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Articles by S Braun
Total Records ( 4 ) for S Braun
  R Werdehausen , S Fazeli , S Braun , H Hermanns , F Essmann , M. W Hollmann , I Bauer and M. F. Stevens

Local anaesthetics are known to induce apoptosis in clinically relevant concentrations. Hitherto, it is unknown what determines the apoptotic potency of local anaesthetics. Therefore, we compared apoptosis induction by local anaesthetics related to their physicochemical properties in human neuronal cells.


Neuroblastoma cells (SHEP) were incubated with eight local anaesthetics, two of the ester and six of the amide types. At least, five concentrations of each local anaesthetic were evaluated. After incubation for 24 h, rates of cells in early apoptotic stages and overall cell death were evaluated by annexin V and 7-amino-actinomycin D double staining by flow cytometry. The concentrations that led to half-maximal neurotoxic effects (LD50) were calculated and compared for all local anaesthetics.


All local anaesthetics were neurotoxic in a concentration-dependent manner. All drugs induced similar rates of early apoptotic cell formation at low concentrations, whereas at high concentrations, late apoptotic or necrotic cell death predominated. Comparison of LD50 values of the different local anaesthetics resulted in the following order of apoptotic potency from high to low toxicity: tetracaine>bupivacaine>prilocaine=mepivacaine=ropivacaine>lidocaine>procaine=articaine. The toxicity correlated with octanol/buffer coefficients and also with experimental potency of the local anaesthetic, but was unrelated to the structure (ester or amide type).


All commonly used local anaesthetics induce neuronal apoptosis in clinically used concentrations. The neurotoxicity correlates with lipid solubility and thus with the conduction blocking potency of the local anaesthetic, but is independent of the chemical class (ester/amide).

  S Braun , N Gaza , R Werdehausen , H Hermanns , I Bauer , M. E Durieux , M. W Hollmann and M. F. Stevens

Ketamine has been shown to have neurotoxic properties, when administered neuraxially. The mechanism of this local toxicity is still unknown. Therefore, we investigated the mechanism of cytotoxicity in different human cell lines in vitro.


We incubated the following cell types for 24 h with increasing concentrations of S(+)-ketamine and racemic ketamine: (i) human Jurkat T-lymphoma cells overexpressing the antiapoptotic B-cell lymphoma 2 protein, (ii) cells deficient of caspase-9, caspase-8, or Fas-associated protein with death domain and parental cells, and (iii) neuroblastoma cells (SHEP). N-Methyl-d-aspartate (NMDA) receptors and caspase-3 cleavage were identified by immunoblotting. Cell viability and apoptotic cell death were evaluated flowcytometrically by Annexin V and 7-aminoactinomycin D double staining. Mitochondrial metabolic activity and caspase-3 activation were measured.


Ketamine, in a concentration-dependent manner, induced apoptosis in lymphocytes and neuroblastoma cell lines. Cell lines with alterations of the mitochondrial pathway of apoptosis were protected against ketamine-induced apoptosis, whereas alterations of the death receptor pathway did not reduce apoptosis. S(+)-Ketamine and racemic ketamine induced the same percentage of cell death in Jurkat cells, whereas in neuroblastoma cells, S(+)-ketamine was slightly less toxic.


Ketamine at millimolar concentrations induces apoptosis via the mitochondrial pathway, independent of death receptor signalling. At higher concentrations necrosis is the predominant mechanism. Less toxicity of S(+)-ketamine was observed in neuroblastoma cells, but this difference was minor and therefore unlikely to be mediated via the NMDA receptor.

  R Wessely , T Koppara , C Bradaric , M Vorpahl , S Braun , S Schulz , J Mehilli , A Schomig , A Kastrati and for the Contrast Media and Nephrotoxicity Following Coronary Revascularization by Angioplasty (CONTR

Background— No clinical trial has yet focused on contrast-mediated nephrotoxicity in patients with chronic renal failure exclusively undergoing percutaneous coronary intervention (PCI). Therefore, the aim of this study was to compare the effect of contemporary contrast media on nephrotoxicity in this high-risk patient population.

Methods and Results— This prospective, randomized, double-blind, comparative clinical trial randomly selected 939 patients with chronic renal failure undergoing coronary angiography with potential PCI to receive either the iso-osmolar contrast medium iodixanol or the low-osmolar contrast medium iomeprol. Of those 939 patients, 615 received diagnostic angiography only and were not included in the primary study analysis, but were followed up in a registry. Three hundred twenty-four patients underwent PCI, of which one-half received iodixanol or iomeprol, respectively, and were included in the primary study analysis. The primary end point was the peak increase in S-creatinine during hospitalization for PCI. Maximum increase in S-creatinine after PCI was lower than expected and thus impaired the power of the study. It was not significantly different between the 2 contrast groups (0.19±0.40 mg/dL for iodixanol and 0.21±0.34 mg/dL for iomeprol; P=0.53). Albeit contrast media-induced nephropathy rates were lower with iodixanol (22.2% compared with 27.8% for iomeprol), this difference was not statistically different (P=0.25). Subgroup analysis suggested a favorable outcome regarding nephrotoxicity in patients who received higher contrast volumes (>340 mL) in the iodixanol group (Pinteraction=0.016).

Conclusions— Routine use of iso-osmolar contrast medium is not associated with a significant reduction of nephrotoxicity compared with low-osmolar contrast medium in patients with chronic renal failure undergoing PCI. However, a positive effect was seen in the iso-osmolar contrast group for patients receiving high amounts of contrast medium, which awaits confirmation of a specifically designed randomized clinical trial.

Clinical Trial Registration— Identifier: NCT00390585

  S Braun , P. J Millett , C Yongpravat , J. D Pault , T Anstett , M. R Torry and J. E. Giphart

The clinical importance of the biceps reflection pulley (BRP), which stabilizes the long head of the biceps tendon (LHB) as it exits the joint, has been shown. However, there is controversy on the pathomechanism of injury to the BRP. The angular orientation of the LHB relative to its origin and distal course changes with joint positions and may place the BRP at risk for injury.


To measure the course of the LHB in common arm positions and to determine the shear and normal (stabilizing) force vectors as well as the excursion of the LHB.

Study Design

Descriptive laboratory study.


The LHBs of 8 fresh-frozen cadaveric shoulders were marked with arthroscopically injected microbeads and mounted in a custom-built shoulder rig. Data for neutral arm position, forward flexion, and abduction were collected in internal, neutral, and external rotation using biplane fluoroscopy. Bone and LHB position were reconstructed in 3 dimensions.


The shear component of the resulting vector was significantly higher during internal (28.4% ± 18.1%) compared with external rotation (18.9% ± 9.7%; P = .0157) and was highest in neutral arm position with internal rotation (39.2% ± 12.7%) and forward flexion with neutral rotation (36.2% ± 10.7%). The normal force vector, stabilizing the LHB, was significantly higher in abduction (55.2% ± 9.6%) compared with forward flexion (39.1% ± 12.4%; P <.0001) and neutral positions (39.1% ± 11.4%; P <.0001). The LHB excursion was significantly lower for neutral arm positions (0.7 ± 6.0 mm) compared with forward flexion (12.6 ± 8.3 mm; P <.0001) and abduction (12.0 ± 6.5 mm; P <.0001).


Increased shear load at forward flexion with internal or neutral arm rotation and internal rotation at neutral arm position may cause injury to the BRP. Additionally, a sawing mechanism caused by the 12-mm linear excursion combined with a load of the LHB through the BRP during elevation may also lead to lesions.

Clinical Relevance

Knowledge of the pathomechanisms of BRP injury may help in developing specific treatment and rehabilitation strategies as well as tests for physical examination.

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