Katarzyna Strawa-Zakoscielna, Monika Lenart-Lipinska, Aneta Szafraniec, Grzegorz Rudzki and Beata Matyjaszek-Matuszek
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Grzegorz Mizerski, Pawel Kicinski and Andrzej Jaroszynski
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Danish Ahmed, Mohd. Ibrahim Khan, Manju Sharma and Mohd. Faiyaz Khan
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Viera Kristová, Milan Kriška, Róbert Vojtko, Miriam Petrová, Silvia Líšková, Radoslav Villáris, Zoltán Varga and Martin Wawruch
Trends in vascular pharmacology research in the Department of Pharmacology and Clinical Pharmacology, Faculty of Medicine, Comenius University, Bratislava
Research in the Department of Pharmacology started to focus intensively on fetal circulation in the 60s. Results of experiments contributed to clarification of the conversion of fetal circulation type to the adult type: the mechanism of the ductus arteriosus closure, examination of fetal and neonatal pulmonary vessel responses. In the early 80s, increased attention was dedicated to fetal vascular endothelium, later on to vascular reactivity in relation to the endothelium in adult animals. We developed original models of vascular endothelial damage using the perfusion method (repeated vasoconstrictive stimuli, deendothelization by air bubbles). We developed a new technique for in vitro endothelial loss quantification on Millipore filters. Under in vitro conditions, the protective effects of sulodexide and pentoxifylline on vascular endothelium were evaluated. In recent years were studied protective effects of selected substances in vivo in models of endothelial damage (e.g. stress, toxic tissue damage, diabetes mellitus, hypertension). The role of potassium channels in the hypertension model was studied in cooperation with the Czech Academy of Sciences. Assessment of vascular reactivity in the diabetic model was significantly improved by computer. In addition to experimental work, the department is solving problems of clinical pharmacology - especially drug risk evaluation (non-steroidal anti-inflammatory drugs). Recently, we have dealt with pharmacoepidemiological studies in geriatric patients and with cardiovascular risk of NSAIDs in relation to pharmacotherapy. The results of these studies may be an impulse for targeted problem solving in our experiments.
Štefan Bezek, Eduard Ujházy, Mojmír Mach, Jana Navarová and Michal Dubovický
Developmental origin of chronic diseases: toxicological implication
Human epidemiological and experimental animal studies show that suboptimal environments in fetal and neonatal life exerts a profound influence on physiological function and risk of disease in adult life. The molecular, cellular, metabolic, endocrine and physiological adaptations to intrauterine nutritional conditions result in permanent alterations of cellular proliferation and differentiation of tissues and organ systems, which in turn can manifest by pathological consequences or increased vulnerability to chronic diseases in adulthood. Intrauterine growth restriction (IUGR) due to intrauterine development derangements is considered the important factor in development of such diseases as essential hypertension, diabetes mellitus, ischemic diseases of the heart, osteoporosis, respiratory, neuropsychiatric and immune system diseases.
An early life exposures to dietary and environmental exposures can have a important effect on epigenetic code, resulting in diseases developed later in life. The concept of the "developmental programming" and Developmental Origins of Adult Diseases (DOHaD) has become well accepted because of the compelling animal studies that have precisely defined the outcomes of specific exposures. The environmental pollullutants and other chemical toxicants may influence crucial cellular functions during critical periods of fetal development and permanently alter the structure or function of specific organ systems. Developmental epigenetics is believed to establish "adaptive" phenotypes to meet the demands of the later-life environment. Resulting phenotypes that match predicted later-life demands will promote health, while a high degree of mismatch will impede adaptability to later-life challenges and elevate disease risk. The rapid introduction of synthetic chemicals, environmental pollutants and medical interventions, may result in conflict with the programmed adaptive changes made during early development, and explain the alarming increases in some diseases.
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Ružena Sotníková, Jana Nedelčevová, Jana Navarová, Viera Nosáľová, Katarína Drábiková, Katalin Szöcs, Peter Křenek, Zuzana Kyseľová, Štefan Bezek, Vladimír Knezl, Ján Dřímal, Zuzana Brosková, Viera Kristová, Ľudmila Okruhlicová, Iveta Bernátová and Viktor Bauer
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