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Biomedical subjects

J Gmiński

Publications and source records attributed to J Gmiński.

At least 19 recordsLinked to original sources
PubMed2003

Activity of antioxidant enzymes in children from families at high risk of premature coronary heart disease.

A positive family history of coronary heart disease (CHD) is one of the most predictive risk factors of CHD. Many children with increased risk of CHD because of their positive family history of CHD do not present other risk factors, such as altered serum lipid profile. Oxidative stress plays an important part in the pathogenesis of atherosclerosis. Serum antioxidants and intracellular enzymatic antioxidants composed mainly of glutathione peroxidase (GSH-Px), catalase (CAT), superoxide dismutase (SOD) and glutathione reductase counterbalance oxidative stress. Diminished activity of this system may lead to accelerated progression of atherosclerosis. The aim of this study was to assess the activity of CAT, GSH-Px, SOD and glutathione reductase in children with a family history of premature CHD who did not present any other major risk factors of CHD (diabetes, obesity, dyslipidaemia or hypertension). Twenty-two healthy children from high-risk families, selected according to the National Cholesterol Education Program definition, were enrolled in the study. The control group comprised 18 children without a family history of CHD. All the children were healthy and had been screened for hyperlipidaemia, diabetes, hypertension and obesity prior to the study. The erythrocyte activity of CAT, GSH-Px, SOD and glutathione reductase was assessed. Children at high risk of CHD had a statistically significant lower level of GSH-Px and CAT activity than the children in the control group. There were no statistically significant differences in the activity of SOD and glutathione reductase.

Adolescent↗
PubMed2001

Plasma levels of von willebrand factor, endothelin-1, prostacyclin and thromboxane in children from families with high risk of premature coronary artery disease.

The aim of the study was to assess the plasma levels of endothelial injury markers in children from families with high risk of premature coronary heart disease (CHD) without other common CHD risk factors (hyperlipidaemia, obesity, hypertension, low physical activity). The study comprised 48 children, including 24 children from high-risk families (HR), according to the NCEP (National Cholesterol Education Programme) criteria: one or two parents had clinical manifestation of cardiovascular disease before the age of 65 years (mother) or 55 years (father). The control group included 24 healthy children with no familial history of cardiovascular disease. All the children were normolipidaemic according to the NCEP and the European Atherosclerosis Society criteria for children aged 2-19 years. In the HR group, the concentration of vWf was significantly elevated in comparison to that in the control group (p<0.0001). Plasma concentrations of ET-1 and TxB2 did not differ significantly between the HR group and the controls. Plasma concentrations of the 6-ketoPGF1alpha in the HR group and in the respective age and gender HR subgroups were significantly lower compared with those of the control group (p<0.00005). Concentration of vWf in the HR group was negatively correlated with the concentration of 6-ketoPGF1alpha (r = -0.47; p<0.05) and positively correlated with TxB2 (r=0.39; p<0.01). In a logistic regression analysis, we found that the 6-ketoPGF1alpha concentration in the lower quartile (< 16.1 pmol/L) was associated with a 3.4-fold odds of inclusion in the high-risk group versus the upper quartile (>23.0 pmol/L).

6-Ketoprostaglandin F1 alpha↗
PubMed2000

[Genetic predisposition to cardiovascular diseases].

The development of cardiovascular system disorders depends on both environmental and genetic factors. Precise mechanism by which genetic factors may promote atherosclerotic lesion formation is still under investigation. From multiple candidate genes for cardiovascular disorders the special attention should be paid to that which control synthesis of molecules involved in atherosclerosis process. For now lots of experiments have been done to test specific genes speculated to be crucial for the onset and progression of atherosclerosis, including genes of lipoprotein metabolism, coagulation and fibrinolysis system, renin-angiotensin system and substances influencing the metabolism of arterial wall. Many of them showed the association between tested polymorphisms and pathogenesis of cardiovascular diseases.

Blood Coagulation↗
PubMed2000

[HMG-CoA reductase inhibitors in prevention of cardiovascular diseases: new mechanisms, aspects and trials].

Use of lipid-lowering drugs in both primary and secondary prevention of cardiovascular disease (CVD) decreases significantly risk of myocardial infarction, stroke, incidence of cardiovascular events, reduces the cardiovascular mortality and morbidity as well as total mortality. HMG-CoA reductase inhibitors (statins) are most potent cholesterol-lowering drugs. Statins act by inhibition of HMG-CoA reductase activity, a rate--limiting step in synthesis of cholesterol and important metabolites of mevalonate--isoprenoids. The mechanisms by which favourable antiatherogenic actions of statins occur are complex. Statins inhibit proliferation and migration of vascular smooth muscle cells, reduce free-radicals generation and LDL modification, lower Lp(a) concentration, inhibit macrophage-derived foam cells accumulation and inhibit activation of platelets, thromboxane and PAI-1 synthesis. Use of statins in the therapy of hypercholesterolemia is presently recommended by NCEP, especially in high-risk groups (diabetes, post-CABG and PTCA, kidney and heart transplantation). Nevertheless, patients with CAD and moderately elevated LDL-C levels also benefit from the treatment with statins. Because of high costs of the therapy, statins of most favourable pharmacoeconomic profile should be used.

Cardiovascular Diseases↗
PubMed1999

[The influence of angiotensin-converting enzyme inhibitors on collagen content of the aorta wall in experimental hypercholesterolemia].

In atherosclerosis numerous qualitative and quantitative changes in connective tissue metabolism parameters in serum and aorta occur. In atherosclerosis there is an enhanced activity of local renin-angiotensin systems. It leads to overexpression of ANG II, both in serum and arterial wall. ANG II stimulates SMC to over-synthesize the collagens type I and III. Hyper-cholesterolemia is a form of metabolic injury which can both induce phenotypic change of SMC and activate RA system in arterial wall. ACEI lower the accumulation of collagens type I and III, and enhance elastin content in arterial wall in experimental hypertension. The aim of this study was to assess the influence of captopril, enalapril and quinapril on connective tissue metabolism of the aorta in experimental hyper-cholesterolemia. 64 male New Zealand rabbits were used. Animals were fed with standard fodder, special diet (1% cholesterol content) or special diet + tested ACEI. Two doses of ACE inhibitors were used: 1st--equivalent to doses applied to human subjects (in mg/kg of body weight), 2nd--dose 10 times higher. The animals were divided into 8 equal groups: K--standard fodder, B--special diet, C1, C2--special diet + captopril in doses 2.5 and 25 mg/kg/24 hours, respectively, E1, E2--special diet + enalapril in doses 0.75 and 7.5 mg/kg/24 hours, respectively, Q1 i Q2--special diet + quinapril in doses 0.75 and 7.5 mg/kg per day, respectively. The experiment lasted for 6 months. After 24 weeks the animals were sacrificed and aortae were excised for collagens assay. The statistical analysis was performed using ANOVA, followed by LSD test; p < 0.05 was considered statistically significant. The aorta collagens content of cholesterol-fed rabbits significantly increased. The tested ACEI (captopril, enalapril in both doses and quinapril in lower dose) had a preventive effect against the increase of aorta collagen content.

Analysis of Variance↗
PubMed1997

[The role of DNA polymorphism in the renin-angiotensin system and the pathogenesis of cardiovascular diseases].

Myocardial infarction and stroke are the major cause of death in developed countries and are the clinical manifestation of atherosclerosis and hypertension. Both the environmental factors and genetic predisposition have an influence on the pathogenesis of these diseases. Despite we know lots of environmental risk factors and we made important advances in the prevention and treatment of mentioned diseases, our knowledge about the pathogenic linkage between genetic predisposition and cardiovascular diseases is still very little. Activation of the renin-angiotensin system has been proposed as a very important step in the pathogenesis of hypertension and atherosclerosis. In spite of vasoconstrictor activity, angiotensin II can stimulate migration and proliferation of vascular smooth muscle cells, macrophage-foam cells formation, adhesion and aggregation of platelets and fibrinolytic system inhibition. Angiotensin convertin enzyme inhibitors reduce the development of the atherosclerotic process after vascular injury and in hyperlipidemic animals. Blockade of renin-angiotensin system seems to be also effective in secondary prevention of myocardial infarction in men. In sum, the genetic variations inside the renin-angiotensin system which may affect the function of its components might have an influence on genetic predisposition to cardiovascular diseases. The paper deals with the current state of knowledge on association between polymorphic variations in renin gene, angiotensinogen gene, angiotensin converting enzyme gene and AT1 receptor gene and primary hypertension, ischaemic heart disease and myocardial infarction.

Animals↗
PubMed1997

[Anti-atherosclerotic actions of HMG-CoA reductase inhibitors].

Statins are most potent lipid-lowering drugs. The mechanisms of their action is specific inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) activity. HMG-CoA reductase catalyses the reduction of HMG-CoA o mevalonate and is rate-limiting step in cholesterol biosynthesis pathway. Mevalonate is considered to be not only an important intermediate of cholesterol synthesis, but also the source of isoprenoids which play important role in DNA replication and cell growth. It was shown that statins inhibit the proliferation and migration of vascular smooth muscle cell--key events in atherogenesis. HMG-CoA reductase inhibitors lower the reactivity of arterial wall to vasoconstrictor agents, decrease the concentration of lipoprotein [a]--an independent risk factor of atherosclerosis, inhibit the generation of free radicals and lipid peroxidation, decrease the number of macrophages in atherosclerotic lesion and finally, equilibrate the clotting-fibrynolysis processes of attennuating platelets function, reducing the tissue factor synthesis and decreasing the concentration of plasminogen activator inhibitors. Statins are presently considered by NCEP to be the drugs of first choice for treatment of hypercholesterolemia.

Animals↗
PubMed1997

[Treatment of hypertension in postmenopausal women].

Epidemiological and clinical studies have defined the lower incidence of atherosclerotic vascular disease in women than in age-matched men. After menopause the difference becomes less significant, what is due to estrogen deficiency. The mechanism of vascular protective effect of estrogen involves inhibition of smooth muscle cell proliferation, protection of endothelium function and improvement of lipid metabolism. One of the most important risk factor of atherosclerosis is hypertension. The prevalence of hypertension in elderly women is extremely high-up to 80%. Because of absence of the hormonal replacement therapy effect on blood pressure, there is an indication for antihypertensive therapy in postmenopausal women. Angiotensin-converting enzyme inhibitors are the class of drugs which can lower cardiovascular mortality due to hypertension and atherosclerosis in elderly women. They improve impaired insulin sensitivity and inhibit activation of renin-angiotensin system, both processes leading to the development of hypertension in postmenopausal women. Angiotensin-converting enzyme inhibitors also possess a direct anti-atherosclerotic properties, like inhibition of smooth muscle cell proliferation and migration, protection of endothelium function, reduced macrophages activation and foam cell accumulation, protection of LDL particles and improvement of fibrinolysis.

Aged↗
PubMed1996

[Anti-atherosclerotic action of ACE inhibitors. I. Inactivation of the renin-angiotensin system].

The activation of the renin-angiotensin system has been proposed as a very important step in the pathogenesis of atherosclerosis. Accordingly, ACE-inhibitors and angiotensin II receptors antagonists showed their ability to reduce the atherosclerotic process in animals. Inhibition of renin-angiotensin system reduces the development of atherosclerotic lesion either in cholesterol-fed animals and in animals after vascular injury. The precise mechanism for this action may depend on the inhibition of other than hypertensive property of angiotensin II.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

[Anti-atherosclerotic action of angiotensin converting enzyme II. Effect on metabolism of kinin, free radical reaction, sensitivity to insulin and lipid metabolism].

Blockade of the renin-angiotensin system reduces the development of the atherosclerotic process after vascular injury and in hyperlipidemic animals. ACE-inhibitors inhibit vascular smooth muscle cells migration and proliferation, macrophage-foam cell accumulation and preserve the antiaggregatory and antithrombotic function of the endothelium in atherosclerotic vessels. In addition to the inhibition of angiotensin II synthesis, reduced degradation of kinins and improvement of insulin action after ACE-inhibition may be responsible for observed actions. ACE-inhibitors may have also influence on lipids metabolism, including low density lipoprotein oxidation. Despite this, ACE-inhibitors failed to prevent restenosis after coronary angioplasty in humans. One reason for the lack of ACE-inhibitors effect in human restenosis might depend on the activation of the alternative angiotensin II-generating system in human arteries after vascular injury.

Angiotensin II↗
PubMed1996

[Pharmacologic treatment of lipid metabolism disorders].

The aim of the treatment of dyslipidaemia is the primary and secondary prevention of coronary heart disease (CHD). Dietary therapy is the first line in the management of hyperlipidaemia. Lipid-lowering drugs should be used in patients with an inadequate dietary response, with CHD and/or multiple CHD risk factors. The choice of drug depends on the lipid disorder type, the desired plasma lipids reduction and presence of contraindications. Lipid-lowering drugs-anion-exchange resins, nicotinic acid and acipimox, fibrates, statins, probucol and two new classes used in experimental studies (ansamycins and ACAT inhibitors) are presented. Antiatherosclerotic properties of statins are characterized.

Female↗
PubMed1996

[Lipids and atherosclerosis].

Atherosclerosis is a degenerative pathology of blood vessels leading to coronary heart disease, myocardial infarction and stroke. The basic lesion of atherosclerosis is the fibrous plaque, which consists of lipids, smooth muscle cells, macrophages and connective tissue matrix. Data derived from experimental and clinical studies indicate the crucial role of elevated serum LDL-cholesterol concentration in the formation of atherosclerotic lesions. HDL removes cholesterol from the arterial wall, stimulates arterial prostacyclin synthesis, inhibits adhesion molecules expression, has antioxidant properties and protects against atherosclerosis. Lipoprotein (a) competes with plasminogen for its binding site, leading to reduced fibrinolysis and is an important link between thrombogenesis and atherosclerosis. The pathogenic role of lipids in atherogenesis is discussed.

Arteriosclerosis↗
PubMed1996

[Anti-atherosclerotic action of hypotensive drugs].

Hypertension is an important risk factor for the development of atherosclerosis. Traditional antihypertensive therapy is not fully effective in prevention of cardiovascular abnormalities of hypertension. Two classes of hypotensive drugs, calcium antagonists and angiotensin-converting enzyme (ACE) inhibitors, reduce atherosclerosis in several experimental models in animals. Anti-atherosclerotic effects of calcium antagonists include attenuation of endothelial dysfunction, prevention of LDL modification, stimulation of LDL receptor activity, inhibition of superoxide radical generation and inhibition of vascular smooth muscle cells proliferation and migration. In large angiographic trials calcium antagonists reduced the development of new atherosclerotic plaques. ACE inhibitors also lead to the lower incidence of atherosclerosis in experimental animals. They inhibit migration and proliferation of vascular smooth muscle cells, reduce macrophage-derived foam cell accumulation, preserve protective endothelium function, reduce LDL modification and increase fibrinolytic activity. It depends on reduced angiotensin II synthesis, increased concentration of kinins, substance P and angiotensin-(1-7), inhibition of leukotriene B4 formation and improvement of insulin action. In some studies they also reduce plasma lipids concentration, including lipoprotein (a). ACE inhibitors were found to be ineffective in prevention of restenosis after PTCA in human but data derived from large, multicenter trials indicate that they are effective in the secondary prevention of myocardial infarction.

Angioplasty, Balloon, Coronary↗
PubMed1994

[Antiatherogenic action of heparin].

Heparin is a highly sulfated glycosaminoglycan with many functions such as antilipemic and antithrombotic. In spite of these activities heparin is able to inhibit vascular smooth muscle cells proliferation and migration what seems to be very important event in the pathogenesis of atherosclerosis. The molecular mechanism of the action of heparin on smooth muscle cells has not been completely understood. Heparin inhibits growth factors binding to their receptors, oncogenes expression and has influence on the extracellular matrix protein deposition in the artery wall.

Animals↗
PubMed1993

[Renin-angiotensin system and atherosclerosis].

Based upon literature the renin-angiotensin system involvement in the pathogenesis of atherosclerosis has been discussed. Angiotensin II leads to the increased production of growth factors such as PDGF, TGF-beta, FGF and extracellular matrix proteins. There are evidences that angiotensin II stimulates expression of egr-1, c-jun, c-fos and c-myc oncogenes in vascular smooth muscle cells. Proliferation of aortic smooth muscle cells in response to the injury can be reduced by inhibitors of renin-angiotensin system what supports the hypothesis that angiotensin II can contribute to the pathogenesis of atherosclerosis.

Angiotensin II↗
PubMed1993

Elastin metabolism parameters in sera of patients with lung cancer.

Elastin metabolism parameters (elastin-derived peptides and elastase-like activity) were determined in sera of patients with lung cancer and in healthy controls. The concentration of elastin-derived peptides was statistically significantly elevated in the lung cancer group. There was no statistically significant difference in the serum elastase-like activity between the groups studied. These data seem to indicate an enhanced metabolism of elastin in patients with lung cancer.

Adenocarcinoma↗