Resections involving circumferential mucosal defects of more than five-sixths increased the likelihood of stricture formation in patients given prophylactic locoregional triamcinolone injections after esophageal ESD.

No abstract

with propofol or propofol/fentanylPurpose: To observe the changes in EEG bispectral index (BIS), 95% spectral edge frequency (95% SEF) and median frequency (MF)with haemodynamic changes to intubation during induction with propofol or propofol and 2 ~ug.l,,g -I fentanyl/v. Methods: Twenty four ASA I-II patients were randomized to receive either propofol infusion preceded by normal saline (group P, n= 12) or propofol preceded by 2/./g.kg -I fentanyl (group PF, n= 12). Intubation was performed five minutes after maintenance of BIS within 45 ---S. EEG and haemodynamic variables were recorded at before induction, and before and after intubation. Results: l-laemodynamiC responses to intubation were greater in group P than in group PF (P < 0.05). Postintubation SBP, DBP and HR increased, compared with preinduction values, more in group P than in group PE Postintubation BIS values increased from 45.5 ___ 3.5 and 44.2 ___ 4. I to 51. I ___ 4. I and 50.9 +_ 5.3 in groups P and PF, respectively, compared with preintubation values. The BIS values were not different between treatment groups before and after intubation, and 95% SEF and MF values did not increase after intubation. Conclusion: Fentanyl, 2/dg.kg -~/v, blunted the haemodynamic responses to intubation, but failed to attenuate the arousal of cerebral cortical activity. The different haemodynamic responses postintubation but similar BIS and 95% SEF changes in the two groups suggest that BIS or 95% SEF cannot predict the haemodynamic responses to intubation during anaesthesia induction with propofol and fentanyl.Objectif : Observer les alt6rations de rindex I~EG bispectral (BIS), sur la fr~quence spectrale de marge (95% SEF) et la fr&luence moyenne (FM) caus~es par les changements h~modynamiques de l'intubation pendant l'induction au propofol ou au propofol associ~ au fentanyl 2/./g.kg -i iv.M&hodes : Vingt-quatre patients ASA I -I I ont re~u al~atoirement soit une perfusion de propofol pr&~d~e de sol. phys. (groupe P, n = 12) ou de propofol pr&~d,6 de fentanyl 2 jug'kg -I (groupe PF, n = 12). On intubait cinq minutes apr& la stabilisation du BIS entre 45 _+ S. I'EEg et les variables h~modynamiques ~taient enregistr~es avant l'induction, et avant et apr~s l'intubation. R~sultats : Les r~ponses h~modynamiques ~ l'intubation &aient plus importantes dans le groupe P que dans le groupe PF (P<0,05). Apt& l'intubation, la pression art&ielle systolique et diastolique et la Fc augmentaient comparativement aux valeurs de pr~induction, mais plus dans le groupe P que dans le groupe PE Apr~s l'intubation, les valeurs du BIS augmentaient de 45 ___ 3,5 ~ 51 +__ 4. I dans le groupe Pet de 44 _+ 4, I ~ 50,9 ---5,3 dans les groupes PF comparativement aux valeurs pr&~dant l'intubation ; les valeurs SEF 95% et MF n'augmentaient pas apt& l'extubation.Conclusion : Le fentanyl 2 pg.kg-% att~nue les r~ponses h~modynamiques ~ l'intubation mais ne parvient pas att~nuer l'~veil de l'activit~ corticale c&~brale. La diff&ence des r~ponses h~modynamiques postintubation mais la similarit~ des cha...

Our results suggest additive interaction between propofol and ketamine (Groups PK0.5 and PK0.75) for achieving the hypnotic endpoints; however, ketamine did not depress the EEG variables in proportion to its hypnotic effect. The paradoxically higher BIS and 95% SEF values at the hypnotic endpoints may be due to lower propofol concentrations and/or no effect of ketamine on the EEG variables.

Purpose: Ketamine reduces endotoxin-induced production of proinflammatory cytokines, including tumour necrosis factor-α (TNF), in several types of inflammatory cells, including monocytes and macrophages. Transcription of the genes that encode production of these proinflammatory cytokines is regulated by nuclear factor-kappa B (NF-6B). Cytoplasmic B protein is activated by endotoxin (LPS) as well as by TNF, allowing B protein to migrate into the cell nucleus to activate gene transcription for these inflammatory mediators. Because NF-6B is likely involved in brain injury and inflammatory neurodegenerative disease, such as multiple sclerosis, we examined whether ketamine inhibits LPS-induced activation of NF-6B in human glioma cells in vitro and intact mouse brain cells in vivo. Methods: Endotoxin-induced NF-6B expression in both the human glioma cells in vitro and the intact mouse brain cells in vivo was determined by electrophoretic mobility shift assays (EMSA) of nuclear extracts and measurement of NF-6B expression by densitometry. Endotoxin was injected intracerebroventricularly in vivo and intact brain was harvested. Klenow fragment labeling was used to identify NF-6B protein for both the in vivo and vitro experiments.Results: Endotoxin treatment increased NF-6B expression (P < 0.05) both in vivo and vitro compared with control (untreated) cells. Ketamine suppressed endotoxin-induced neuronal NF-6B activation in a dose-dependent manner (P < 0.05, except for the 10 -5 M concentration in vitro) both in vivo and vitro.Conclusion: Ketamine inhibits endotoxin-induced NF-6B expression in brain cells in vivo and vitro and it is suggested that this may have implications in the neuroprotective effects of ketamine reported by other investigators.Objectif : La kétamine réduit la production de cytokines pro-inflammatoires induite par endotoxine, y compris le facteur nécrosant des tumeurs (TNF), dans certains types de cellules inflammatoires comprenant les monocytes et les macrophages. La transcription des gènes qui encodent la production de ces cytokines pro-inflammatoires est réglée par le facteur-kappa B nucléaire (NF-6B).La protéine cytoplasmique 6B est activée par l'endotoxine (LPS) et par le TNF et peut ainsi migrer dans le noyau cellulaire et activer la transcription génique pour ces médi-ateurs de l'inflammation. Comme le NF-6B participe probablement aux lésions cérébrales et aux maladies inflammatoires neurodégénératives, dont la sclérose en plaques, notre but était de savoir si la kétamine inhibe l'activation de NF-6B induit par LPS dans des cellules de gliome humain in vitro et dans des cellules cérébrales intactes de souris in vivo. Méthode : L'expression du NF-6B induite par endotoxine dans les cellules humaines in vitro et dans les cellules de souris in vivo a été déterminée par une étude de retardement de la mobilité électrophorétique (ERME) d'extraits nucléaires et la mesure de l'expression du NF-6B a été faite par densitométrie. L'endotoxine a été injectée dans les ventricules cérébraux in vivo et du tissu...