Biomedical subjects
Publications and source records attributed to Hartmut Gehring.
To determine the impact of acute hypoxia on prohepcidin concentrations in humans, we measured concentrations of this peptide in serum collected during and after a transient period (30 min) of hypoxia and during normoxia. Prohepcidin concentrations were significantly lower 150 min after the end of hypoxia than after normoxia (p=0.028).
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Resting energy expenditure (REE) is known to be influenced by various ambient conditions such as oxygen supply. Investigations in healthy subjects during acute hypoxia revealed a drop in REE, but persistent effects after hypoxia had ended have not been examined so far. Although indirect calorimetry is a well-established method to measure REE, it may lead to false conclusions when hyperventilation, rise in lactate or catecholamines, and decrease of food intake accompany hypoxia. Therefore, we determined REE in healthy men after hypoxia had ended and under conditions of controlled energy supply during a glucose clamp. In a double-blind crossover study design, we induced hypoxia for 30 minutes by decreasing oxygen saturation to 75% (vs 96% in a control session) in 13 healthy men. Indirect calorimetry was performed at baseline and 150 minutes after hypoxia had ended. Plasma glucose was held stable between 4.5 and 5.5 mmol/L, and lactate as well as catecholamine concentrations were monitored. In parallel, we measured alterations in hormones of the hypothalamic-pituitary-thyroid axis, which is one known factor mediating changes in REE. Resting energy expenditure was decreased after hypoxia (from 1656+/-80 to 1564+/-97 kcal/d) as compared with the normoxic control condition (1700+/-82 to 1749+/-79 kcal/d, P=.037), whereas the respiratory quotient remained stable (P=.79). Plasma lactate, catecholamine levels, and the pituitary thyroid secretory activity were unchanged after hypoxia (P>.2). Our data demonstrate that the REE decrease persists 150 minutes after acute hypoxia, indicating an adaptation of energy metabolism. This should be valued as an additive pathogenic factor in diseases with disturbed energy metabolism.
BACKGROUND: Analyzing propofol concentration in expired alveolar gas (cPA) may be considered as a convenient, noninvasive method to follow the propofol concentration in plasma (cPPL). In the current study, the authors established procedures to measure cPA and cPPL for the assessment of their relation in two animal models during anesthesia. METHODS: Expired alveolar gas and mixed venous and arterial blood were simultaneously sampled during continuous application of propofol for general anesthesia to three goats and three pigs. Propofol infusion rates were varied to modify plasma concentrations. cPA, sampled cumulatively over several respiratory cycles, was quantified by thermal desorption gas chromatography-mass spectrometry. cPPL was determined using reversed phase high-performance liquid chromatography with fluorescence detection. RESULTS: cPA ranged from 0 to 1.4 and from 0 to 22 parts per billion in goats and pigs, respectively, at cPPL of 0-8 microg/ml. The relation between cPA and cPPL was linear; however, the slopes of the regression lines varied between animals. CONCLUSION: Propofol can be quantified in expired alveolar gas. The results stress the role of marked species-specific variability.
BACKGROUND: Since there is a growing use of analgesia and sedation in spontaneously breathing patients undergoing diagnostic or therapeutic interventions, recommendations by national societies of anesthesiologists call for the application of capnometry during all anesthetic procedures. METHODS: We compared readings from a transcutaneous capnometer (Tosca) and an end-tidal capnometer (Microcap Plus) to P(aCO2) measurements made via arterial-blood-gas analysis. We studied 30 spontaneously breathing patients who were recovering from general anesthesia, and we used Bland Altman analysis to compare the capnometry readings to the arterial-blood-gas values. Expiratory gas samples for end-tidal capnometry were taken either from a conventional face mask or an oral/nasal cannula. RESULTS: The Tosca significantly overestimates P(aCO2) (mean +/- SD difference 5.6 + 3.4 mm Hg). The Microcap Plus significantly underestimates P(aCO2) (mean +/- SD difference -14.1 +/- 7.4 mm Hg). There was no significant difference between the face mask and oral/nasal cannula with regard to collecting end-tidal samples. CONCLUSION: Both the Tosca and Microcap Plus provide just an approximate estimation of P(aCO2). Clinical use of these monitors can not be proposed under actual conditions but will be advantageous after correction of the limiting errors.
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.
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.
Mannitol is an osmotically active polyalcohol often present in fluids used for irrigation of exposed tissue during minimal invasive surgery. Since this polyol normally is not detected in human plasma to any significant extent, it may be used as a laboratory marker of absorption of mannitol-containing irrigative fluids during surgery. For this aim, we developed a photometric assay of mannitol in human blood or serum that may be performed in a near-patient setting. Following deproteinization of the sample with trichloroacetic acid, the supernatant is mixed with NAD+ and a commercially available preparation of mannitol 2-dehydrogenase and is incubated at pH 7.8 and at 37 degrees C for 30 to 60 minutes. At the end of the incubation period the solution is appropriately diluted and the concentration of NADH formed by oxidation of mannitol is determined photometrically at 340 nm. The limit of detection of serum mannitol with this assay is 0.05 mmol/l, the linear range of measurement extends to about 3 mmol/l. At analyte concentrations of 0.48, 1.38 and 3.48 mmol/l, coefficients of inter-assay variation of 12.1, 6.7 and 4.9%, respectively, were obtained. The analytical recovery of mannitol added to serum samples was close to 100%. Of 27 polyalcohols, monosaccharides and oligosaccharides tested, none exhibited a measurable substrate activity and only D-fructose significantly inhibited the oxidation of mannitol at sample concentrations above 10 mmol/l; the enzymatic reaction, however, was strongly affected by EDTA. The suitability of the assay as a routine diagnostic tool for detection and quantification of intraoperatively absorbed irrigation fluid was demonstrated by analyzing mannitol in serum samples obtained from 24 patients undergoing transurethral prostatectomy.
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INTRODUCTION: Motion artifact and low perfusion often lead to faulty or absent pulse oximetry readings in clinical practice. OBJECTIVE: Determine the impact of motion artifact and low perfusion on newly introduced pulse oximetry technologies during hypoxemic episodes in healthy volunteers. METHODS: Five different pulse oximeters from 4 manufacturers (the Datex Ohmeda 3900P; the Agilent; the Nellcor N-3000; the Nellcor N-395; and the Schiller OX-1, which is the European version of the Ivy SatGuard 2000 with Masimo SET) were compared with respect to their ability (separated or in combination) to provide accurate readings in the presence of motion artifact and low perfusion. Four of these oximeters represent the latest available oximetry technology, and one (the N-3000) represents a previous generation of oximeters. Oxygen saturation values (S(pO(2))) and pulse rate from the oximeters were recorded during episodes of induced hypoxemia in 10 healthy volunteers. Standardized and repeatable motion artifacts were generated by a motion machine and by having the test subject perform tapping and scratching motions. Perfusion to the finger was reduced by an inflatable balloon impinging on the brachial artery. The pulse oximetry readings from the test oximeters were compared to readings from control pulse oximeters on the unperturbed reference hand. The pulse rates from the test oximeters were compared to the electrocardiographically-measured heart rate. RESULTS: The frequency of faulty readings was increased by increasing motion interference and decreasing perfusion. The S(pO(2)) deviation was within +/- 3% of the reference reading > 95% of the time for all instruments during the control desaturation period in the absence of motion and with normal perfusion. With the combination of motion and low perfusion, the S(pO(2)) error was within +/- 3% less than 62% of the time for all oximeters tested. A significant difference in the frequency of large S(pO(2)) errors was observed only in the direct comparison of the N-395 and N-3000. The N-395 exhibited less frequent S(pO(2)) error exceeding 6% of S(pO(2)) in the combination of the most challenging situations (motion and motion with reduced perfusion). In the same situation the Datex-Ohmeda 3900P and Nellcor N-3000 showed significantly higher pulse rate errors than the other devices (Datex-Ohmeda 3900P 53% of the time and N-3000 37% of the time). CONCLUSIONS: The established model of creating motion artifact and low perfusion is capable of simulating a hierarchy of severe clinical situations. With solely motion or solely reduced perfusion the percentage of errors exceeding +/- 3% of S(pO(2)) increased by 20% and 10%, respectively, compared to the control period. Simultaneous presence of motion and reduced perfusion leads to a relative incidence of > 35% of errors > 3% of S(pO(2)) for the various oximeters. In this situation the N-3000 and the Datex-Ohmeda 3900P exhibited differences between estimated pulse rate and electrocardiographically-measured heart rate > 25 beats/min > 37% of the time.
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