Monitors of the hypnotic component of anesthesia - correlation between bispectral index and cerebral state index.

BACKGROUND: The current study examines whether analysis of identical EEG data results in a high correlation coefficient of BIS and CSI values during all anesthetic levels and assesses the concordance of both EEG monitors for displaying the level of anesthesia as defined by the manufacturers. METHODS: EEG data of 40 patients undergoing elective surgery under general anesthesia with either sevoflurane/remifentanil or propofol/remifentanil were replayed to an EEG player and reanalysed by a BIS A-2000® monitor and a Cerebral State Monitor. Further, research into differences between CSI and BIS index values was performed, e.g., extraction of differences of ≥ 10 and ≥ 20 index points and of the EEG length with differing index values. RESULTS: The overall correlation coefficient was 0.68 without significant difference between propofol or sevoflurane group. In 51.8% of all recordings, both EEG monitors agreed in their classification of the anesthetic level. The number and length of differing index pairs was influenced by varying time delays of index calculation and different algorithms of index computation. CONCLUSION: In contrast to previous studies, our current approach combines the following conditions: analysis on basis of identical underlying EEG data from deep to light anesthesia, no guidance of anesthetic administration by one of the EEG-based monitors, avoidance of simultaneous EEG readings and the use of two different anesthetic regimens. Though the result of EEG analysis during anesthesia is similar with both monitors, CSI performance during propofol anesthesia was superior to sevoflurane anesthesia. Consequently, a lower agreement of classification of anesthetic levels between BIS and CSI was reached with the use of sevoflurane. Thus, CSI calculation seems not to be independent from anesthetic agent.

Time delay of electroencephalogram index calculation: analysis of cerebral state, bispectral, and Narcotrend indices using perioperatively recorded electroencephalographic signals.

BACKGROUND: Monitoring of anaesthetic depth with EEG-derived indices may detect EEG changes associated with awareness and thereby help to decrease the incidence of intraoperative awareness with postoperative recall. All currently available monitors need varying time periods to calculate a new index when reacting to changes in anaesthetic depth. The exact time delay for calculation of new index values is unknown. In a previous study, we used simulated EEG signals and found considerable time lags for the cerebral state index (Danmeter, Odense, Denmark), the bispectral index (Aspect Medical Systems Inc., Newton, MA, USA), and the Narcotrend index (MonitorTechnik, Bad Bramstedt, Germany). The aim of this study was to investigate whether the time delays observed with simulated EEG signals also applied to real EEG data. METHODS: We used perioperatively recorded EEG data from a database corresponding to the awake state, general anaesthesia, and suppression of cortical activity, respectively. After a switch from one state of consciousness to another, the time necessary for all indices to adjust the index value to the underlying input signal was measured. RESULTS: We found time delays for all indices between 24 (7) and 122 (23) s before the new state was indicated. In accordance with our previous results, these time delays were not constant and depended on the particular starting and target index value. Results were different for decreasing and increasing values. CONCLUSIONS: Our results may show a limitation of the value of electronic EEG indices in prevention of awareness with recall. Furthermore, due to different time delays for ascending and descending values, the results of pharmacodynamic studies may be influenced by this phenomenon.

[Transport of blood gas samples: is the pneumatic tube system safe?]. / Transport von Blutgasproben: Ist die Rohrpost sicher?

BACKGROUND: Transport of blood gas samples via a pneumatic tube system and subsequent analysis in the central laboratory can reduce costs and errors compared to on-site testing in the operating theatre or the intensive care unit. In this study, a modern pneumatic tube transport system was tested for its usability for this purpose. METHODS: A total of 4 consecutive blood gas samples were obtained intraoperatively from 54 different patients and sent to the central laboratory. Of these, 3 samples were transferred using the pneumatic tube system but by different methods and 1 sample was transported personally which served as a reference. The results of sample analysis concerning blood gases, electrolytes and haemoglobin were compared and examined for differences. RESULTS: No statistically significant differences could be determined between the different modes of transportation. CONCLUSION: Transport of samples for blood gas analysis via a modern pneumatic tube system is safe when samples are correctly prepared.

Gastrin induces expression and promoter activity of the vesicular monoamine transporter subtype 2.

Gastric enterochromaffin-like cells produce histamine in response to the antral hormone gastrin and accumulate the biogenic amine in secretory organelles via vesicular monoamine transporter subtype 2. The putative effects of gastrin on vesicular monoamine transporter subtype 2 expression and promoter activity are poorly understood. In the present study we used highly enriched rat enterochromaffin-like cells (purity, >90%) and rat pheochromocytoma cells stably transfected with a gastrin/cholecystokinin B receptor to investigate the expression and transcriptional regulation of vesicular monoamine transporter subtype 2. Stimulation of vesicular monoamine transporter subtype 2 mRNA and protein expression was observed in isolated enterochromaffin-like cells after 3- to 7-h incubation with gastrin (10(-7) M), forskolin (10(-5) M), or ionomycin (10(-5) M). Deletion analysis of the rat vesicular monoamine transporter subtype 2 promoter defined the minimal promoter sequence necessary for full basal activity as a -121 bp segment upstream of exon 1 containing two Sp1 sites (-97 to -88 bp and -68 to -59 bp) and a cAMP-responsive element (-44 to -35 bp). Gastrin (10(-7) M) stimulated extracellular signal related kinase1/2 phosphorylation, activated Sp1 and cAMP-responsive element-binding protein, and further induced activity of the complete rat vesicular monoamine transporter subtype 2 promoter (-800 bp) in gastrin/cholecystokinin B receptor cells. The -121-bp fragment was able to confer full gastrin responsiveness, and site-directed mutagenesis of the Sp1 and cAMP-responsive element motifs demonstrated their crucial importance for basal and inducible activities. Comparison of promoter activity of histidine decarboxylase, chromogranin A, or vesicular monoamine transporter subtype 2 in transfected cell lines revealed significant differences in basal and gastrin-stimulated activities. Our current study provides the first evidence that gastrin directly stimulates the expression and promoter activity of vesicular monoamine transporter subtype 2. Sp1 and cAMP-responsive element-binding protein recognition motifs located within 121 bp upstream of exon 1 appear to be indispensable for full basal and inducible promoter activities. Diverging effects of gastrin on histidine decarboxylase, chromogranin A, and vesicular monoamine transporter subtype 2 promoter may account for the coordinated synthesis and storage of histamine in this neuroendocrine cell type.

The mechanism of histamine secretion from gastric enterochromaffin-like cells.

Enterochromaffin-like (ECL) cells play a pivotal role in the peripheral regulation of gastric acid secretion as they respond to the functionally important gastrointestinal hormones gastrin and somatostatin and neural mediators such as pituitary adenylate cyclase-activating peptide and galanin. Gastrin is the key stimulus of histamine release from ECL cells in vivo and in vitro. Voltage-gated K(+) and Ca(2+) channels have been detected on isolated ECL cells. Exocytosis of histamine following gastrin stimulation and Ca(2+) entry across the plasma membrane is catalyzed by synaptobrevin and synaptosomal-associated protein of 25 kDa, both characterized as a soluble N-ethylmaleimide-sensitive factor attachment protein receptor protein. Histamine release occurs from different cellular pools: preexisting vacuolar histamine immediately released by Ca(2+) entry or newly synthesized histamine following induction of histidine decarboxylase (HDC) by gastrin stimulation. Histamine is synthesized by cytoplasmic HDC and accumulated in secretory vesicles by proton-histamine countertransport via the vesicular monoamine transporter subtype 2 (VMAT-2). The promoter region of HDC contains Ca(2+)-, cAMP-, and protein kinase C-responsive elements. The gene promoter for VMAT-2, however, lacks TATA boxes but contains regulatory elements for the hormones glucagon and somatostatin. Histamine secretion from ECL cells is thereby under a complex regulation of hormonal signals and can be targeted at several steps during the process of exocytosis.