The goal of the study was to determine whether postconditioning protects against different ischemia durations in the rabbit. Rabbits were assigned to a 20-, 25-, 45- or 60-min coronary occlusion followed by 24-h of reperfusion. Rabbits received no further intervention (control) or were postconditioned with four cycles of 30-s occlusion and 30-s reperfusion after myocardial infarction. Plasma levels of troponin I were quantified throughout reperfusion. In control conditions, infarct sizes (% area at risk using triphenyltetrazolium chloride) after 20, 25, 45 and 60 min of coronary occlusions were 23±3, 51±4, 70±3 and 81±3 %, respectively. With 20 and 25 min occlusion, postconditioning reduced infarct size by 43±10 and 73±21 %, respectively. On the other hand, with 45 or 60 min occlusion, postconditioning had no significant effects on infarct size (61±3 and 80±2 % of area at risk). Preconditioning protocol was performed with 25- and 60-min coronary occlusion. As expected, preconditioning significantly reduced infarct size. In conclusion, in the rabbit, the cardioprotection afforded by postconditioning is limited to less than 45 min coronary occlusion., R. Létienne, Y. Calmettes, B. Le Grand., and Obsahuje seznam literatury
There is accumulating evidence showing that ischemic preconditioning (PC) may lose its cardioprotective effect in the diseased states. The present study investigated whether PC can be effective in hypothyroidism, a clinical condition which is common and often accompanies cardiac diseases such as heart failure and myocardial infarction. Hypothyroidism was induced in rats by 3-week administration of 6n-propyl-2-thiouracil in water (0.05 %). Normal and hypothyroid hearts (HYPO) were perfused in Langendorff mode and subjected to 20 min of zero-flow global ischemia and 45 min of reperfus ion. A preconditioning protocol (PC) was also applied prior to ischemia. HYPO hearts had significantly improved post-ischemic recovery of left ventricular developed pressure, end-diastolic pressure and reduced lactate dehydrogenase release. Furthermore, phospho-JNK and p38 MAPK levels after ischemia and reperfusion were 4.0 and 3.0 fold lower in HYPO as compared to normal hearts ( P<0.05). A different response to PC was observed in normal than in HYPO hearts. PC improved the post-ischemic recovery of function and reduced the extent of injury in normal hearts but had no additional effect on the hypothyroid hearts. This response, in the preconditioned normal hearts, resulted in 2.5 and 1.8 fold smaller expression of the phospho-JNK and phospho-p38 MAPK levels at the end of reperfusion, as compared to non-PC hearts ( P<0.05), while in HYPO hearts, no additional reduction in the phosphorylation of these kinases was observed after PC. Hypothyroid hearts appear to be tolerant to ischemia-reperfusion injury. This response may be, at least in part, due to the down-regulation of ischemia-reperfusion induced activation of JNKs and p38 MAPK kinases. PC is not associated with further reduction in the activation of these kinases in the hypothyroid hearts and fails to confer added protection in those hearts., I. Mourouzis ... [et al.]., and Obsahuje seznam literatury
The founder of physiology studies in the Balkans and the pioneer of research on hypothermia, Ivan Djaja (Jean Giaja) was born 1884 in L’Havre. Giaja gained his PhD at the Sorbonne in 1909. In 1910 he established the first Chair of Physiology in the Balkans and organized the first Serbian In stitute for Physiology at the School of Philosophy of the University of Belgrade. He led this Institute for more than 40 subsequent years. His most notable papers were in the field of thermoregulation and bioenergetics. Djaja became member of the Serbian and Croatian academies of science and doctor honoris causa of Sorbonne. In 1952 for the seminal work on the behavior of deep cooled warm blooded animals he became associate member of the National Medical Academy in Paris. In 1955 the French Academy of Sciences elected him as associate member in place of deceased Sir Alexander Fleming. Djaja died in 1957 during a congress held in his honor. He left more than 200 scientific and other papers and the golden DaVincian credo “Nulla dies sine experimento”. His legacy was continued by several generations of researchers, the most prominent among them being Stefan Gelineo, Radoslav Andjus and Vojislav Petrović ., P. R. Andjus, S. S: Stojilkovic, G. Cvijic., and Obsahuje bibliografii a bibliografické odkazy
Článek se zabývá taxonomií, reprodukční biologií, fylogenetikou, fylogeografií a introdukční historií ryb rodu karas (Carassius). Článek poskytuje souhrn poznatků, které jsou značně komplikované a spojené s jedinečným způsobem rozmnožování, definicí druhu a nepřesným chápáním biologie a systematiky těchto ryb v minulosti. Celá problematika je ještě daleko od svého kompletního vyřešení, ale současný pohled nám může pomoci v lepší péči o vodní prostředí., This article deals with the taxonomy, reproductive biology, phylogenetics, phylogeography and introduction history of the fishes of the genus Carassius. It summarizes findings associated with their unique mode of reproduction, challenging species delimitation and insufficient understanding of the biology and systematics of these fishes in the past. Deeper insight into the biology of Prussian Carp (Carassius gibelio) will require more research, but the available results can improve our understanding and management of the aquatic environment., Lukáš Kalous., and Obsahuje seznam literatury
Regulatory volume decrease (RVD) is essential for the survival of animal cells. The aim of this study was to observe the RVD process in rat ventricular myocytes, and to determine if the KATP channels are involved in the RVD process in these cells. By using reverse transcriptase polymerase chain reaction and Western blot analysis, we demonstrated that there are two types of KATP channels expressed in rat ventricular myocytes: Kir6.1 and Kir6.2. When rat cardiac myocytes were exposed to hypotonic solution, cell volume increased significantly within 15 min and then gradually recovered. This typical RVD process could be inhibited by a Cl– channel blocker (0.5 mM 9-anthracene-carboxylic acid , 9-AC), a K+ channel blocker (5.0 mM CsCl) and a KATP channel blocker glibenclamide (10 μM). Electrophysiological results showed that hypotonic solution activated a whole-cell current, which had similar biophysical characteristics with KATP opener (pinacidil)-induced currents. This current could be blocked by glibenclamide. Our data suggested that the RVD process in rat ventricular myocytes is dependent on the activation of K+ channels, and that KATP channels are involved in this process., L. Shi ... [et al.]., and Obsahuje seznam literatury