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Your search keyword '"Riegger, Günter A. J."' showing total 193 results
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193 results on '"Riegger, Günter A. J."'

23. Technical complications during veno-venous extracorporeal membrane oxygenation and their relevance predicting a system-exchange--retrospective analysis of 265 cases

Author

Lubnow, Matthias, Philipp, Alois, Foltan, Maik, Enger, Tone Bull, Lunz, Dirk, Bein, Thomas, Haneya, Assad, Schmid, Christof, Riegger, Günter A. J., Müller, Thomas, and Lehle, Karla

Subjects
Adult, Lung Diseases, Male, Critical Care and Emergency Medicine, Pulmonology, 610 Medizin, lcsh:Medicine, Hemolysis, Extracorporeal Membrane Oxygenation, Respiratory Failure, Medicine and Health Sciences, Humans, Prospective Studies, lcsh:Science, Blood Coagulation, Lung, Retrospective Studies, ddc:610, Hemostasis, Respiratory Distress Syndrome, lcsh:R, Biology and Life Sciences, Thrombosis, Middle Aged, Oxygen, Female, Vascular Resistance, Medical Devices and Equipment, lcsh:Q, Blood Gas Analysis, Respiratory Insufficiency, Research Article, Biotechnology
Abstract

OBJECTIVES: Technical complications are a known hazard in veno-venous extracorporeal membrane oxygenation (vvECMO). Identifying these complications and predictive factors indicating a developing system-exchange was the goal of the study. METHODS: Retrospective study on prospectively collected data of technical complications including 265 adult patients (Regensburg ECMO Registry, 2009-2013) with acute respiratory failure treated with vvECMO. Alterations in blood flow resistance, gas transfer capability, hemolysis, coagulation and hemostasis parameters were evaluated in conjunction with a system-exchange in all patients with at least one exchange (n = 83). RESULTS: Values presented as median (interquartile range). Patient age was 50(36-60) years, the SOFA score 11(8-14.3) and the Murray lung injury Score 3.33(3.3-3.7). Cumulative ECMO support time 3411 days, 9(6-15) days per patient. Mechanical failure of the blood pump (n = 5), MO (n = 2) or cannula (n = 1) accounted for 10% of the exchanges. Acute clot formation within the pump head (visible clots, increase in plasma free hemoglobin (frHb), serum lactate dehydrogenase (LDH), n = 13) and MO (increase in pressure drop across the MO, n = 16) required an urgent system-exchange, of which nearly 50% could be foreseen by measuring the parameters mentioned below. Reasons for an elective system-exchange were worsening of gas transfer capability (n = 10) and device-related coagulation disorders (n = 32), either local fibrinolysis in the MO due to clot formation (increased D-dimers [DD]), decreased platelet count; n = 24), or device-induced hyperfibrinolysis (increased DD, decreased fibrinogen [FG], decreased platelet count, diffuse bleeding tendency; n = 8), which could be reversed after system-exchange. Four MOs were exchanged due to suspicion of infection. CONCLUSIONS: The majority of ECMO system-exchanges could be predicted by regular inspection of the complete ECMO circuit, evaluation of gas exchange, pressure drop across the MO and laboratory parameters (DD, FG, platelets, LDH, frHb). These parameters should be monitored in the daily routine to reduce the risk of unexpected ECMO failure.

Published
2014

24. Antidiabetic treatment restores adiponectin serum levels and APPL1 expression, but does not improve adiponectin-induced vasodilation and endothelial dysfunction in Zucker diabetic fatty rats

Author

Schmid, Peter M., Resch, Markus, Schach, Christian, Birner, Christoph, Riegger, Günter A. J., Luchner, Andreas, and Endemann, Dierk H.

Subjects
ddc:610, endocrine system diseases, Endocrinology, Diabetes and Metabolism, Adiponectin, APPL1, AdipoR, eNOS, Insulin, Metformin, Diabetes mellitus type 2, 610 Medizin, nutritional and metabolic diseases, Cardiology and Cardiovascular Medicine, hormones, hormone substitutes, and hormone antagonists
Abstract

Background Adiponectin is able to induce NO-dependent vasodilation in Zucker lean (ZL) rats, but this effect is clearly alleviated in their diabetic littermates, the Zucker diabetic fatty (ZDF) rats. ZDF rats also exhibit hypoadiponectinemia and a suppressed expression of APPL1, an adaptor protein of the adiponectin receptors, in mesenteric resistance arteries. Whether an antidiabetic treatment can restore the vasodilatory effect of adiponectin and improve endothelial function in diabetes mellitus type 2 is not known. Methods During our animal experiment from week 11 to 22 in each case seven ZDF rats received an antidiabetic treatment with either insulin (ZDF+I) or metformin (ZDF+M). Six normoglycemic ZL and six untreated ZDF rats served as controls. Blood glucose was measured at least weekly and serum adiponectin levels were quantified via ELISA in week 11 and 22. The direct vasodilatory response of their isolated mesenteric resistance arteries to adiponectin as well as the endothelium-dependent and -independent function was evaluated in a small vessel myograph. Additionally, the expression of different components of the adiponectin signaling pathway in the resistance arteries was quantified by real-time RT-PCR. Results In ZDF rats a sufficient blood glucose control could only be reached by treatment with insulin, but both treatments restored the serum levels of adiponectin and the expression of APPL1 in small resistance arteries. Nevertheless, both therapies were not able to improve the vasodilatory response to adiponectin as well as endothelial function in ZDF rats. Concurrently, a downregulation of the adiponectin receptors 1 and 2 as well as endothelial NO-synthase expression was detected in insulin-treated ZDF rats. Metformin-treated ZDF rats showed a reduced expression of adiponectin receptor 2. Conclusions An antidiabetic treatment with either insulin or metformin in ZDF rats inhibits the development of hypoadiponectinemia and downregulation of APPL1 in mesenteric resistance arteries, but is not able to improve adiponectin induced vasodilation and endothelial dysfunction. This is possibly due to alterations in the expression of adiponectin receptors and eNOS.

Published
2013
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27. Association of Early Repolarization Pattern on ECG with Risk of Cardiac and All-Cause Mortality: A Population-Based Prospective Cohort Study (MONICA/KORA)

Author

Sinner, Moritz F., primary, Reinhard, Wibke, additional, Müller, Martina, additional, Beckmann, Britt-Maria, additional, Martens, Eimo, additional, Perz, Siegfried, additional, Pfeufer, Arne, additional, Winogradow, Janina, additional, Stark, Klaus, additional, Meisinger, Christa, additional, Wichmann, H.-Erich, additional, Peters, Annette, additional, Riegger, Günter A. J., additional, Steinbeck, Gerhard, additional, Hengstenberg, Christian, additional, and Kääb, Stefan, additional

Published
2010
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29. Contractile Reserve and Extent of Transmural Necrosis in the Setting of Myocardial Stunning: Comparison at Cardiac MR Imaging

Author

Bodí, Vicente, primary, Husser, Oliver, additional, Sanchis, Juan, additional, Núñez, Julio, additional, López-Lereu, María P., additional, Monmeneu, José V., additional, Mainar, Luis, additional, Chaustre, Fabian, additional, Riegger, Günter A. J., additional, Bosch, María J., additional, Chorro, Francisco J., additional, and Llácer, Angel, additional

Published
2010
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30. White Blood Cell Subtypes after STEMI: Temporal Evolution, Association with Cardiovascular Magnetic Resonance—Derived Infarct Size and Impact on Outcome

Author

Husser, Oliver, primary, Bodi, Vicente, additional, Sanchis, Juan, additional, Nunez, Julio, additional, Mainar, Luis, additional, Chorro, Francisco Javier, additional, Lopez-Lereu, Maria Pilar, additional, Monmeneu, Jose Vicente, additional, Chaustre, Fabian, additional, Forteza, Maria J., additional, Trapero, Isabel, additional, Dasi, Francisco, additional, Benet, Isabel, additional, Riegger, Günter A. J., additional, and Llacer, Angel, additional

Published
2010
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33. Apoptosis in myocardial infarction.

Author

Schunkert, Heribert, Riegger, G. A. J., Sigel, Andreas V., and Riegger, Günter A. J.

Abstract

Accumulating evidence suggests that programmed cell death plays an important role in myocardial infarction. The occurrence of programmed cell death has clearly been shown in several clinical (1,2,3) and experimental settings involving myocardial injury. Experimental data in vivo and in vitro suggest that cardiomyocytes are able to undergo apoptosis during hypoxia (4,5), hypoxia-reoxygenation (6,7), myocardial infarction (8,9), ischemia-reperfusion (10,11), and heart failure (12,13). Based on these studies the present concept of myocardial injury attributes the major portion of cell loss during cardiac ischemia and reperfusion to primary necrosis (14,15). However, based on the observation that apoptosis can be the early and predominant form of cell death in infarcted human myocardium, the possibility of apoptosis as inducer of secondary necrosis has already been raised (9,16). Thus, investigating the role of programmed cell death in myocardial infarction as well as documenting its underlying mechanisms may lead to new therapeutic strategies to prevent serious cell loss following ischemia and reperfusion. [ABSTRACT FROM AUTHOR]

Published
2000
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35. Effects of growth hormone on renal renin gene expression in normal rats and rats with myocardial infarction

Author

Kammerl, Martin C., primary, Grimm, Daniela, additional, Nabel, Caroline, additional, Schweda, Frank, additional, Bach, Matthias, additional, Fredersdorf, Sabine, additional, Piehler, Harald, additional, Holmer, Stephan R., additional, Riegger, Günter A. J., additional, Kromer, Eckhard P., additional, and Krämer, Bernhard K., additional

Published
2000
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46. Gene expression of 5-, 12-, and 15-lipoxygenases and leukotriene receptors along the rat nephron.

Author

Reinhold, Stephan W., Vitzthum, Helga, Filbeck, Thomas, Wolf, Konrad, Lattas, Christos, Riegger, Günter A. J., Kurtz, Armin, and Krämer, Bernhard K.

Subjects
KIDNEY tubules, GENE expression, LIPOXYGENASES, LEUKOTRIENES, LABORATORY rats, CYTOCHROME P-450
Abstract

The arachidonate signaling pathways comprise prostanoids formed by cyclooxygenases, EETs, and HETEs formed by cytochrome P-450 (CYP) enzymes and HETEs and leukotrienes generated by lipoxygenases. Whereas the intrarenal localization of cyclooxygenases and of some CYP enzymes along the nephron has already been determined, the localization of lipoxygenases and leukotriene-forming enzymes together with leukotriene receptors in the kidney is less clear. This study therefore aimed to determine the expression of 5-, 12-, and 15-lipoxygenases as well as the leukotriene receptors along the rat nephron. The kidneys were dissected into cortex and outer and inner medulla, and the microdissected nephron segments were collected after a collagenase digestion. mRNA abundance was determined by RT-PCR and real-time PCR. 15-LOX mRNA showed a characteristic expression pattern along the distal nephron. 12-LOX mRNA was only found in the glomerulus. Similarly, 5-LOX mRNAs together with 5-LOX-activating protein mRNAs were expressed in the glomerulus and also in the vasa recta. The leukotriene A4 hydrolase was found in all nephron segments, whereas leukotriene C4 synthase mRNA could not be found in any nephron segment. The leukotriene receptor B4 and the cysteinyl leukotriene receptor type 1 were selectively expressed in the glomerulus, whereas cysteinyl receptor type 2 was not found in any nephron segment. Our data suggest that the glomerulus is a major source and target for 5- and 12-HETE and for leukotrienes. The collecting duct system, on the other hand, appears to be a major source of 15-HETE. [ABSTRACT FROM AUTHOR]

Published
2006
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50. Association of the heart rate turbulence with classic risk stratification parameters in postmyocardial infarction patients.

Author

Jeron A, Kaiser T, Hengstenberg C, Löwel H, Riegger GAJ, Holmer S, Jeron, Andreas, Kaiser, Tanja, Hengstenberg, Christian, Löwel, Hannelore, Riegger, Günter A J, and Holmer, Stephan

Abstract

The heart rate turbulence (HRT) parameters were introduced for risk stratification of ventricular arrhythmias in postmyocardial infarction patients. However, the relationship of these parameters with other risk stratificators such as heart rate variability (HRV), repolarization parameters or left ventricular function is unknown. Furthermore, the influence of age and medication on HRT remains to be evaluated. Holter ECG's of 509 post-MI patients (1-10 years after MI) were screened for single ventricular extrasystole. In 196 patients the parameters' turbulence onset (TO) and turbulence slope (TS) could be computed. A pathological TO (>0%) and TS (<2.5 ms) was found in 58 and 54 patients, respectively. HRT was not related to gender, but was correlated with age (TS: r = 0.209, P < 0.01). No relationship was observed between QT interval, QTc interval or QT dispersion and HRT parameters. Individuals with a pathological HRT showed decreased HRV values (e.g., PNN50: 2.8 vs. 11.5; P < 0.001). Of all MI patients with systolic left ventricular dysfunction (EF < 45%, n = 46), 18 showed a pathological TO (39%) compared to 34 out of 142 patients (24%) with an EF > 45%. In contrast, the percentage of pathological HRT was not different between patients with left ventricular hypertrophy (16 out of 59, 27%) compared to patients without LVH (38 out of 133, 28%). The HRT was pathological in 14 out of 24 patients with diabetes mellitus (58%) compared to 40 out of 172 (23%) normoglycemic patients (TO: -0.6 +/- 3.1 vs. -2.5 +/- 5.5, P < 0.02). HRT was similar in patients with ss-blockers (n = 96) as in patients without ss-blockers (n = 100). In stable post-MI patients, HRT is influenced by age and left ventricular function and correlates with heart rate variability. Therapy with ss-blockers has no influence on HRT, while diabetic patients may have an increased likelihood of pathological HRT. [ABSTRACT FROM AUTHOR]

Published
2003

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