Pollen-based quantitative reconstructions of Holocene regional vegetation cover (plant-functional types and land-cover types) in Europe suitable for climate modelling.

We present quantitative reconstructions of regional vegetation cover in north-western Europe, western Europe north of the Alps, and eastern Europe for five time windows in the Holocene [around 6k, 3k, 0.5k, 0.2k, and 0.05k calendar years before present (bp)] at a 1° × 1° spatial scale with the objective of producing vegetation descriptions suitable for climate modelling. The REVEALS model was applied on 636 pollen records from lakes and bogs to reconstruct the past cover of 25 plant taxa grouped into 10 plant-functional types and three land-cover types [evergreen trees, summer-green (deciduous) trees, and open land]. The model corrects for some of the biases in pollen percentages by using pollen productivity estimates and fall speeds of pollen, and by applying simple but robust models of pollen dispersal and deposition. The emerging patterns of tree migration and deforestation between 6k bp and modern time in the REVEALS estimates agree with our general understanding of the vegetation history of Europe based on pollen percentages. However, the degree of anthropogenic deforestation (i.e. cover of cultivated and grazing land) at 3k, 0.5k, and 0.2k bp is significantly higher than deduced from pollen percentages. This is also the case at 6k in some parts of Europe, in particular Britain and Ireland. Furthermore, the relationship between summer-green and evergreen trees, and between individual tree taxa, differs significantly when expressed as pollen percentages or as REVEALS estimates of tree cover. For instance, when Pinus is dominant over Picea as pollen percentages, Picea is dominant over Pinus as REVEALS estimates. These differences play a major role in the reconstruction of European landscapes and for the study of land cover-climate interactions, biodiversity and human resources.

Inhibitory CD200R and proapoptotic CD95/CD95L molecules on innate immunity cells are modulated by cardiac surgery.

INTRODUCTION: Cardiac surgery directly initiates a systemic inflammatory response with the activation of both cellular and humoral parts of the immune system. Exaggerated immune system activation is associated with a risk of life-threatening multi-organ dysfunction (MOD) and increased morbidity and mortality in the postoperative period. The immune system response is regulated and terminated by inhibitory mechanisms, including the regulatory membrane molecules, such as CD200R, CD95, CD95L and soluble sCD200R. METHODS: We measured the expression of CD95, CD95L, CD200R and sCD200R molecules in granulocyte and monocyte populations in blood samples of 30 patients who underwent coronary artery bypass grafting (CABG) using cardiopulmonary bypass (CPB). Samples collected before surgery, after surgery and in the postoperative period were analyzed by flow cytometry and ELISA. RESULTS: We found a significant increase in the percentage of granulocytes featuring the anti-inflammatory molecule CD200R (from 5% to 17.8%) after surgery. We presume that these cells were less susceptible to apoptosis because they rarely expressed CD95 as the CD200R(+)CD95(-) granulocyte sub-population prevailed. Only a small percentage of CD200R(+) granulocytes expressed simultaneously CD95 (from 0.5 to 2.06 %). This small population of CD200R(+)CD95(+) cells decreased expression of CD200R after surgery and, thus, was likely to be a source of increased sCD200R in serum (from 96 to 294 ng/mL). Also, the expression of CD95L on CD200R(+) granulocytes and CD95 on CD200R(+) monocytes was affected by surgery. The percentage of CD200R(+) monocytes was elevated on the 1(st) postoperative day (from 30.6 to 49.4 %) and dropped below the preoperative value on the 7(th) day after surgery (from 30.6 to 19.8 %). This population comprised mainly CD200R(+)CD95(+) monocytes in which the enhanced expression of CD95 was found. CONCLUSION: Our data show that the expression of CD200R, CD95 and CD95L was influenced by cardiac surgery and imply the role of these membrane molecules in cell regulation-inhibition and apoptosis following cardiac surgery.

Actual position of interleukin(IL)-33 in atherosclerosis and heart failure: Great Expectations or En attendant Godot?

Atherosclerosis has been recognized as an inflammatory/autoimmune disease. The long-standing low-grade inflammation which fuels its development is primarily focused on the components of the vessel wall. Originally, inflammation in atherogenesis was supposed to be driven by the pro-inflammatory Th1 cellular and cytokine immune response. On the basis of accumulating evidence, this view has been re-evaluated to include the Th17/Th1 axis which is shared by most diseases of sterile inflammation. The anti-inflammatory Th2 cellular and cytokine immune response is initiated concomitantly with the former two, the latter dampening their harmful reactions which culminate in full-blown atherosclerosis. Interleukin-33, a novel member of the IL-1 cytokine superfamily, was suggested to take part in the anti-atherogenic response by mediating the Th1-to-Th2 switch of the immune reactions. However, IL-33 is a multifaceted mediator with both pro- and anti-inflammatory activities, also called a "dual factor" or a "Janus face" interleukin. IL-33 occurs both in an extracellular (cytokine-like) and in a nuclear-bound (transcription factor-like) form, each of them performing distinct activities of their own. This review article presents the latest data relevant to IL-33's role in atherosclerosis and cardiac diseases as perceived by a cardiologist and a cardiac surgeon.

The long pentraxin PTX3: a candidate anti-inflammatory mediator in cardiac surgery.

Coronary artery bypass grafting (CABG) is performed with the use of cardiopulmonary bypass (CPB) and cardioplegic arrest (CA) of the heart. The advantage of this technique, alternatively referred to as "on-pump" surgery, resides, for the surgeon, in relatively easy access to and manipulation with the non-beating, bloodless heart. However, the advantage that is, thereby, gained by the patient is paid off by an increased susceptibility to postoperative systemic inflammatory response syndrome (SIRS). Under unfavorable conditions, the inflammatory syndrome may develop into life-threatening forms of MODS (multiple organ dysfunction syndrome) or even MOFS (multiple organ failure syndrome). Deliberate avoidance of CPB, also known as "off-pump" surgery, attenuates early postoperative inflammation throughout its trajectory of SIRS→MODS→MOFS, but, in the long run, there appears to be no substantial difference in the overall mortality rates. In the last years, our knowledge of the pathophysiology of surgical inflammation has increased considerably. Recent findings, highlighting the as yet rather obscure role of pentraxin 3 (PTX3) in these processes, are discussed in this review article.

Pentraxin 3(PTX 3): an endogenous modulator of the inflammatory response.

Inflammatory or anti-inflammatory? That is the question as far as the acute-phase response and its mediators, the pentraxins, are concerned. Only some ten years ago, the classical or short pentraxin C-reactive protein and the newly discovered long pentraxin PTX3 were considered to exert most of the detrimental effects of acute inflammation, whether microbial or sterile in origin. However, accumulating evidence suggests an at least dichotomous, context-dependent outcome attributable to the pentraxins, if not a straightforward anti-inflammatory nature of the acute-phase response. This paper is focused on the inherent effects of pentraxin 3 in inflammatory responses, mainly in coronary artery disease and in Aspergillus fumigatus infection. Both are examples of inflammatory reactions in which PTX3 is substantially involved; the former sterile, the latter infectious in origin. Apart from different inducing noxae, similarities in the pathogenesis of the two are striking. All the same, the introductory question still persists: is the ultimate impact of PTX3 in these conditions inflammatory or anti-inflammatory, paradoxical as the latter might appear? We try to provide an answer such as it emerges in the light of recent findings.

Impact of methylprednisolone in priming solution of cardiopulmonary bypass on anti-inflammatory CD163 receptor during cardiac surgery.

We evaluated the influence of methylprednisolone in cardiopulmonary bypass fluid on scavenger receptor for hemoglobin CD163 molecule expression on monocytes of patients who underwent elective coronary artery bypass grafting with cardiopulmonary bypass with either exposure to methylprednisolone present in the cardiopulmonary bypass fluid (20 patients), or without methylprednisolone in the cardiopulmonary bypass fluid (22 patients) and operated on without cardiopulmonary bypass (42 patients). The dynamics of CD163 expression was also followed in patients operated on without cardiopulmonary bypass. This study was a retrospective analysis of a comparison of two studies. The expression of CD163 was determined quantitatively by standardized flow cytometry technique. The similarities in the dynamics of CD163 monocyte expression, comparing the patients operated on with or without cardiopulmonary bypass, were found. Compared to the preoperative level, CD163 monocyte expression was significantly elevated on the 1(st) postoperative day. Monocyte CD163 expression on the 1(st) postoperative day was evidently similar in both groups of patients operated without cardiopulmonary bypass (median value of mean fluorescence intensity (MFI) 18,896; interquartile range from 27,538 to 57,711; median value of MFI 18,863; interquartile range from 16,514 to 26,559; n.s.), suggesting high reproducibility of our flow cytometric method; the monocyte CD163 expression was significantly higher (median value of MFI 37,902; interquartile range from 27,538 to 57,711) on the 1(st) postoperative day in patients exposed to methylprednisolone compared to patients without this exposure (median value of MFI 20,995; interquartile range from 16,321 to 29,623) (p<0.001). We concluded that the expression of hemoglobin scavenger receptor CD163 on monocytes of cardiac surgical patients is induced by methylprednisolone present in cardiopulmonary bypass fluid.

Interferon gamma receptor expression on granulocytes of cardiac surgical patients is modulated differently by the type of cardiopulmonary bypass used.

AIMS: To follow the IFNγ receptor expression on monocytes and granulocytes of cardiac surgical patients with respect to the type of cardiopulmonary bypass (CPB). METHODS: Expression of IFNγ receptor on monocytes and granulocytes of 26 cardiac surgical patients operated with the use of either "standard" or "miniaturised" CPB was determined by flow cytometry. RESULTS: The significant increase in IFNγ receptor expression on monocytes on the 1(st) and on the 3(rd) postoperative days was revealed in both groups of patients (p<0.001) irrespective of the type of CPB used, being non-significantly different between groups. In contrast, the expression of IFNγ on granulocytes displayed significant differences in terms of the CPB used. Whereas, in "standard" CPB patients, granulocyte INFγ receptor expression reached its maximum immediately after surgery (p<0.01), in "miniivasive" CPB patients, the peak in INFγ receptor expression was postponed to the 1(st) postoperative day (p<0.05). Statistically significantly higher IFNγ receptor expression on granulocytes was found in "standard" CPB patients (p<0.05). CONCLUSION: Compared to "miniaturised" CPB patients, the significantly higher IFNγ receptor expression on granulocytes was found in "standard" CPB patients (p<0.05) on the 1(st) postoperative day.

Interleukin-33, a novel member of the IL-1/IL-18 cytokine family, in cardiology and cardiac surgery.

Interleukin-33 is a newly recognized cytokine of the IL-1 family. Unlike its other members IL-1α, IL-1ß and IL-18, interleukin-33 induces predominantly Th2-skewed immune responses. In this context, the effects of IL-33 are mostly anti-inflammatory. However, depending on the actual cytokine and cellular milieu, IL-33 can promote both Th1 and Th2 immune reactions. Most importantly for cardiology and cardiac surgery, IL-33 has emerged to represent the as yet unknown ligand of the orphan receptor ST2. Before the advent of IL-33, the ST2 receptor, currently recognized as the soluble one of its two isoforms, was considered to be an unfavorable prognostic marker in myocardial infarction, congestive heart failure and trauma/sepsis shock patients. Now we know that IL-33, when bound to the cellular membrane-anchored ST2L isoform of the receptor, can have certain beneficial effects on the aforementioned conditions. Various forms of IL-33 interaction with the respective isoforms of its cognate receptor are discussed here. The focus is on physiological and prognostic values in cardiac patients.

Neutrophil apoptosis by Fas/FasL: harmful or advantageous in cardiac surgery?

Polymorphonuclear leukocytes or neutrophils are the main executors of cellular death, both in septic inflammation during bacterial infection and in sterile inflammation during trauma or surgery. Whereas in septic inflammation neutrophils perform a useful function to fortify the host's defense against infection, in sterile inflammation, by contrast, they contribute to unwelcome tissue damage. Regardless of the situation, activated neutrophils exhibit a prolonged lifespan and delayed apoptotic death which, under normal conditions, is a prerequisite for their natural renewal. Traditionally, delayed neutrophil apoptosis was considered to promote trauma or surgical injury. According to the results of recent studies, however surprising they may appear, the reverse might be in keeping with what happens IN VIVO. Apoptotic signaling in neutrophils could, by contrast, contribute to intrinsic protection of the host's tissues. This review article, aimed preferentially but not exclusively at the cardiac surgeon, presents some new information in support of this viewpoint, which fits in with our own observations.

[Transcription factor Egr-1 in cardiovascular biology]. / Transkripcní faktor Egr-1 v kardiovaskuláirni biologii.

The zinc finger transcription factor Egr-l plays an important role in cardiovascular biology. While binding complementary motifs on DNA in the target genes, Egr-1 either increases or decreases proteosynthesis of many proinflammatory and antiinflammatory mediators. In physiologic circumstances, these mediators support healing and regeneration of damaged tissue, mainly by conducting angioneogenesis. In pathologic circumstances these same mediators take an active part in promoting tissue injury. The participation of the transcription factor Egr-1 in the pathogenesis of atherosclerosis can be traced from the initial phases with the generation of foam cells as far as the onset of acute cardiovascular or cerebrovascular ischemic events. At the same time, transcription factor Egr-1 presents a would-be linker at the level of which converge many seemingly heterogenous atherogenic risk factors such as hyperlipidemic disorders, untoward rheologic changes of blood flow often encountered in arterial hypertension or various infectious agents, with Chlamydia pneumoniae belonging to the most deeply investigated ones. Protective effects of the known anti-atherogenic factors, such as the endogenous antiinflammatory cytokine interleukin-10 or the "pleiotropic" effects of statins can be, at least in part, explained by their inhibitory influence on the activities of the transcription factor Egr-1.

[Cardiac surgery operations and their influence on serum level of antiinflammatory cytokine interleukin-10]. / Kardiochirurgické operace a jejich vliv na sérovou hladinu protizánetového cytokinu interleukinu-10.

BACKGROUND: Cardiac surgical operation is followed by the development of inflammatory reaction. This reaction is regulated in many ways including the production of antiinflammatory cytokines such as IL-10 to avoid potentially harmful effects of inflammation. METHODS AND RESULTS: We compared serum levels of cytokines IL-10, IL-6, and IL-13 in the group of patients undergoing cardiac surgical operation using either cardiopulmonary bypass (CPB, n=17) or surged on the beating heart (n=17). We found significant elevation in the serum level of IL-10 during surgery with the peak immediately after finishing surgery in CPB patients and at the first postoperative day in non-CPB patients, respectively. There is statistically significantly higher level of IL-10 in CPB patients in comparison with non-CPB patients at the end of surgery. Serum level of IL-6 is elevated in both groups during surgery reaching maximum immediately after surgery in CPB patients and at the first postoperative day in patients without CPB, respectively. The serum levels of IL-13 are only nonsignificantly changed during operation and in postoperative period in both groups. CONCLUSIONS: The intensity of inflammatory response in CPB patients which is enhanced by massive contact activation of blood and extensive ischemia-reperfusion injury is regulated by the production of antiiflammatory IL- 10 cytokine.

[Transcription factor KLF2 (Krüppel-like factor 2) and natural defence of vascular endothelium]. / Transkripcní faktor KLF2 (Krüppel-like factor 2) a prirozená ochrana cévního endotelu.

Vascular endothelium, monocytes and T-lymphocytes belong to the key cellular populations, which take an active part in the host's defence reactions. A successful course of these reactions is determined by a meticulous control of all phases since the very first steps until final healing of all incurred wounds. Any failure of the control mechanisms may lead to the development of chronic inflammatory diseases with an autoimmune component, such as the rheumatoid arthritis or atherosclerosis. An inflammatory reaction which is already under way is regulated by anti-inflammatory cytokines. However, of equal importance is the maintenance of cellular participants of inflammatory reactions in a quiescent state while no pro-inflammatory stimuli are present. One of the most important endogenous mediators, which prevent a self-initiated activation of endothelial cells, monocytes and T-lymphocytes, is represented by the transcription factor Krüppel-like factor 2. Its impact on the mentioned cells is almost identical with the so-called pleiotropic effects of inhibitors of the enzyme HMG CoA reductase or statins. This review article offers an insight into basic preventive mechanisms exerted by KLF2, notably those related to atherosclerosis.

[Shared pathogenesis of infectious and cardiovascular diseases--year 2005's view]. / Spolecné patogenetické mechanizmy infekcních a kardiovaskulárních chorob: pohled roku 2005.

Entry of microorganisms into the blood stream provokes a decline in the contractile function of the cardiac muscle. Lipopolysaccharide of Gram-negative bacteria sets off production of pro-inflammatory cytokines including bactericidal concentrations of nitric oxide which set up the first defence line against bacteremia. At the same time, however, the performance of the cardiovascular system is negatively affected. The immediate menace resides in the occurrence of septic shock, while chronic infectious diseases that are accompanied by low-grade inflammation have been suspected to take an active part in the initiation and progression of atherosclerosis. This hypothesis, as attractive as it may appear, has not yet been accepted unequivocally. The article offers an up-to-date review of the signalling cascades which permit activation by lipopolysaccharide of the target cells. The same holds true for cellular activation by non-infectious stimuli. An emerging paradigm seems plausible that the same biologic events which serve to combat acute infection might be in the long run involved in the pathogenesis of atherosclerosis.

[The role of pentraxin 3 in the inflammatory and immune response]. / Pentraxin 3 v zánetlivé a imunitní odpovedi.

Pentraxin 3 is the first detected and so far the most important protein from the recently recognized group called the long pentraxins. The structure and function of PTX3 resembles in many aspects that of the short or classical pentraxins, i.e. C-reactive protein and the serum amyloid P component. There are, however, several important differences between the two groups of pentraxins that will be mentioned in more detail in the article. All of the above mentioned pentraxins take an acitve part in the first-line defense of the host against invading pathogenic microorganisms and in the clearance of the host's own apoptotic cells. The latter mechanism impedes the onset of destructive autoimmune reactions. A biologically relevant antipode of PTX3 is represented by TNFalpha. Physiologic course of the defense reactions depends on a closely co-ordinated activity of both peptides. In case of an unchecked or missing activity of either peptide, a disturbance in their mutual balance results in increased susceptibility of the host to conditionally pathogenic fungi or in increased damage to host's own tissues inflicted by the defense reactions. This review article deals with the physiopathologic importace of pentraxin 3 as has been gained on the basis of the most up-to-date information.

[C-reactive protein in the pathogenesis of atherosclerosis: advantage and pitfalls of the "Mainz hypothesis"]. / C-reaktivní protein v patogenezi aterosklerózy: prednosti a úskalí "Mohucské hypotézy"

C-reactive protein can be viewed as a basic marker of activity of the inflammatory response, which modulates the development and the progression of atherosclerosis including its life-threatening complications. At the same time, C-reactive protein represents an active partaker or mediator of this same inflammatory reaction. However, at the very beginning of atherosclerotic disease, C-reactive protein exerts a clear-cut antiatherogenic activity. The two aspects of CRP's function, i.e. both the pro-inflammatory and the anti-inflammatory one, respectively, stem from CRP's extent of co-operation with the complement system. From the evolutional point of view, the anti-inflammatory activity of CRP is the primary one, in that it sets stage for the host to remove foreign particles and to accelerate wound healing. The influence of well-known atherogenic risk factors converts the originally beneficial influence of CRP into pro-inflammatory and pro-atherogenic effects. This review article presents new conclusions from the "Mainz hypothesis". It shows that the primary protective action of CRP resides in its regulatory influence on the extent of activation of the complement system after the latter has been triggered by enzymatically remodeled low-density lipoproteins. In further course of atherosclerotic disease, C-reactive protein exhibits a full-blown proinflammatory activity. It can result in the progression of the primary morphologic lesions up to the development of sudden vascular events.

[Innate immunity, receptors for exogenous and endogenous danger patterns in immunopathogenesis of atherosclerosis--part II: TLR receptors, significance of genetic polymorphism of danger signals receptors]. / Pirrozená imunita, receptory pro exogenní a endogenní nebezpecné vzory v imunopatogenezi aterosklerózy II. cast. Receptory TLR, význam polymorfizmu receptoru pro nebezpecné vzory.

The most important set of receptors for danger patterns are TLR receptors. Together ten different TLR receptors were identified so far. Majority of TLR receptors is expressed on the cell surface to identify extracellulary localized danger signals. Some TLR receptors are also expressed in the intracellular compartment to identify intracellular danger signals. Receptors for danger signals display individual differences delineated by genetic polymorphism. The individual immune reactivity is developed in the context of genetic predisposition and the exposition to variable environmental factors. The differences in an individual immune reactivity are probably responsible for individual susceptibility or resistance to the development of immunopathological reactivity, which is involved in the immunopathogenesis of atherosclerosis.

[Innate immunity, receptors for exogenous and endogenous danger patterns in immunopathogenesis of atherosclerosis--part 1: identification of danger signals by innate immunity]. / Prirozená imunita, receptory pro exogenní a endogenní nebezpecné vzory v imunopatogenezi aterosklerózy I. cást: Prirozená imunita, rozlisení signálu nebezpecí.

Cellular and humoral components of innate immunity are able to identify danger signals both of the exogenous and endogenous origin. Exogenous danger signals are evolutionary conserved mosaics of danger patterns which are frequent in pathogenic microbes. Endogenous danger signals are raised during damage of self structures, by oxidative stress and/or by chemical modification of self molecules. Danger signals are identified by several families of molecules which are expressed on the surfaces of innate immunity cells. Among them the TLR receptors family which is associated with intracellular signaling pathway NF-kappaB is one of the most important. The inflammatory response is induced via activated NF-kappaB transcription factor.

Changes in metabolism and blood flow in peripheral tissue (skeletal muscle) during cardiac surgery with cardiopulmonary bypass: the biochemical microdialysis study.

The aim of this study was to monitor the metabolism and blood flow in the interstitium of the skeletal muscle during cardiac surgery with cardiopulmonary bypass (CPB) and in the early postoperative period by means of microdialysis and to compare metabolic changes during CPB at normothermia (NT) and hypothermia (HT). Surgical revascularization using CPB was performed in 50 patients, 25 patients (group HT) were operated using hypothermic CPB, 25 (group NT) using normothermic CPB. Interstitial microdialysis was performed by two CMA 60 probes (CMA Microdialysis AB, Solna, Sweden) inserted into the patient's deltoid muscle. Constituents analysed in the obtained dialysates, collected at intervals, were glucose, urea, glycerol and lactate. Tissue blood flow was monitored by dynamic microdialysis with gentamicin as a marker. In both groups, NT versus HT, similar dynamics of concentrations were found. Low initial concentrations were followed by gradual increases during CPB and in the following phase of the operation. Concentrations were higher in the NT group. Immediately after the operation, the decrease in values continued, with a gradual increase in the succeeding postoperative period in both groups. Similar dynamic changes in the lactate concentration were found in both groups. The gentamicin concentrations were lower in the NT group (versus the HT group). The results showed dynamic changes in the interstitial concentrations of glucose, urea, glycerol and lactate, which depend on the phase of the surgery in the CPB and early postoperative phase in the both groups of patients. Higher tissue perfusion of the skeletal muscle was noted in those patients operated on in normothermia. The dynamics of the concentration changes of these substances in the interstitium of the skeletal muscle has been proven to be caused by both the metabolic activity of the tissue and by the blood flow through the interstitium of the muscle.

[Interstitial microdialysis study of changes in metabolism and blood flow in skeletal muscles during cardiac surgery with normothermic and hypothermic extracorporeal circulation]. / Sledování zmen metabolismu a krevního prutoku v kosterním svalu behem srdecní operace v mimotelním obehu v normotermii a hypotermii pomocí intersticiální mikrodialýzy.

AIM: Hypoperfusion of peripheral tissues and splanchnic organs during cardiac surgery in extracorporeal circulation may lead to the origin of serious complications. The aim of the study was to monitor metabolism and blood pressure in interstital peripheral tissue, skeletal muscle, during the operation on the patient with extracorporeal circulation (ECC) in an early post-operation period by means of microdialysis. METHODS: The interstitial microdialysis is a minimally invasive method for the biochemical monitoring of metabolic changes and blood pressure in extracellular space of tissue. The substances in interstitium pass across a semipermeable membrane of the inserted microdialysis probe and may be analyzed. Microdialysis in this study was performed by means of two microdialysis probes CMA (CMA Microdialysis AB, Sweden) inserted into the deltoid muscle of the surgically treated patient. The probes were perfused by the Ringer solution at the rate of 0.3 ml/hour. The dialysates were sampled in the following intervals: beginning of the operation, beginning of ECC, end of ECC, end of the operation, two hours during the post-operation period. Standard biochemical methods were to evaluate, in the dialysates, glucose, urea, glycerol and lactate. The blood flow in the interstitium was monitored by means of dynamic microdialysis of gentamycine as a marker. Microdialysis was performed in 40 patients with ischemic heart disease, operated on in the extracorporeal circulation. In 20 patients the ECC was performed in normothermia (NT), while in the other 20 patients it was made in hypothermia (HT). RESULTS: In both groups, NT versus HT, a similar dynamism of interstitial concentration of the observed substances in relation to the operation phase and in early post-operation period. Low initial concentrations were gradually increasing during the extracorporeal circulation and increased further after the end of extracorporeal circulation and also in the subsequent phase of the operation. The concentration values of the analytes under observation were higher in the groups operated on under normothermia, apparently due to normal cellular activity during normothermia (versus values in hypothermia). Immediately after the operation the observed values decreased in the both groups and subsequently gradually increased in the post-operation period in the both groups. The trend of dynamic changes of the observed analytes, selected as compounds indicating metabolic activity of skeletal muscles during hypothermia documents a lower metabolic activity of the cells during hypothermia and its marked increase (against NT) in the phase of subsequent normalization of the tissue temperature. Analysis of the concentrations of lactate, as a compounds mapping anaerobic metabolism of skeletal muscle, revealed similar dynamic changes in the both groups (NT vs. HT). There were no significant differences, related to the phase of the operation or the phase of immediate post-operation course when the both groups were compared. The analysis of gentamycine concentrations as a flow marker revealed lower gentamycine concentrations in dialysate during the operation, ECC and the early post-operation course in the group operated on in normotheramia (vs. HT), indicating a higher tissue flow in skeletal muscle against the group of patients operated on under hypothermia. CONCLUSION: The results of the microdialysis study demonstrated dynamic changes in interstitial concentrations of the observed compounds (glucose, urea, glycerol and lactate) related to the phase of operation on the heart in extracorporeal circulation and in early post-operation period. A higher perfusion of skeletal muscle was documented in patients operated on under normothermia. It became obvious that the dynamism in the changes of the compounds observed in the interstitium of skeletal muscle was determined by metabolic activity of the tissue as well as by blood flow in the muscle interstitium.

[Frequency of occurrence of traumatic aortic rupture in automobile passengers involved in a frontal crash with a static or dynamic obstacle]. / Cetnost výskytu úrazové ruptury aorty u posádek automobilu pri celním stretu se statickou ci dynamickou protijedoucí prekázkou.

There is a lesion of aortic thoracic complex in car-passengers during the frontal clash to a static or to a dynamic antipodal obstacle is described in this study. It is a retrospective analysis. Facts were noted especially from dissectional documents. All from 298 men died. The main cause of car-passengers death was a weighty traumatic lesion of cardiovascular system in 58.7%. The aortic rupture was noted in 98 (32.9%) people, the death was in 90.8% directly on the road and 9.2% at hospital. From the whole people who were accepted to a hospital were 9 (8.9%) with a traumatic aortic rupture. But nobody of them was transported to a special center and everyone died due to traumatic lesion of cardiovascular system. Statistical significant cofactors of aortic rupture were atherosclerosis of aortic wall and intensity of clash. Therefore we can expect an aortic rupture in every third dead frontal car crash participant on a dynamic or static obstacle. Nearly 10% from men with traumatic aortic rupture were transported to a hospital. No aortic rupture was diagnosed.