Hypoxic respiratory diseases are frequently accompanied by glucose intolerance. We examined whether hypoxia is a cause of glucose intolerance in healthy subjects. In a double-blind within-subject crossover design, hypoxic versus normoxic conditions were induced in 14 healthy men for 30 minutes by decreasing oxygen saturation to 75% (versus 96% in control subjects) under the conditions of a euglycemic clamp. The rate of dextrose infusion needed to maintain stable blood glucose levels was monitored. Neurohormonal stress response was evaluated by measuring catecholamine and cortisol concentrations as well as cardiovascular parameters, and symptoms of anxiety. To differentiate between the effects of stress hormonal response, and hypoxia itself, on glucose intolerance, we performed hypoglycemic clamps as a nonspecific control. We found a significant decrease in dextrose infusion rate over a period of 150 minutes after the start of hypoxia (p < 0.01). Hypoxia also increased plasma epinephrine concentration (p < 0.01), heart rate (p < 0.01), and symptoms of anxiety (p < 0.05), whereas the other parameters remained unaffected. Glucose intolerance was closely comparable between hypoxic and hypoglycemic conditions (p < 0.9) despite clear differences in stress hormonal responses. Hypoxia acutely causes glucose intolerance. One of the factors mediating this effect could be an elevated release of epinephrine.

EIT is suitable for monitoring the dynamic effects of PEEP variations on the regional change of tidal volume. It is superior to global ventilation parameters in assessing the beginning of alveolar recruitment and lung collapse.

Background: Anesthesia per se and pneumoperitoneum during laparoscopic surgery lead to atelectasis and impairment of oxygenation. We hypothesized that a ventilation with positive end-expiratory pressure (PEEP) during general anesthesia and laparoscopic surgery leads to a more homogeneous ventilation distribution as determined by electrical impedance tomography (EIT). Furthermore, we supposed that PEEP ventilation in lung-healthy patients would improve the parameters of oxygenation and respiratory compliance. Methods: Thirty-two patients scheduled to undergo laparoscopic cholecystectomy were randomly assigned to be ventilated with ZEEP (0 cmH 2 O) or with PEEP (10 cmH 2 O) and a subsequent recruitment maneuver. Differences in regional ventilation were analyzed by the EIT-based center-of-ventilation index (COV), which quantifies the distribution of ventilation and indicates ventilation shifts. Results: Higher amount of ventilation was examined in the dorsal parts of the lungs in the PEEP group. Throughout the application of PEEP, a lower shift of ventilation was found, whereas after the induction of anesthesia, a remark-

Propofol can be quantified in expired alveolar gas. The results stress the role of marked species-specific variability.

Pulse oximetry is a well-established, noninvasive photoplethysmographic method to monitor vital signs. It allows us to measure cardiovascular parameters, such as heart rate and arterial oxygen saturation, and is considered an essential monitoring tool in clinical routine. However, since many of the conventional systems work in transmission mode, they can only be applied to the thinner or peripheral parts of the body, such as a finger tip. This has the major disadvantage that, in case of shock-induced centralization and a resulting drop in perfusion, such systems cannot ensure valid measurements. Therefore, we developed a reflective in-ear sensor system that can be worn in the ear channel like a headphone. Because the sensor is integrated in an ear mold and positioned very close to the trunk, reliable measurement is expected even in case of centralization. An additional advantage is that the sensor is comfortable to wear and has considerable resistance to motion artifacts. In this paper, we report on hypoxia studies with ten healthy participants which were performed to analyze the system with regard to the detection of heart rate and arterial oxygen saturation. It was shown earlier that, due to the high signal quality, heart rate can easily be detected. Using the conventional calculation principle, based on Beer-Lambert's law combined with a single-point calibration method, we now demonstrate that the detection of arterial oxygen saturation in the human ear canal is possible using reflective saturation sensors.

SUMMARYCardiac surgery with cardiopulmonary bypass (CPB) leads to a systemic inflammatory response with secretion of cytokines (e.g. IL-6, TNF-a , IL-1b and sIL-2R). The objective of the following study was to investigate in vitro and in vivo cytokine responses and white blood cell counts (WBC) of patients with high versus low cytokine secretion after a coronary artery bypass grafting (CABG) procedure. Twenty male patients undergoing elective CABG surgery with CPB under general anaesthesia were enrolled in the study. On the day of surgery (postoperatively), serum levels of TNF-a and IL-1b were significantly higher in patients of the high IL-6 level group compared to the respective values in the patient group with low IL-6 levels. The inter-individual differences in IL-6 release in patients undergoing CABG surgery with CPB were accompanied by differences in the release of other cytokines, such as TNF-a , IL-1b and sIL-2R. To understand whether genetic background plays a role in influencing cytokine plasma levels under surgical stress, we examined the distribution of polymorphic elements within the promoter regions of the TNF-a and IL-6 genes, and determined their genotype regarding the BAT2 gene and TNF-b intron polymorphisms. Our preliminary data suggests that regulatory polymorphisms in or near the TNF locus, more precisely the allele set 140/150 of the BAT2 microsatellite marker combined with the G allele at 2308 of the TNF-a gene, could be one of the genetic constructions providing for a less sensitive response to various stimuli. Our results suggest: (1) close relationships between cytokine release in the postoperative period, and (2) inter-individually varying patterns of cytokine release in patients undergoing CABG surgery with CPB.

Vascular endothelial growth factor (VEGF) is known to be upregulated by hypoxia in vitro. However, in vivo data about VEGF regulation in chronic hypoxic diseases are conflicting. We investigated the effects of hypoxia on plasma VEGF concentration in healthy subjects. To control known confounders, such as insulin, glucose concentrations, or exercise, hypoxic effects on VEGF were studied during experimentally clamping glucose concentrations at rest. In a double-blind crossover study design, we induced hypoxia for 30 min by decreasing oxygen saturation to 75% (vs. normoxic control) in 14 healthy men. Plasma VEGF concentration was determined at baseline, immediately after hypoxia had ended, and after a further 150 min. Levels of its soluble (s)Flt-1 receptor were assessed at baseline and at the end of the clamp. In parallel, catecholamine and cortisol levels were monitored. To investigate potential effects of glucose administration on the release of VEGF, we performed a third session, reducing glucose infusion for 30 min while serum insulin was held stable thereby inducing hypoglycemia. Hypoxia decreased VEGF levels compared with the normoxic control ( P < 0.05). VEGF concentrations increased during hypoglycemia ( P < 0.02) but were comparable to the normoglycemic control at the end of the clamp ( P > 0.80). sFlt-1 receptor concentration remained unchanged during hypoxia and hypoglycemia compared with control (both P > 0.4). Epinephrine concentration ( P < 0.01) increased upon hypoxia, whereas norepinephrine and cortisol did not change. Contrary to in vitro studies, in healthy humans hypoxia decreases plasma VEGF concentration, suggesting that systemic VEGF concentration may be differently regulated than the expression on cellular basis.

Propofol can be measured in exhaled gas from the beginning until the end of propofol anaesthesia. The different time courses of c(P)PL and c(P)G have to be considered when interpreting c(P)G.