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12. Ontogenetic development of cardiac tolerance to oxygen deprivation - possible mechanisms

Creator:
Bohuslav Ošťádal, Ivana Ošťádalová, František Kolář, Zuzana Charvátová, and Ivan Netuka
Type:
article, články, model:article, and TEXT
Subject:
Patologie. Klinická medicína, kardiologie, hypoxie, ischemie, ontogeneze, cardiology, hypoxia, ischemia, ontogeny, odolnost srdce, ochrana srdce, cardiac tolerance, cardiac protection, 14, and 616
Language:
English
Description:
Our present focus on the hypoxic immature heart is driven by clinical urgency: cyanotic congenital cardiac malformations remain the single largest cause of mortality from congenital defects and ischemic heart disease is no more the disease of the fifth and older decades but its origin as well as risk factors are present already during early ontogeny. Moreover, the number of adult patients operated for cyanotic congenital heart disease during infancy steadily increases. This group approaches the age of the rising risk of serious cardiovascular diseases, particularly ischemic heart disease. Experimental results have clearly shown that the immature heart is significantly more tolerant to oxygen deficiency than the adult myocardium. However, the mechanisms of this difference have not yet been satisfactorily clarified; they are likely the result of developmental changes in cardiac energy metabolism, including mitochondrial function. The high resistance of the newborn heart cannot be further increased by ischemic preconditioning or adaptation to chronic hypoxia; these protective mechanisms appear only with decreasing tolerance during development. Resistance of the adult myocardium to acute oxygen deprivation may be significantly influenced by perinatal hypoxia. These results suggest that the developmental approach offers new possibilities in the studies of pathogenesis, prevention and therapy of critical cardiovascular diseases., B. Ošťádal ... [et al.]., and Obsahuje seznam literatury
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

13. Pregnancy-associated plasma protein A and proform eosinophilic major basic protein in the detection of different types of coronary artery disease

Creator:
Petr Hájek, Milan Macek, Magdaléna Hladíková, Běla Houbová, David Alan, Václav Durdil, Jiří Fiedler, Martin Malý, Petr Ošťádal, Josef Veselka, and Alice Krebsová
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Patologie. Klinická medicína, kardiologie, věnčité tepny, troponiny, ateroskleróza, cardiology, coronary arteries, troponins, atherosclerosis, PAPP-A/proMBP, PAPP-A/proMBP (pregnancy-associated plasma protein A), 14, and 616
Language:
English
Description:
Kryptor system was proven to be a rapid, standard method for pregnancy-associated plasma protein A and proform eosinophilic major basic protein (PAPP-A/proMBP) complex detection in coronary artery disease (CAD). No age and/or gender differences in 51 controls and 110 stable coronary artery disease (SCAD) patients were found. SCAD patients did not differ from controls and no difference in PAPP-A/proMBP levels with regards to the number of affected vessels was found. In 21 unstable angina pectoris (UAP), in 35 without and 66 with ST elevation acute myocardial infarctions (NSTEMI, STEMI respectively) patients PAPP-A/proMBP levels were increased (P=0.004 and P<0.0005, respectively). PAPP-A/proMBP levels did not correlate with cardiac troponin I (cTnI) in STEMI and NSTEMI patients. PAPP-A/ proMBP increase was more frequent than cTnI (P=0.036) within the early phase of STEMI. In NSTEMI patients PAPP-A/proMBP positivity was present in 50 % of cTnI negative cases. Receiver operating characteristic (ROC) analysis revealed the highest diagnostic accuracy of PAPP-A/proMBP (0.919) in STEMI cTnI positive cases. The highest specificity/sensitivity PAPP-A/proMBP levels for particular acute coronary syndrome (ACS) types were 10.65-14.75 mIU/l. Combination of PAPP-A/proMBP with cTnI increases their diagnostic efficacy within the early phase of ACS. Our results suggest that PAPP-A/proMBP complex is involved in processes preceding vulnerable plaque development in ACS., P. Hájek, M. Macek, M. Hladíková, B. Houbová, D. Alan, V. Durdil, J. Fiedler, M. Malý, P. Ošťádal, J. Veselka,A. Krebsová., and Obsahuje bibliografii a bibliografické odkazy
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

14. Total β-adrenoceptor deficiency results in cardiac hypotrophy and negative inotropy

Creator:
Lee, S., Grafweg, S., Schneider, T., Jimenez, M., Giacobino, J.-P., Ghanem, A., Tiemann, K., Bloch, W., Müller-Ehmsen, J., Schwinger, R. H. G., and Brixius, K.
Format:
print
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, kardiologie, cardiology, beta-1 adrenoceptor, beta-2 adrenoceptor, beta-3 adrenoceptor, knockout, mice, 14, and 612
Language:
English
Description:
The present study investigated cardiac function in hearts of mice with total deficiency of the β1-, β2- and β3-adrenoceptors (TKO) in comparison to wildtype mice (WT). We investigated cardiac morphology and echocardiographic function, measured protein expression of Ca2+-regulatory proteins, SERCA 2a activity, myofibrillar function, and performed running wheel tests. Heart weight and heart-to-body weight ratio were significantly smaller in TKO as compared to WT. This was accompanied by a decrease in the size of the cardiomyocytes in TKO. Heart rate and ejection fraction were significantly diminished in TKO as compared to WT. Protein expressions of SERCA 2a, ryanodine receptor and Na+/Ca2+-exchanger were similar in TKO and WT mice, but phospholamban protein expression was increased. PKAdependent phosphorylation of phospholamban at serine 16 was absent and CaMKII-dependent phosphorylation at threonine 17 was decreased in TKO. All alterations were paralleled by a decrease in SERCA 2a-activity. A similar maximal calciumdependent tension but an increased myofibrillar calciumsensitivity was measured in TKO as compared to WT. We did not observe relevant functional impairments of TKO in running wheel tests. In the absence of β-agonistic stimulation, SERCA 2a activity is mainly regulated by alterations of phospholamban expression and phosphorylation. The decreased SERCA 2a activity following β-adrenoceptor deficiency may be partly compensated by an increased myofibrillar calcium-sensitivity., S. Lee ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public