EMT-led laryngeal tube vs. face-mask ventilation during cardiopulmonary resuscitation - a multicenter prospective randomized trial.

BACKGROUND: Laryngeal tube (LT) application by rescue personnel as an alternate airway during the early stages of out-of-hospital cardiac arrest (OHCA) is still subject of debate. We evaluated ease of handling and efficacy of ventilation administered by emergency medical technicians (EMTs) using LT and bag-valve-mask (BVM) during cardiopulmonary resuscitation of patients with OHCA. METHODS: An open prospective randomized multicenter study was conducted at six emergency medical services centers over 18 months. Patients in OHCA initially resuscitated by EMTs were enrolled. Ease of handling (LT insertion, tight seal) and efficacy of ventilation (chest rises visibly, no air leak) with LT and BVM were subjectively assessed by EMTs during pre-study training and by the attending emergency physician on the scene. Outcome and frequency of complications were compared. RESULTS: Of 97 eligible patients, 78 were enrolled. During pre-study training EMTs rated efficacy of ventilation with LT higher than with BVM (66.7% vs. 36.2%, p = 0.022), but efficacy of on-site ventilation did not differ between the two groups (71.4% vs. 58.5%, p = 0.686). Frequency of complications (11.4% vs. 19.5%, p = 0.961) did not differ between the two groups. CONCLUSIONS: EMTs preferred LT ventilation to BVM ventilation during pre-study training, but on-site there was no difference with regard to efficacy, ventilation safety, or outcome. The results indicate that LT ventilation by EMTs during OHCA is not superior to BVM and cannot substitute for BVM training. We assume that the main benefit of the LT is the provision of an alternative airway when BVM ventilation fails. Training in BVM ventilation remains paramount in EMT apprenticeship and cannot be substituted by LT ventilation. TRIAL REGISTRATION: ClinicalTrials.gov (NCT01718795).

Dexamethasone impairs the gastric mucosal integrity in rats treated with a cyclooxygenase-1 but not with a cyclooxygenase-2 inhibitor.

In rats, neither the cyclooxygenase-1 inhibitor SC-560 nor the cyclooxygenase-2 inhibitor rofecoxib damages the gastric mucosa. Coadministration of dexamethasone induced injury in SC-560- but not in rofecoxib-treated rats. High levels of cyclooxygenase-1 protein occurred in the gastric mucosa of control rats, with no change after administration of SC-560. In contrast, the gastric cyclooxygenase-2 protein levels were low in control rats, but increased in a time-dependent manner after administration of SC-560. Dexamethasone prevented the increase in cyclooxygenase-2 protein levels. Our findings show that inhibition of cyclooxygenase-1 upregulates cyclooxygenase-2. When the upregulation is prevented by dexamethasone, gastric damage develops, suggesting that induction of cyclooxygenase-2 represents a compensatory mechanism that counteracts the injurious effect of cyclooxygenase-1 inhibition.

Vitamin E (alpha-tocopherol) attenuates cyclo-oxygenase 2 transcription and synthesis in immortalized murine BV-2 microglia.

One of the immediate early microglial genes that are up-regulated in response to proinflammatory stimuli is cyclo-oxygenase 2 (COX-2). In the present study, we have investigated the effects of alpha-tocopherol (alpha TocH), an essential constituent of the nervous system, on the activation of COX-2 in lipopolysaccharide (LPS)-stimulated mouse BV-2 microglia. In unstimulated BV-2 cells, COX-2 mRNA and protein were almost undetectable but were strongly up-regulated in response to LPS. Activation of COX-2 protein synthesis in LPS-stimulated BV-2 cells involved activation of the extracellular-signal-regulated kinase 1/2 (ERK1/2) and p38 mitogen-activated protein kinase (MAPK) pathway and was sensitive to the protein kinase C (PKC) inhibitors staurosporine and chelerythrine, and the MAP kinase/ERK kinase 1/2 inhibitors PD98059 and U0126. Supplementation of BV-2 cells with alpha TocH before LPS stimulation resulted in pronounced up-regulation of protein phosphatase 2A (PP2A) activity, down-regulation of PKC activity, ERK1/2 phosphorylation and nuclear factor kappa B (NF kappa B) activation. As a result, COX-2 protein levels and prostaglandin E(2) production were significantly lower in alpha TocH-supplemented cells. The effects of alpha TocH on PKC activity could be reverted by calyculin A and okadaic acid, two PP inhibitors. In summary, our results suggest that alpha TocH activates microglial PP2A activity and thereby silences an LPS-activated PKC/ERK/NF kappa B signalling cascade resulting in significantly attenuated COX-2 protein synthesis. These in vitro results imply that alpha TocH could induce quiescence to pathways that are associated with acute or chronic inflammatory conditions in the central nervous system.