(Pro)renin receptor (PRR) contributes to regulating many physiological and pathological processes; however, the role of PRR-mediated signaling pathways in myocardial ischemia/reperfusion injury (IRI) remains unclear. In this study, we used an in vitro model of hypoxia/reoxygenation (H/R) to mimic IRI and carried out PRR knockdown by siRNA and PRR overexpression using cDNA in H9c2 cells. Cell proliferation activity was examined by MTT and Cell Counting Kit-8 (CCK-8) assays. Apoptosis-related factors, autophagy markers and beta-catenin pathway activity were assessed by real-time PCR and western blotting. After 24 h of hypoxia followed by 2 h of reoxygenation, the expression levels of PRR, LC3B-I/II, Beclin1, cleaved caspase-3, cleaved caspase-9 and Bax were upregulated, suggesting that apoptosis and autophagy were increased in H9c2 cells. Contrary to the effects of PRR downregulation, the overexpression of PRR inhibited proliferation, induced apoptosis, increased the expression of pro-apoptotic factors and autophagy markers, and promoted activation of the beta-catenin pathway. Furthermore, all these effects were reversed by treatment with the beta-catenin antagonist DKK-1. Thus, we concluded that PRR activation can trigger H/R-induced apoptosis and autophagy in H9c2 cells through the beta-catenin signaling pathway, which may provide new therapeutic targets for the prevention and treatment of myocardial IRI.

• MeSH
• apoptóza fyziologie   MeSH
• autofagie fyziologie   MeSH
• beta-katenin metabolismus   MeSH
• buněčné linie MeSH
• hypoxie buňky fyziologie   MeSH
• kardiomyocyty metabolismus   patologie   MeSH
• krysa rodu rattus MeSH
• kyslík metabolismus   MeSH
• receptory buněčného povrchu metabolismus   MeSH
• reperfuzní poškození myokardu metabolismus   patologie   MeSH
• signální transdukce MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

The incorporation of the RGD peptide (arginine-glycine-aspartate) into biomaterials has been proposed to promote cell adhesion to the matrix, which can influence and control cell behaviour and function. While many studies have utilised RGD modified biomaterials for cell delivery, few have examined its effect under the condition of reduced oxygen and nutrients, as found at ischaemic injury sites. Here, we systematically examine the effect of RGD on hMSCs in hyaluronic acid (HA) hydrogel under standard and ischaemic culture conditions, to elucidate under what conditions RGD has beneficial effects over unmodified HA and its effectiveness in improving cell viability. Results demonstrate that under standard culture conditions, RGD significantly increased hMSC spreading and the release of vascular endothelial factor-1 (VEGF) and monocyte chemoattractant factor-1 (MCP-1), compared to unmodified HA hydrogel. As adhesion is known to influence cell survival, we hypothesised that cells in RGD hydrogels would exhibit increased cell viability under ischaemic culture conditions. However, results demonstrate that cell viability and protein release was comparable in both RGD modified and unmodified HA hydrogels. Confocal imaging revealed cellular morphology indicative of weak cell adhesion. Subsequent investigations found that RGD was could exert positive effects on encapsulated cells under ischaemic conditions but only if hMSCs were pre-cultured under standard conditions to allow strong adhesion to RGD before exposure. Together, these results provide novel insight into the value of RGD introduction and suggest that the adhesion of hMSCs to RGD prior to delivery could improve survival and function at ischaemic injury sites. STATEMENT OF SIGNIFICANCE: The development of a biomaterial scaffold capable of maintaining cell viability while promoting cell function is a major research goal in the field of cardiac tissue engineering. This study confirms the suitability of a modified HA hydrogel whereby stem cells in the modified hydrogel showed significantly greater cell spreading and protein secretion compared to cells in the unmodified HA hydrogel. A pre-culture period allowing strong adhesion of the cells to the modified hydrogel was shown to improve cell survival under conditions that mimic the myocardium post-MI. This finding may have a significant impact on the use and timelines of modifications to improve stem cell survival in harsh environments like the injured heart.

• MeSH
• buněčná adheze účinky léků   MeSH
• buněčné kultury MeSH
• hydrogely chemie   MeSH
• hypoxie buňky fyziologie   MeSH
• kyselina hyaluronová chemie   MeSH
• lidé MeSH
• mezenchymální kmenové buňky cytologie   fyziologie   MeSH
• oligopeptidy chemie   MeSH
• tkáňové inženýrství metody   MeSH
• tkáňové podpůrné struktury chemie   MeSH
• viabilita buněk účinky léků   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Background: Exposure to intermittent hypoxia (IH) may play a role in the development of metabolic impairments in the context of obstructive sleep apnea syndrome, probably by elevated plasma levels of free fatty acids. Employing gas-permeable cultureware to grow differentiated human and mouse adipocytes in vitro, we directly studied the effects of pericellular oxygen fluctuations on key adipocyte metabolic functions-spontaneous lipolytic rates, triglyceride accumulation, de novo lipogenesis, and expression of adipocyte-specific marker genes. Materials and Methods: 3T3-L1 fibroblasts and human subcutaneous preadipocytes were differentiated under conditions that induced repetitive pericellular-oxygen cycles IH between 1% O2 (5 min) and 16% O2 (5 min), continuously for 14 days or under control conditions. Chemicals were used to inhibit the flux of acetyl-CoA from glycolysis (alfa-cyano-4-hydroxy cinnamate) or the tricarboxylic acid cycle (SB204990), or to stimulate the flux of acetyl-CoA from pyruvate to the lipogenic pool. Lipolytic rate, intracellular lipids, and expression of adipocyte differentiation markers were assessed and t-test or ANOVA were used to find significant differences. Results: The rate of lipolysis increased by 211% in 3T3-L1 cells and by 39% in obese human adipocytes. Exposure to IH reduced intracellular lipid stores by 37% and reduced the expression of adipocyte differentiation markers. Pharmacological stimulation or inhibition of de novo lipogenesis did not modify the intracellular lipid content under IH. Conclusions: Pericellular oxygen fluctuations directly stimulated lipolysis, but did not increase de novo lipogenesis from endogenous substrates. Similarly, IH hampered adipocyte differentiation from precursors.

• MeSH
• acetylkoenzym A metabolismus   MeSH
• buněčná diferenciace genetika   fyziologie   MeSH
• buňky 3T3-L1 MeSH
• citrátový cyklus MeSH
• glykolýza MeSH
• hypoxie buňky genetika   fyziologie   MeSH
• kinetika MeSH
• lidé MeSH
• lipogeneze genetika   fyziologie   MeSH
• lipolýza genetika   fyziologie   MeSH
• myši MeSH
• spotřeba kyslíku genetika   MeSH
• stanovení celkové genové exprese MeSH
• triglyceridy metabolismus   MeSH
• tukové buňky metabolismus   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Ample experimental evidence suggests that sepsis could interfere with any mitochondrial function; however, the true role of mitochondrial dysfunction in the pathogenesis of sepsis-induced multiple organ dysfunction is still a matter of controversy. This review is primarily focused on mitochondrial oxygen consumption in various animal models of sepsis in relation to human disease and potential sources of variability in experimental results documenting decrease, increase or no change in mitochondrial respiration in various organs and species. To date, at least three possible explanations of sepsis-associated dysfunction of the mitochondrial respiratory system and consequently impaired energy production have been suggested: 1. Mitochondrial dysfunction is secondary to tissue hypoxia. 2. Mitochondria are challenged by various toxins or mediators of inflammation that impair oxygen utilization (cytopathic hypoxia). 3. Compromised mitochondrial respiration could be an active measure of survival strategy resembling stunning or hibernation. To reveal the true role of mitochondria in sepsis, sources of variability of experimental results based on animal species, models of sepsis, organs studied, or analytical approaches should be identified and minimized by the use of appropriate experimental models resembling human sepsis, wider use of larger animal species in preclinical studies, more detailed mapping of interspecies differences and organ-specific features of oxygen utilization in addition to use of complex and standardized protocols evaluating mitochondrial respiration.

• MeSH
• buněčné dýchání fyziologie   MeSH
• hypoxie buňky fyziologie   MeSH
• lidé MeSH
• mitochondrie metabolismus   patologie   MeSH
• multiorgánové selhání metabolismus   patologie   MeSH
• sepse metabolismus   patologie   MeSH
• spotřeba kyslíku fyziologie   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

Syndrom obstrukční spánkové apnoe (OSA) je u diabetiků 2. typu velmi časté onemocnění, které významně zvyšuje kardiovaskulární morbiditu i mortalitu. OSA byla řadou studií identifikována jako nezávislý rizikový faktor rozvoje inzulinové rezistence, glukózové intolerance a diabetes mellitus 2. typu. Porucha glukózové homeostázy u pacientů s OSA je pravděpodobně zprostředkována chronickou intermitentní hypoxií nebo spánkovou fragmentací skrze aktivaci sympatického nervového systému, hypotalamo-hypofyzární-adrenální osy, prozánětlivých drah či oxidačního stresu. Navzdory vysoké prevalenci OSA mezi diabetiky 2. typu i prokázanému benefitu léčby kontinuálním pozitivním přetlakem (CPAP) na redukci mortality zůstává většina pacientů s OSA nediagnostikovaná. Na místě je proto provádění aktivního screeningu OSA u všech diabetiků 2. typu nejlépe pomocí domácí monitorace saturace a dýchání ve spánku. Ačkoli efekt léčby CPAP na zlepšení kompenzace cukrovky (snížení glykovaného hemoglobinu) nebyl u diabetiků 2. typu zatím jednoznačně prokázán, byly zaznamenány slibné výsledky při léčbě pacientů s prediabetem.

Obstructive sleep apnoea syndrome (OSA) is a disease very frequently occurring in people with type 2 diabetes, that significantly increases cardiovascular morbidity and mortality. In a number of studies, OSA has been identified as an independent risk factor for the development of insulin resistance, glucose intolerance and type 2 diabetes mellitus. Disorders of glucose homeostasis in patients with OSA are probably mediated by chronic intermittent hypoxia and/or sleep fragmentation through activation of the sympathetic nervous system, the hypothalamic-pituitary-adrenal stress axis, pro-inflammatory paths or oxidative stress. Despite the high prevalence of OSA among patients with type 2 diabetes as well as the proven benefit of the continuous positive airway pressure (CPAP) therapy on reduction of mortality, most patients with OSA remain undiagnosed. Active OSA screening should therefore be performed in all patients with type 2 diabetes, ideally through home monitoring of oxygen saturation and breathing during sleep. Although the effect of CPAP therapy on the improvement in diabetes control (decrease in glycated hemoglobin) has not been clearly proven in patients with type 2 diabetes so far, promising outcomes have been observed during the treatment of patients with prediabetes.

• Klíčová slova
• intermitentní hypoxie,
• MeSH
• diabetes mellitus 2. typu * diagnóza   mortalita   MeSH
• hypoxie buňky fyziologie   MeSH
• komplikace diabetu MeSH
• krevní glukóza metabolismus   MeSH
• lidé MeSH
• obstrukční spánková apnoe * diagnóza   terapie   MeSH
• prevalence MeSH
• rizikové faktory MeSH
• spánková deprivace komplikace   metabolismus   patologie   MeSH
• trvalý přetlak v dýchacích cestách přístrojové vybavení   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• práce podpořená grantem MeSH

Kyslík je absolútne nevyhnutný pre fungovanie živých organizmov a zmeny v jeho koncentrácii majú dramatické následky. V nádorovom tkanive zohráva kyslík významnú úlohu v produkcii energie a modulácii oxidačno-redukčnej rovnováhy. Výsledkom jeho nedostatočnej hladiny je hypoxia, ktorá predstavuje charakteristickú črtu nádorového mikroprostredia. Kľúčovým koordinátorom odpovede na hypoxiu na bunkovej úrovni je hypoxiou-indukovaný transkripčný faktor, ktorý reguluje expresiu viac ako stovky génov zapojených do významných bunkových procesov. Z klinického hľadiska sú fenotypové zmeny navodené hypoxiou veľmi závažné. Nádorová hypoxia je asociovaná s rezistenciou voči terapii, progresiou a rekurenciou ochorenia ako aj so zvýšenou mortalitou. Preto intratumorová hypoxia predstavuje vážny terapeutický problém a jej detekcia môže prispieť k zlepšeniu stratifikácie pacientov pre vhodnú terapiu. V súčasnej dobe dostupné stratégie zamerané na detekciu hypoxie v nádorovom tkanive prinášajú pomerne dosť limitácií, napr. invazívnosť, nedostupnosť tkaniva, nízku citlivosť, nepresnú interpretáciu a pod. Na druhej strane sa však ponúka využitie endogénnych markerov hypoxie, ktorých detekcia prostredníctvom imunohistochémie je pomerne ľahká, dostupná, reprodukovateľná a použiteľná nielen prospektívne, ale aj retrospektívne na archivovaných vzorkách tkanív. Patrí medzi ne napr. karbonická anhydráza IX (CA IX), ktorá v súčasnosti predstavuje jeden z prominentných indikátorov chronickej hypoxie v nádoroch. Hypoxiou-indukované proteíny (vrátane CA IX) sú zároveň aj potenciálnymi terčami protinádorovej terapie a ich praktické využitie je predmetom intenzívneho výskumu.

Oxygen is absolutely essential for correct functioning of living organisms and alterations in its concentration lead to serious consequences. In tumor tissues, oxygen plays an important role in energy production and modulation of red-ox balance. Insufficient oxygen supply within tissues results in hypoxia that is a characteristic feature of the tumor microenvironment. Hypoxia-inducible transcriptional factor represents a key executor of a cellular and molecular response to hypoxia and can activate the expression of more than hundred genes involved in various essential cellular processes. From the clinical point of view, phenotypic alterations caused by hypoxia are serious. Tumor hypoxia has been associated with resistance to therapy, disease progression and recurrence as well as increased mortality. Therefore, intratumoral hypoxia represents a clinically relevant problem, and its detection within tumors is very important for patient stratification for a suitable treatment. Currently available strategies directed towards the detection of hypoxic regions within tumor tissue suffer from numerous limitations e. g. invasiveness, inaccessibility of tumor tissue, low sensibility, inaccurate interpretation etc. On the other hand, the use of an intrinsic endogenous hypoxic marker, which can be detected through immunohistochemistry, is relatively simple, routinely available, and reproducible and can be performed on both prospective and retrospective samples. These include carbonic anhydrase IX (CA IX), one of the most strongly hypoxia-induced proteins and a prominent indicator of chronic hypoxia. Moreover, hypoxia-induced proteins (including CA IX) are also potential targets of anticancer therapy, and their practical application is a subject of intense research. Key words: hypoxia – tumor microenvironment – hypoxia-inducible factor – resistance – carbonic anhydrase IX This study was supported by European Regional Development Fund and the state budget of the Czech Republic for Regional Centre for Applied Molecular Oncology – RECAMO (CZ.1.05/2.1.00/03.0101), the project MEYS – NPS I – LO1413, European Regional Development Fund and the State Budget of the Slovak Republic (ITMS 26240220087) and the Slovak Scientific Grant Agency VEGA 2/0152/12. The authors declare they have no potential conflicts of interest concerning drugs, products, or services used in the study. The Editorial Board declares that the manuscript met the ICMJE “uniform requirements” for biomedical papers. Submitted: 27. 3. 2015 Accepted: 13. 4. 2015

• Klíčová slova
• karbonická anhydráza IX, radiorezistence,
• MeSH
• chemorezistence MeSH
• faktor 1 indukovatelný hypoxií - podjednotka alfa metabolismus   MeSH
• faktor 1 indukovatelný hypoxií * metabolismus   MeSH
• hypoxie buňky * fyziologie   účinky léků   účinky záření   MeSH
• hypoxie MeSH
• imunohistochemie MeSH
• karboanhydrasa IV analýza   MeSH
• karboanhydrasy MeSH
• lidé MeSH
• nádorové biomarkery MeSH
• nádorové mikroprostředí * fyziologie   MeSH
• nádory metabolismus   MeSH
• pozitronová emisní tomografie MeSH
• radioterapie MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• práce podpořená grantem MeSH
• přehledy MeSH

Mitochondrial NADPH-dependent isocitrate dehydrogenase, IDH2, and cytosolic IDH1, catalyze reductive carboxylation of 2-oxoglutarate. Both idh2 and idh1 monoallelic mutations are harbored in grade 2/3 gliomas, secondary glioblastomas and acute myeloid leukemia. Mutant IDH1/IDH2 enzymes were reported to form an oncometabolite r-2-hydroxyglutarate (2HG), further strengthening malignancy. We quantified CO2-dependent reductive carboxylation glutaminolysis (RCG) and CO2-independent 2HG production in HTB-126 and MDA-MB-231 breast carcinoma cells by measuring (13)C incorporation from 1-(13)C-glutamine into citrate, malate, and 2HG. For HTB-126 cells, (13)C-citrate, (13)C-malate, and (13)C-2-hydroxyglutarate were enriched by 2-, 5-, and 15-fold at 5mM glucose (2-, 2.5-, and 13-fold at 25 mM glucose), respectively, after 6 h. Such enrichment decreased by 6% with IDH1 silencing, but by 30-50% upon IDH2 silencing while cell respiration and ATP levels rose up to 150%. Unlike 2HG production RCG declined at decreasing CO2. At hypoxia (5% O2), IDH2-related and unrelated (13)C-accumulation into citrate and malate increased 1.5-2.5-fold with unchanged IDH2 expression; whereas hypoxic 2HG formation did not. (13)C-2HG originated by ∼50% from other than IDH2 or IDH1 reactions, substantiating remaining activity in IDH1&2-silenced cells. Relatively high basal (12)C-2HG levels existed (5-fold higher vs. non-tumor HTB-125 cells) and (13)C-2HG was formed despite the absence of any idh2 and idh1 mutations in HTB-126 cells. Since RCG is enhanced at hypoxia (frequent in solid tumors) and 2HG can be formed without idh1/2 mutations, we suggest 2HG as an analytic marker (in serum, urine, or biopsies) predicting malignancy of breast cancer in all patients.

• MeSH
• glutaráty metabolismus   MeSH
• hypoxie buňky fyziologie   MeSH
• isocitrátdehydrogenasa genetika   metabolismus   MeSH
• kyslík metabolismus   MeSH
• lidé MeSH
• nádorové biomarkery genetika   metabolismus   MeSH
• nádorové buněčné linie MeSH
• nádory prsu enzymologie   genetika   metabolismus   MeSH
• parciální tlak MeSH
• Check Tag
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Changes in endocrine function of adipose tissue during surgery, such as excessive production of proinflammatory cytokines, can significantly alter metabolic response to surgery and worsen its outcomes and prognosis of patients. Therapeutic hypothermia has been used to prevent damage connected with perioperative ischemia and hypoperfusion. The aim of our study was to explore the influence of deep hypothermia on systemic and local inflammation, adipose tissue hypoxia and adipocytokine production. We compared serum concentrations of proinflammatory markers (CRP, IL-6, IL-8, sIL-2R, sTNFRI, PCT) and mRNA expression of selected genes involved in inflammatory reactions (IL-6, TNF-α, MCP-1, MIF) and adaptation to hypoxia and oxidative stress (HIF1-α, MT3, GLUT1, IRS1, GPX1, BCL-2) in subcutaneous and visceral adipose tissue and in isolated adipocytes of patients undergoing cardiosurgical operation with hypothermic period. Deep hypothermia significantly delayed the onset of surgery-related systemic inflammatory response. The relative gene expression of the studied genes was not altered during the hypothermic period, but was significantly changed in six out of ten studied genes (IL-6, MCP-1, TNF-α, HIF1-α, GLUT1, GPX1) at the end of surgery. Our results show that deep hypothermia suppresses the development of systemic inflammatory response, delays the onset of local adipose tissue inflammation and thus may protect against excessive expression of proinflammatory and hypoxia-related factors in patients undergoing elective cardiac surgery procedure.

• MeSH
• cytokiny metabolismus   MeSH
• endarterektomie metody   MeSH
• hypoxie buňky fyziologie   MeSH
• lidé středního věku MeSH
• lidé MeSH
• terapeutická hypotermie * MeSH
• transkriptom MeSH
• tuková tkáň metabolismus   patofyziologie   MeSH
• zánět metabolismus   MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Cells of solid malignancies generally adapt to entire lack of oxygen. Hypoxia induces the expression of several genes, which allows the cells to survive. For DNA transcription, it is necessary that DNA structure is loosened. In addition to structural characteristics of DNA, its epigenetic alterations influence a proper DNA transcription. Since histones play a key role in epigenetics, changes in expression levels of acetylated histones H3 and H4 as well as of hypoxia-inducible factor-1α (HIF-1α) in human neuroblastoma cell lines cultivated under standard or hypoxic conditions (1% O2) were investigated. Moreover, the effect of hypoxia on the expression of two transcription factors, c-Myc and N-myc, was studied. Hypoxic stress increased levels of acetylated histones H3 and H4 in UKF-NB-3 and UKF-NB-4 neuroblastoma cells with N-myc amplification, whereas almost no changes in acetylation of these histones were found in an SK-N-AS neuroblastoma cell line, the line with diploid N-myc status. An increase in histone H4 acetylation caused by hypoxia in UKF-NB-3 and UKF-NB-4 corresponds to increased levels of N-myc transcription factor in these cells.

• MeSH
• acetylace MeSH
• histony metabolismus   MeSH
• hypoxie buňky fyziologie   MeSH
• lidé MeSH
• nádorové buněčné linie MeSH
• neuroblastom metabolismus   patologie   MeSH
• protoonkogenní proteiny c-myc biosyntéza   MeSH
• regulace genové exprese u nádorů fyziologie   MeSH
• western blotting MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Sepse je spojena s velkou morbiditou a mortalitou v intenzívní péči. Je také nejčastější příčinou syndromu multiorgánového selhání. I když máme k dispozici možnosti terapeutické podpory většiny orgánů, nejsme u cca třetiny pacientů úspěšní. V přehledu popisujeme hlavní patofyziologické mechanismy od úrovně centrálního nervového systému až k úrovni molekulárněgenetické. I když máme díky extenzívnímu výzkumu k dispozici množství poznatků, je zatím nemožné rozhodnout, zda postižení orgánů je jen nežádoucím efektem systémového procesu, nebo spíše celkovou adaptační reakcí organismu s cílem snížení bazálního metabolismu ve smyslu hibernace. Podkladem je mitochondriální dysfunkce, která je nyní považována již za nepopíratelný fakt v rozvoji orgánové dysfunkce spojené se sepsí, avšak hypotéza tzv. mitochondriálního shut-down zatím zůstává nepotvrzená. Po přehledu nejdůležitějších mechanismů a jejich kritickém zhodnocení se v poslední části věnujeme možnostem terapeutického ovlivnění se zaměřením na manipulace v oblasti dodávky kyslíku a ventilační podporu.

Sepsis in Intensive Care Unit is related with considerable morbidity and mortality. It is also the most common cause of syndrome of multiple organ failure (MOF). Despite of extensive organ support, our therapeutic efforts are not successful in approximately one third of patients. In this review we describe many pathophysiological mechanisms from central nervous system to molecular level. Taken together, due to an extensive research, we have actually large body of evidence in the field of MOF. Nevertheless, the question whether the organ involvement is only an undesirable effect of the systemic inflammation or the whole adaptive reaction of the organism with intention of basal metabolism reduction, like hibernation, remains to be resolved. Underlying mechanism is mitochondrial dysfunction, which is considered to be a proven feature of sepsis related organ dysfunction. However, mitochondrial shut down hypothesis still remains a matter of exciting discussion. After an overview of the most important mechanisms and their critical reappraisal in the last part of our review we discuss the therapeutical potential of organ support predominantly with the scope of oxygen delivery manipulation strategy and ventilatory support.

• Klíčová slova
• orgánová podpora, intenzívní péče, oxidativní stres, patofyziologie,
• MeSH
• centrální nervový systém patofyziologie   patologie   MeSH
• endokrinní systém patofyziologie   patologie   MeSH
• endotel metabolismus   patologie   MeSH
• financování organizované MeSH
• hypoxie buňky fyziologie   imunologie   účinky léků   MeSH
• jednotky intenzivní péče normy   využití   MeSH
• koagulopatie diagnóza   etiologie   MeSH
• lidé MeSH
• mechanické ventilátory využití   MeSH
• mitochondrie imunologie   metabolismus   patologie   MeSH
• multiorgánové selhání diagnóza   komplikace   terapie   MeSH
• oxid dusnatý metabolismus   škodlivé účinky   MeSH
• oxidační stres imunologie   účinky léků   MeSH
• sepse diagnóza   komplikace   terapie   MeSH
• septický šok diagnóza   komplikace   terapie   MeSH
• urgentní lékařství metody   trendy   MeSH
• Check Tag
• lidé MeSH