Convulsions on anaesthetic induction with sevoflurane in young children

Increased worldwide use for paediatric anaesthesia of the volatile anaesthetic agent sevoflurane has mainly resulted from its low blood-gas partition coefficient and low airway irritability, providing smooth conditions for rapid induction of anaesthesia. Nevertheless, there are several clinical and experimental reports suggesting a correlation between exposure to sevoflurane and generalized clonic or tonic seizure activity. We report two clinical episodes of convulsions associated with the induction of sevoflurane anaesthesia in young children. Case 1: during induction of anaesthesia with sevoflurane by facemask in a 3-year-old healthy boy, there were symmetrical clonic seizure-like movements of the upper extremities for 60 s. Case 2: on re-induction of anaesthesia with sevoflurane because of profuse bleeding following nasal adenoidectomy in a 4-year-old healthy girl with a family history of epilepsy, there were symmetrical tonic and clonic seizure-like movements for 30-40 s in the upper and lower extremities. Both episodes ceased spontaneously. Although no EEG was recorded, it cannot be excluded that both episodes resulted from seizure activity within the CNS. Based on our observations and reports by others we suggest that, until further notice, sevoflurane should be avoided or at least used cautiously in patients where clinical epileptic activity has been verified or is strongly suspected

Apoptotic Effects of Antilymphocyte Globulins on Human Pro-inflammatory CD4+CD28− T-cells

BACKGROUND: Pro-inflammatory, cytotoxic CD4(+)CD28(-) T-cells with known defects in apoptosis have been investigated as markers of premature immuno-senescence in various immune-mediated diseases. In this study we evaluated the influence of polyclonal antilymphocyte globulins (ATG-Fresenius, ATG-F) on CD4(+)CD28(-) T-cells in vivo and in vitro. PRINCIPAL FINDINGS: Surface and intracellular three colour fluorescence activated cell sorting analyses of peripheral blood mononuclear cells from 16 consecutive transplant recipients and short-term cell lines were performed. In vivo, peripheral levels of CD3(+)CD4(+)CD28(-) T-cells decreased from 3.7 ± 7.1% before to 0 ± 0% six hours after ATG-F application (P = 0.043) in 5 ATG-F treated but not in 11 control patients (2.9 ± 2.9% vs. 3.9 ± 3.0%). In vitro, ATG-F induced apoptosis even in CD4(+)CD28(-) T-cells, which was 4.3-times higher than in CD4(+)CD28(+) T-cells. ATG-F evoked apoptosis was partially reversed by the broad-spectrum caspase inhibitor benzyloxycarbonyl (Cbz)-Val-Ala-Asp(OMe)-fluoromethylketone (zVAD-fmk) and prednisolon-21-hydrogensuccinate. ATG-F triggered CD25 expression and production of pro-inflammatory cytokines, and induced down-regulation of the type 1 chemokine receptors CXCR-3, CCR-5, CX3CR-1 and the central memory adhesion molecule CD62L predominately in CD4(+)CD28(-) T-cells. CONCLUSION: In summary, in vivo depletion of peripheral CD3(+)CD4(+)CD28(-) T-cells by ATG-F in transplant recipients was paralleled in vitro by ATG-F induced apoptosis. CD25 expression and chemokine receptor down-regulation in CD4(+)CD28(-) T-cells only partly explain the underlying mechanism

Influence of Heat Treatments on the Properties of ZnO Nanorods Prepared by Hydrothermal Synthesis

ZnO nanorods were grown on bare or SiO2-coated Si wafers by the hydrothermal method. The ZnO nanorods were annealed at 200, 400, and 600??C, respectively. The structural, optical, and electrical property variation of the ZnO nanorods with the annealing temperature was investigated by X-ray diffraction, field-emission scanning electron microscopy, photoluminescence, and current???voltage measurements. For the ZnO nanorods, compressive strain was detected, which decreased with annealing. Moreover, annealing at 600??C led to nanorod agglomeration. The ZnO nanorods annealed at 400??C exhibited the highest crystallinity