Does femoral nerve catheter placement with stimulating catheters improve effective placement? A randomized, controlled, and observer-blinded trial.

Continuous peripheral nerve blocks offer the benefit of extended postoperative analgesia and accelerated functional recovery after major knee surgery. Conventional nerve localization is performed over a stimulating needle followed by blind insertion of the peripheral catheter. Correct catheter placement is confirmed by testing for satisfactory analgesia. Stimulating catheters offer the advantage of verifying correct placement close to the nerve during catheter placement. The aim of this randomized trial was to determine whether accurate catheter positioning under continuous stimulation accelerates the onset of sensory and motor block, improves the quality of postoperative analgesia, and enhances functional recovery. We compared femoral nerve catheters inserted under continuous stimulation with catheters that were placed using the conventional technique of blind advancement in 81 patients undergoing major knee surgery. Time of catheter placement was similar in both groups with 4 min (3/7.3; median, 25th/75th percentile) in the conventional group and 5 min (4/8.8) in the stimulating catheter group. In both groups, 42% of the catheters could be correctly placed (motor response of the patella with a current < or =0.5 mA) at first attempt. In 22 patients (58%) of the stimulating catheter group, the catheter had to be redirected 1-20 times, including 2 that could not be correctly placed within 20 min. The onset time of sensory and motor block was almost similar in both groups. There were no differences in the postoperative IV opioid consumption, and visual analog scale pain scores at rest and movement, or maximal bending and stretching of the knee joint during the 5 days after surgery. We conclude that with continuous femoral nerve blocks, blind catheter advancement is as effective as the stimulating catheter technique with respect to onset time of sensory and motor block as well as for postoperative pain reduction and functional outcome.

Stress response to tracheal intubation in patients undergoing coronary artery surgery: direct laryngoscopy versus an intubating laryngeal mask airway.

OBJECTIVE: Stress response caused by endotracheal intubation may be harmful for the coronary or cerebral circulation of high-risk patients. This study evaluated the hypothesis that tracheal intubation via an intubating laryngeal mask airway is associated with less cardiovascular and endocrine stress response than the conventional technique using direct laryngoscopy. DESIGN: Randomized, patient-blinded trial. SETTING: University department (single center). PARTICIPANTS: Eighty-six patients undergoing elective coronary artery surgery. INTERVENTION: Tracheal intubation was performed via an intubating laryngeal mask or by conventional direct laryngoscopy after standardized induction of anesthesia. MEASUREMENTS AND MAIN RESULTS: Electrocardiogram with automatic ST-segment analysis and invasive measured blood pressure were recorded continuously and blood samples to analyze norepinephrine plasma levels were taken at 4 times. Catecholamine concentrations and the pressure-rate product were analyzed by using an analysis of variance for repeated measures. In both groups, the pressure-rate product (p = 0.003) and norepinephrine concentrations (p < 0.0001) significantly decreased after induction of anesthesia. However, the fall was more marked in the patients intubated via the laryngeal mask (p = 0.031) than in patients receiving direct laryngoscopy. There were neither signs of cardiac ischemia nor major adverse events during induction of anesthesia. CONCLUSIONS: Reduction of cardiovascular and endocrine stress response associated with endotracheal intubation is more pronounced when performed via the intubating laryngeal mask. Thus, this technique can be helpful in high-risk cardiac patients.

Reciprocal inhibition of p53 and nuclear factor-kappaB transcriptional activities determines cell survival or death in neurons.

The tumor suppressor and transcription factor p53 is a key modulator of cellular stress responses, and activation of p53 precedes apoptosis in many cell types. Controversial reports exist on the role of the transcription factor nuclear factor-kappaB (NF-kappaB) in p53-mediated apoptosis, depending on the cell type and experimental conditions. Therefore, we sought to elucidate the role of NF-kappaB in p53-mediated neuron death. In cultured neurons DNA damaging compounds induced activation of p53, whereas NF-kappaB activity declined significantly. The p53 inhibitor pifithrin-alpha (PFT) preserved NF-kappaB activity and protected neurons against apoptosis. Immunoprecipitation experiments revealed enhanced p53 binding to the transcriptional cofactor p300 after induction of DNA damage, whereas binding of p300 to NF-kappaB was reduced. In contrast, PFT blocked the interaction of p53 with the cofactor, whereas NF-kappaB binding to p300 was enhanced. Most interestingly, similar results were observed after oxygen glucose deprivation in cultured neurons and in ischemic brain tissue. Ischemia-induced repression of NF-kappaB activity was prevented and brain damage was reduced by the p53 inhibitor PFT in a dose-dependent manner. It is concluded that a balanced competitive interaction of p53 and NF-kappaB with the transcriptional cofactor p300 exists in neurons. Exposure of neurons to lethal stress activates p53 and disrupts NF-kappaB binding to p300, thereby blocking NF-kappaB-mediated survival signaling. Inhibitors of p53 provide pronounced neuroprotective effects because they block p53-mediated induction of cell death and concomitantly enhance NF-kappaB-induced survival signaling.