Klaus Wagner

Klinikum Südstadt Rostock, Rostock, Mecklenburg-Vorpommern, Germany

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Publications (9)19.39 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Primary objective was to assess whether oral analgesia with oxycodone offers superior pain relief after cesareans than patient controlled analgesia (PCA). Secondary outcomes were additional pain medication, time to first mobilization, therapeutic side effects, postoperative restrictions, overall satisfaction and costs. Randomized controlled trial at a University Hospital conduct between July 2009 and November 2009. Of the 1,112 patients, 257 met the inclusion criteria and 239 agreed to participate. Patients were randomly assigned to either receive intravenous piritramide PCA (2 mg piritramide/ml 0.9 % saline) or oral oxycodone (20 mg). Pain was assessed on a visual analog pain scale (VAS) at 2, 12, 24, 32, 40, 48 and 72 h after cesarean. No differences in VAS scores were observed within the general study population. Pain scores of oxycodone versus PCA were comparable at 24 h. Patients randomized to PCA demonstrated increased demand for rescue medication 48 h after cesarean (p = 0.057). In the PCA group, patients with previous cesarean had increased operative times, a trend towards increased VAS scores after 48 h (p = 0.081) and increased VAS scores in comparison to patients who did not have cesarean before (p = 0.044). For this subgroup, no difference was seen in the oxycodone patients (p = 0.883). General satisfaction with both treatment regimes was high. The results support the potential use of oral pain regimes and emphasis the importance of a multimodal approach to treat post-cesarean pain. Oral oxycodone is a not expensive, convenient and comparable analgesic to PCA devices with opioids after cesarean. Trial registration at clinicaltrials.gov identifier: NCT 01115101.
    Archives of Gynecology 05/2012; 286(4):859-65. · 0.91 Impact Factor
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    ABSTRACT: Erythropoietin has been shown to promote tissue regeneration after ischaemic injury in various organs. Here, we investigated whether Erythropoietin could ameliorate ischaemic spinal cord injury in the mouse and sought an underlying mechanism. Spinal cord ischaemia was developed by cross-clamping the descending thoracic aorta for 7 or 9 min. in mice. Erythropoietin (5000 IU/kg) or saline was administrated 30 min. before aortic cross-clamping. Neurological function was assessed using the paralysis score for 7 days after the operation. Spinal cords were histologically evaluated 2 and 7 days after the operation. Immunohistochemistry was used to detect CD34(+) cells and the expression of brain-derived neurotrophic factor and vascular endothelial growth factor. Each mouse exhibited either mildly impaired function or complete paralysis at day 2. Erythropoietin-treated mice with complete paralysis demonstrated significant improvement of neurological function between day 2 and 7, compared to saline-treated mice with complete paralysis. Motor neurons in erythropoietin-treated mice were more preserved at day 7 than those in saline-treated mice with complete paralysis. CD34(+) cells in the lumbar spinal cord of erythropoietin-treated mice were more abundant at day 2 than those of saline-treated mice. Brain-derived neurotrophic factor and vascular endothelial growth factor were markedly expressed in lumbar spinal cords in erythropoietin-treated mice at day 7. Erythropoietin demonstrated neuroprotective effects in the ischaemic spinal cord, improving neurological function and attenuating motor neuron loss. These effects may have been mediated by recruited CD34(+) cells, and enhanced expression of brain-derived neurotrophic factor and vascular endothelial growth factor.
    Journal of Cellular and Molecular Medicine 12/2011; 16(8):1792-802. · 4.75 Impact Factor
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    ABSTRACT: Here we report of a patient who developed a Moschcowitz-like syndrome following a desmopressin treatment of severe postpartum hemorrhage. The patient got an anaphylactic reaction after cervical ripening with dinoproston, leading to an emergency cesarean. A postpartum uterine atony with a blood loss more than 1500 ml resulted in a disseminated intravascular coagulation that was treated with mass transfusion of blood products, including platelets and factor VII. Desmopressin is used as rescue medication in situations of severe bleeding. It was given in this life-threatening situation and presumably triggered a Moschcowitz-like syndrome. Desmopressin exerts its haemostatic effect by releasing von Willebrand factor, which is elevated in pregnancy per se. This results in an increased risk of developing microthrombi, leading to a Moschcowitz-like syndrome. In conclusion, desmopressin should not be administered in pregnant patients owing to its potential risk of triggering the development of thrombotic-thrombocytopenic purpura.
    Blood coagulation & fibrinolysis: an international journal in haemostasis and thrombosis 09/2011; 22(8):749-51. · 1.25 Impact Factor
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    ABSTRACT: Matrigel promotes angiogenesis in the myocardium from ischemic injury and prevents remodelling of the left ventricle. We assessed the therapeutic efficacy of intracardiac matrigel injection and matrigel-mediated stem cell homing in a rat myocardial infarction (MI) model. Following MI, matrigel (250 μl) or phosphate-buffered solution (PBS) was delivered by intracardiac injection. Compared to the MI control group (MI-PBS), matrigel significantly improved left ventricular function (n= 11, P < 0.05) assessed by pressure-volume loops after 4 weeks. There is no significant difference in infarct size between MI-matrigel (MI-M; 21.48 ± 1.49%, n = 10) and MI-PBS hearts (20.98 ± 1.25%, n = 10). The infarct wall thickness of left ventricle is significantly higher (P < 0.01) in MI-M (0.72 ± 0.02 mm, n = 10) compared with MI-PBS (0.62 ± 0.02 mm, n = 10). MI-M hearts exhibited higher capillary density (border 130.8 ± 4.7 versus 115.4 ± 6.0, P < 0.05; vessels per high-power field [HPF; 400×], n = 6) than MI-PBS hearts. c-Kit(+) stem cells (38.3 ± 5.3 versus 25.7 ± 1.5 c-Kit(+) cells per HPF [630×], n = 5, P < 0.05) and CD34(+) cells (13.0 ± 1.51 versus 5.6 ± 0.68 CD34(+) cells per HPF [630×], n = 5, P < 0.01) were significantly more numerous in MI-M than in MI-PBS in the infarcted hearts (n = 5, P < 0.05). Intracardiac matrigel injection restores myocardial functions following MI, which may attribute to the improved recruitment of CD34(+) and c-Kit(+) stem cells.
    Journal of Cellular and Molecular Medicine 06/2011; 15(6):1310-8. · 4.75 Impact Factor
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    ABSTRACT: Organ shortage in liver transplantation has justified usage of marginal donor livers to expand the donor organ pool. The particular susceptibility of steatotic livers to I/R injury necessitates optimal preservation conditions in order to minimize preservation-reperfusion injury for successful transplantation. The effect of erythropoietin (EPO) as additive to HTK preservation solution was studied in a mouse model. Lean and steatotic livers were harvested, stored for 24 h in 4°C HTK solution containing either EPO or saline and reperfused for 2 h with 37°C Krebs-Henseleit buffer. Livers without cold storage served as sham controls. Flushing of livers upon cold storage revealed a transaminase release, which was 2- to 10-fold higher in steatotic versus lean livers. EPO was effective in reducing the enzyme release to 50% in steatotic but not in lean livers. EPO prevented cold storage-induced denudation of the endothelial lining in steatotic livers, but aggravated it in lean livers. During reperfusion, steatotic livers presented with lower oxygen consumption and higher enzyme release than lean livers. In all livers, parameters of reperfusion injury remained unaffected by EPO. Expression of UCP2 was found markedly higher in steatotic livers. After I/R, steatotic livers revealed a significant drop of UCP2, whereas expression in lean livers was only slightly affected. EPO diminished Erk phosphorylation to almost the same extent in both mouse strains. Fortification of the preservation solution by EPO ameliorates cold ischemic injury of steatotic livers and may thus be considered for use as an adjunctive agent to increase the success of transplanting steatotic livers.
    Journal of Surgical Research 11/2010; 173(1):171-9. · 2.02 Impact Factor
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    ABSTRACT: Erythropoietin (EPO) protects the myocardium from ischaemic injury and promotes beneficial remodelling. We assessed the therapeutic efficacy of intracardiac EPO injection and EPO-mediated stem cell homing in a rat myocardial infarction (MI) model. Following MI, EPO (3000 U/kg) or saline was delivered by intracardiac injection. Compared to myocardial infarction control group (MIC), EPO significantly improved left ventricular function (n =11-14, P < 0.05) and decreased right ventricular wall stress (n = 8, P < 0.05) assessed by pressure-volume loops after 6 weeks. MI-EPO hearts exhibited smaller infarction size (20.1 +/- 1.1% versus 27.8 +/- 1.2%; n = 6-8, P < 0.001) and greater capillary density (338.5 +/- 14.7 versus 259.8 +/- 9.2 vessels per mm2; n = 6-8, P < 0.001) than MIC hearts. Direct EPO injection reduced post-MI myocardial apoptosis by approximately 41% (0.27 +/- 0.03% versus 0.42 +/- 0.03%; n = 6, P= 0.005). The chemoattractant SDF-1 was up-regulated significantly assessed by quantitative realtime PCR and immunohistology. c-Kit(+) and CD34(+) stem cells were significantly more numerous in MI-EPO than in MIC at 24 hrs in peripheral blood (n = 7, P < 0.05) and 48 hrs in the infarcted hearts (n = 6, P < 0.001). Further, the mRNAs of Akt, eNOS and EPO receptor were significantly enhanced in MI-EPO hearts (n = 7, P < 0.05). Intracardiac EPO injection restores myocardial functions following MI, which may attribute to the improved early recruitment of c-Kit(+) and CD34(+) stem cells via the enhanced expression of chemoattractant SDF-1.
    Journal of Cellular and Molecular Medicine 05/2009; 13(4):664-79. · 4.75 Impact Factor
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    ABSTRACT: Systemic administration of erythropoietin (Epo) protects the myocardium from an ischemic insult and promotes beneficial remodeling. We hypothesized that intracardiac injection of Epo may exhibit cardioprotective potential with reduced systemic toxicity. Following myocardial infarction (MI), Epo was injected directly into the border of the infarction. Six weeks after an MI, we evaluated infarction size, angiogenesis, and pathologic effects of the treatment. Myocardial performance was assessed with a Forced Swim Test adapted to the study. Anti-inflammatory and cellular proliferative effects of Epo were analyzed by measuring expression of integrin-beta and CdK4 by reverse transcriptase-polymerase chain reaction (RT-PCR). The findings indicated improved cardiac status with direct Epo administration. Exercise capacity detected by the Forced Swim Test was significantly increased. There was radical reduction of absolute infarction size, ventricular dilatation, and hypertrophy in the Epo group. Integrin-beta was down-regulated and CdK4 expression was increased significantly with Epo. In conclusion, the study demonstrated that intramyocardial Epo injection, following MI, reduced inflammation, enhanced angiogenesis and proliferation, improved myocardial functions, and did not lead to intramural thrombus formation.
    Transplantation Proceedings 06/2008; 40(4):962-6. · 0.95 Impact Factor
  • Thoracic and Cardiovascular Surgeon - THORAC CARDIOVASC SURG. 01/2008; 56.
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    Journal of stem cells & regenerative medicine. 01/2007; 2(1):204.