pathophysiological principles of the relation between myocardial hypertrophy of the left ventricle and its regression.

Hypertrophy of the left heart ventricle as a consequence of a haemodynamic overload is a process of ambiguous biological value. Although hypertrophy allows to increase the performance of the ventricle without substantial elevation in wall tension, it represents a risk factor of cardiac morbidity and mortality. The regression of hypertrophy seems to be a rational outcome of this ambivalent situation. Not every reversal of hypertrophied muscle mass, however, can be unambiguously considered therapeutic success. The biological value of hypertrophy regression depends on the type of hypertrophy, on the level of deterioration of the heart by a long-lasting haemodynamic overload, as well as on the way in which the reversal of hypertrophy is achieved. Even in the case when functional characteristics are preserved or even improved compared to the hypertrophied heart, hypertrophy regression need not automatically mean a decrease of the cardiovascular risk induced by ventricular hypertrophy. Regression of hypertrophy may be even disadvantageous in those situations when reduction of hypertrophy and reduction of the haemodynamic overload proceed in a disproportional manner. Spontaneously developing regression of the hypertrophied left ventricle as demonstrated on the model of aortal insufficiency, is an explicitly pathological state, resulting in heart failure. Regression of myocardial hypertrophy should not be considered the primary therapeutic aim but rather a part of the management of haemodynamic overload of the heart. The main aim is to achieve optimal perfusion of the periphery, yet at the same time to provide such conditions which would prevent the working load of the heart to become a limiting factor of survival.

Animals↗
PubMed1994

Some actual aspects of ischemic heart disease.

The 59th annual conference of the German Society for Heart and Vessel Research was held from 15th to 17th April 1993 in Mannheim. More than six hundred lectures and posters were presented (including those invited from abroad) introducing the topics of current experimental and clinical cardiology. The primary lectures dealt with problems of etiology and pathogenesis of atherosclerosis and its complications. Also the principles of treatment of ischemic heart disease were discussed. Moreover, insights into confusing problems of reperfusion injury, hibernating myocardium and stunned myocardium were introduced. The presented data have shown that myocardial ischemia, its etiology, pathogenesis, manifestations and treatment form a bulk of challenging problems of present cardiology. Many such phenomena were described, which provoke more questions than give answers. Only close interdisciplined cooperation can help to solve some of them in the near future. (Ref. 35.)

Humans↗
PubMed1991

[The effect of long-term administration of metipranolol on passive diastolic properties of the hypertrophic ventricle].

In the course of adaptation of the rabbit heart to volume load passive diastolic properties of the hypertrophic ventricle and myocardium were changing significantly. On day 30 following perforation of the aortic valve stiffness of the ventricle was reduced, yet normalized ventricular stiffness and myocardial stiffness were increased. These changes were prevented by beta adrenergic blockade during development of adaptation of the heart to volume load. Although ventricular stiffness was reduced, normalized ventricular stiffness and myocardial stiffness remained at the level of control values. The demonstrated effect of beta adrenergic blockade on passive diastolic properties of the ventricle and myocardium may be of value in preventing heart failure due to chronic hemodynamic load. (Tab.3,Ref.15.).

Animals↗
PubMed1991

[Modification of the composition of the hypertrophic myocardium by beta adrenergic blockade].

Adaptation of the rabbit heart to volume load of the left ventricle is characterized by hypertrophic growth. This process involves an increase in the mass and changes in the composition of the myocardium. In the fifth week after perforation of the aortic valve an increase in phospholipid content and in mitochondria and a decrease in protein content was observed in the myocardium. These changes precondition a transient hyperfunction of the cardiomyocytes, but they presumably lead also to the eventual loss of contractile capacity. When the hypertrophic process occurs under conditions of nonspecific beta-adrenergic blockade, the required increase in left ventricular mass is achieved yet the content of phospholipids, proteins and mitochondria remains unchanged. Long-term blockade of beta-adrenergic receptors may be one of the modes of affecting the expression of cardiac genes in such a way that the hypertrophic myocardium does not develop conditions resulting in heart failure.

Animals↗
PubMed1990

[Strategies in the use of isolated cardiomyocytes in relation to other models in experimental cardiology].

Selection of the optimal model for a specific experiment considerably determines the results and their correct interpretation. The model of the isolated cardiomyocyte is increasingly being used in experimental cardiology as it provides several advantages in comparison to models in which the heart tissue remains relatively complete. Similarly as in other models, the factors limiting its use have to be known also in the case of the isolated cardiomyocyte. To minimalize misinterpretation of results the given problem is to be handled at all available levels.

Heart↗
PubMed1989

[Passive diastolic properties of the left ventricle during development of cardiac hypertrophy].

Induced insufficiency of the aortal valve in rabbits is followed by gradual adaptation of the heart to volume load. In the period of developing hypertrophy, we studied the changes in the passive diastolic properties of the ventricle. By analyzing the passive relationship between the volume of the ventricular cavity and the intraventricular pressure, the stiffness of the ventricle, normalized ventricular stiffness, and myocardial stiffness were determined. On day 30 after inducing the volume verload, the stiffness constant of the ventricle was statistically significantly reduced, whereas the constant of normalized ventricular stiffness and the constant of myocardial stiffness were statistically significantly increased. The increased stiffness of the myocardium, which characterizes the volume verloaded, left ventricle in the period of developing hypertrophy, may represent one of the changes causing reversal of the adaptive response of the heart to hemodynamic verload after a certain period of time, gradually resulting in the development of the syndrome of heart failure.

Animals↗
PubMed1986

Calcium transport by intracellular membrane structures in the myocardium of hypertrophied and failing hearts.

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.

Animals↗