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Biomedical subjects

F Simko

Publications and source records attributed to F Simko.

At least 37 records · Page 2Linked to original sources
PubMed1999

Captopril increased mitochondrial coenzyme Q10 level, improved respiratory chain function and energy production in the left ventricle in rabbits with smoke mitochondrial cardiomyopathy.

The aim of the study was to show whether the ACE inhibitor captopril is able to protect the heart against the deleterious effect of passive cigarette smoking on left ventricular mitochondria. Four groups of rabbits were investigated: control (C), passive smoking of three cigarettes twice daily/30 minutes (S), control + captopril (7.5 mg/kg body weight twice daily) (Cap), and smoking + captopril (SCap) as in group 2 and 3. Three weeks lasting passive smoking impaired oxidative phosphorylation, diminished cytochrome oxidase activity and increased the mitochondrial F1-ATPase protein concentration. Moreover, the level of coenzyme Q10 (CoQ10) and coenzyme Q9 were decreased. Simultaneous treatment with captopril prevented partly the decrease of CoQ10 level, deterioration of oxidative phosphorylation, diminution of cytochrome oxidase activity and enhancement of F1-ATPase level. We conclude that captopril protected the myocardium against the harmful effect of passive smoking in rabbits.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

Heart failure and angiotensin converting enzyme inhibition: problems and perspectives.

Heart failure has become the most widely studied syndrome in cardiology over the recent years. Despite the encouraging achievements by angiotensin converting enzyme (ACE) inhibitors, the mortality of patients with chronic heart failure remains high. There are several factors which can potentially be responsible for the fact that about 80% of patients with a failing heart defy protection by ACE inhibitors: different activation of tissue and systemic renin-angiotensin system (RAS) in a particular heart disease and the distinct ability of various ACE inhibitors to block cardiac ACE, alternative pathways for angiotensin II formation (chymase), genetic polymorphism of the RAS system and the complexity of neuroendocrine activation. Moreover, chronic heart failure can provoke disturbances in the reactivity of peripheral vessels and metabolism of striated muscles. These factors may then potentiate the vicious circle of heart failure. New therapeutic approaches, which could further reduce the mortality in patients with heart failure involve angiotensin II type 1 receptor antagonists, beta-blockers, aldosterone antagonists and blockers of the endothelin receptor. A number of questions associated with functions of the RAS still remain open and their solution could be of substantial benefit for patients with a failing heart.

Adrenergic beta-Antagonists↗
PubMed1999

Effect of captopril in L-NAME-induced hypertension on the rat myocardium, aorta, brain and kidney.

Long-term administration of NG-nitro-L-arginine methyl ester (L-NAME) induces development of hypertension and hypertrophy of the left ventricle in rats. The aim of the present study was to demonstrate the effect of chronic L-NAME treatment on DNA and RNA concentration, and protein synthesis in the rat heart, aorta, brain and kidney and to determine the effect of angiotensin converting enzyme (ACE) inhibitor captopril on these potential alterations. Four groups of rats were investigated: control, L-NAME (40 mg kg-1 day-1), captopril (100 mg kg-1 day-1), and L-NAME (40 mg kg-1 day-1) + captopril (100 mg kg-1 day-1). NO synthase activity in the heart, aorta, brain and kidney was found to be decreased in the L-NAME group. In the group of rats treated with L-NAME + captopril, captopril did not affect NO synthase inhibition. Captopril, however, completely prevented development of hypertension and left ventricular hypertrophy in this group. In the L-NAME group, DNA and RNA concentrations, as well as [14C]leucine incorporation, were significantly increased in all the tissues investigated. In the L-NAME + captopril group, captopril completely prevented the enhancement of DNA and RNA concentrations and [14C]leucine incorporation in all tissues compared to the L-NAME group. Moreover, a significant decrease in RNA concentration and [14C]leucine incorporation below control values was found in the captopril group as well as the L-NAME + captopril group in all the tissues investigated. We conclude that captopril prevented the development of hypertension and increase in nucleic acid concentration and protein synthesis in the heart, aorta, brain and kidney in rats treated with L-NAME + captopril. However, this protective effect of captopril was not associated with increased NO synthase activity in this model of hypertension.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

[Diagnosis of Duchenne and Becker muscular dystrophy in Slovak patients using multiplex polymerase chain reaction].

The authors of the paper describe the diagnostic method of deletion in the dystrophin gene by means of an improved variant of the polymerase chain reaction--so called multiplex PCR. The authors analyzed a group of 66 patients with developed clinical symptoms of the disease. The deletion screening included 22 exones of the dystrophine gene and it was performed in 5 multiplex PCR reactions. 20 patients yielded a verified deletion which was pre-assessed by Southern's hybridization. The relative simplicity of multiplex PCR which does not require the use of radioisotopes, its low time and financial needs, make this method to represents an appropriate alternative of Southern's hybridization in the assessment of deletion of the dystrophine gene. (Fig. 1, Ref. 19.)

Dystrophin↗
PubMed1998

Captopril attenuates proteosynthesis in the aorta and decreases endothelaemia in rabbits with aortic insufficiency.

The effect of the angiotensin converting enzyme (ACE) inhibitor, captopril, on proteosynthesis in the aorta, acetylcholine-stimulated aortic relaxation and endothelaemia (circulating endothelial cells) was investigated in rabbits with aortic insufficiency. The animals were studied 28 days after experimental intervention. Cardiac volume overload stimulated proteosynthesis in the aorta as reflected by increased ribonucleic acid (RNA) concentration and [14C] leucine incorporation into proteins of the aorta. Moreover, the number of endothelial cells in the blood was increased. The administration of captopril starting from the second day of the haemodynamic overload, partially prevented the increase both in aortic proteosynthesis and in endothelaemia. Despite these alterations, the relaxing ability of the aorta to acetylcholine was not changed either by the haemodynamic overload or by captopril. We conclude that the increase of proteosynthesis in the aorta and of endothelaemia in the early period of chronic cardiac volume overload in rabbits were partially prevented by chronic captopril treatment. Neither aortic insufficiency nor captopril changed the acetylcholine-induced relaxation of the aorta.

Acetylcholine↗
PubMed1997

Protein remodelling of the heart in NO-deficient hypertension: the effect of captopril.

Long-term administration of NG-nitro-L-arginine methyl ester (L-NAME) induces development of NO-deficient hypertension. The aim of the present study was to determine whether treatment with the angiotensin-converting enzyme (ACE) inhibitor captopril can prevent hypertension, left ventricular (LV) hypertrophy, changes in nucleic acid concentration, protein synthesis and protein profile of the left ventricle. Four groups of rats were investigated: control, L-NAME 40 mg/kg/day, captopril 100 mg/kg/day, L-NAME 40 mg/kg/day along with captopril 100 mg/kg/day. NO-synthase activity in the left ventricle was found to be decreased by 69% in the L-NAME group. Captopril did not influence this inhibition of NO-synthase activity. However, it completely prevented hypertension and left ventricular hypertrophy development. The increase in left ventricular RNA and DNA concentration and -14C-leucine incorporation observed in the L-NAME group was completely prevented by simultaneous captopril treatment. The protein profile of the left ventricle in the L-NAME group was characterized by higher concentration of metabolic proteins (MP), soluble collagenous proteins (SCP) and of hydroxyproline in insoluble collagenous proteins (ICP). The concentration of hydroxyproline in ICP was significantly decreased by simultaneous captopril treatment. We conclude that captopril prevented the development of hypertension, left ventricular hypertrophy, increase in nucleic acid concentration and diminished collagen concentration by mechanisms different from affecting NO-synthase activity.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

Effect of captopril on the development of left ventricular hypertrophy in rabbits with aortic insufficiency.

We investigated the effect of captopril on the growth of the left ventricle in an experimental model of aortic insufficiency. Four groups of rabbits were studied 28 days after experimental intervention: 1. control, 2. control with captopril (10 mg/kg/day), 3. aortic insufficiency, 4. aortic insufficiency with captopril (10 mg/kg/day). Aortic insufficiency induced hypertrophic growth of the left ventricle demonstrated by increased weight and ribonucleic acid (RNA) concentration. Administration of captopril only slightly attenuated the weight increase of the left ventricle and the increase in concentration of left ventricular RNA. However, captopril reduced the concentration of left ventricular deoxyribonucleic acid (DNA) both in the control and even more in the group with aortic insufficiency. The chronic haemodynamic overload enhanced mitochondrial respiration in the left ventricle which was not influenced by captopril. We conclude that captopril in the dose 10 mg/kg/day did not prevent hypertrophy of the left ventricle but reduced left ventricular DNA concentration.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Left ventricular hypertrophy regression as a process with variable biological implications.

OBJECTIVE: To determine whether myocardial hypertrophy regression, similarly to hypertrophy itself, is a process of variable nature with different biological implications. DATA SOURCES: Current Contents and MEDLINE searches under myocardial hypertrophy and regression of hypertrophy-related headings were conducted. DATA EXTRACTION: The search covered the period from 1969 to 1994, and 89 articles dealing with both human and animal studies were used. DATA SYNTHESIS: The positive adaptive effect of left ventricular myocardial hypertrophy may be counterbalanced by increased incidence of heart failure, myocardial infarction or sudden death. The risk of undesirable cardiovascular events varies according to the character of hypertrophic growth. Reduction of cardiac mass to that of a normal heart need not always mean that the ventricle is normal in all aspects. Several forms of left ventricular hypertrophy regression may be distinguished. The hypertrophy regression of the athletic heart is of a physiological nature. The spontaneous regression of left ventricular hypertrophy as seen in the rabbit model of aortic insufficiency has a pathological aspect resulting in heart failure. The nature of therapeutically induced regression of hypertrophy may vary according to fibrotic tissue concentration, energetical state and the function of the regressed heart. CONCLUSION: The biological implication of hypertrophy regression varies especially with respect to the nature of hypertrophy and the mode of achievement of hypertrophied mass reversal. Only long term prospective studies can clarify the question as to which types of hypertrophy regression result in decreased cardiovascular risk.

Animals↗
PubMed1996

[ACE-inhibitors in the treatment of chronic heart failure: pathophysiologic principles of protective effects].

The aim of modern therapy of heart failure is not a pure removal of symptoms but an improvement of survival. The angiotensin-converting enzyme (ACE)-inhibitors reduced morbidity and mortality in several large clinical trials in patients with dysfunctional left ventricle or manifestant heart failure. Thus, ACE inhibitors are recommended for heart failure treatment as a drug of primary option, unless contraindications are present, and if tolerated by patient. The mechanism of action of ACE inhibitors in heart failure is hypothetical. Participation of three factors is supposed: improvement in the pumping function of the failing heart, reduction on the risk of sudden death and reduction in myocardial infarction incidence. Reduction of hemodynamic load, antiischemic action and reduction of fibrotic tissue proliferation in failing myocardium are responsible for heart function improvement. These mechanisms together with potential antiatherosclerotic, antiaggregative, fibrinolytic and protective effect on endothelial function are supposed to participate in reduction of acute myocardial infarction and sudden death origin. The mentioned effects are determined by interaction with both circulating and local renin-angiotensin systems. The negative hemodynamic effects and undesirable restructuralisation of the affected ventricle are thus influenced on systematic and local-tissue level. Similarly as any other therapy also the treatment of heart failure with ACE inhibitors needs experience and a rational well tailored individual approach. (Fig.1, Ref. 32.).

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Captopril prevents NO-deficient hypertension and left ventricular hypertrophy without affecting nitric oxide synthase activity in rats.

The aim of the study was to assess whether angiotensin converting enzyme (ACE) inhibition with captopril prevents the development of hypertension and myocardial hypertrophy and affects nitric oxide synthase (NOS) activity in rats. Animals were divided into five groups: control, two groups receiving NG-nitro-L-arginine methyl ester (L-NAME) 20 or 40 mg/kg/day, a group receiving captopril 100 mg/kg/day and a group concomitantly treated with 40 mg/kg/day L-NAME plus 100 mg/kg/day captopril. After four weeks, systolic blood pressure (SBP) significantly increased in both L-NAME groups by 30% and 34%, respectively. In the captopril group, SBP significantly decreased by 30% and in the captopril plus L-NAME group SBP was not changed as compared to the control. Although left ventricular weight/body weight (LVW/BW) ratio in both L-NAME groups was significantly elevated by 19% and 29%, respectively, no alterations in LVW/BW ratio were found in the captopril group and captopril plus L-NAME group. In both groups receiving L-NAME, NOS activity significantly decreased by 17% and 69% in the heart, by 14% and 26% in the aorta, by 60% and 73% in the brain and by 13% and 30% in the kidney, respectively. Captopril did not influence NO synthase activity in any of the studied tissues. We conclude that captopril prevents the development of hypertension and LV hypertrophy without affecting NO formation.

Administration, Oral↗
PubMed1995

Spontaneous regression of left ventricular hypertrophy in a rabbit model of aortic insufficiency: possible clinical implications.

The right timing of surgical intervention in patients with aortic insufficiency is the crucial precondition for optimal postoperative course. To meet this demand, it is essential to have precise knowledge of the pathogenesis of this disease. Within the rabbit model of aortic insufficiency, four periods of adaptational changes to chronic haemodynamic overload were distinguished: developing hypertrophy, developed hypertrophy, regression of hypertrophy, and heart failure. The period of spontaneously developing regression of hypertrophy is linked with deterioration of function, metabolism, and structure of the left ventricle and represents an indication preceding heart failure. This paper presents the hypothesis that, in patients with severe aortic insufficiency, the left ventricle may undergo spontaneous regression of hypertrophy. Detection of this period may contribute to the insight into the pathogenesis of this disease and help to identify the patients who are candidates for surgery. Moreover, the onset of left ventricular diminution might represent the optimal phase for this intervention.

Animals↗