The effects of fenoterol inhalation after acid aspiration-induced lung injury.

BACKGROUND: Acid aspiration is a serious complication that can occur during general anesthesia. Studies show that beta-agonists have beneficial effects on lung injury. Therefore, we tested the effect of the nebulized beta-agonist fenoterol on lung variables in a rodent model of acid-induced lung injury. METHODS: In a prospective, randomized, and controlled study, we evaluated the effects of fenoterol inhalation on lung oxygenation, inflammation, and pulmonary histology in a rat model of acid-induced lung injury. Sprague-Dawley rats underwent sevoflurane anesthesia with tracheotomy and carotid catheter insertion. Lung injury was induced by instillation of 0.4 mL/kg 0.1 M hydrochloric acid. The lungs were ventilated for 6 h and randomized to receive either fenoterol inhalation 10 microg or saline inhalation, both at 15 and 180 min after acid aspiration. Mean arterial blood pressures and peak airway pressures were documented, arterial blood gases were determined at 30, 90, 180, 270, and 360 min, and postmortem histology was subsequently examined. Additionally, fenoterol concentrations in bronchoalveolar lavage fluid (BALF) and plasma were determined by liquid chromatography/tandem mass spectroscopy. After 360 min tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 were determined in the BALF, and lungs were dried for determination of the wet/dry ratio. RESULTS: Inhalation treatment with 10 microg fenoterol significantly increased oxygenation after 270 and 360 min when compared with placebo. Fenoterol-treated rats showed a significant decrease in IL-6 and TNF-alpha levels and in the wet/dry weight ratio of the lungs. The histologic appearance showed significantly less interstitial edema and leukocyte infiltration in the fenoterol group. The concentration of fenoterol was 10.3 microg/L (median) in the BALF and <1 microg/L in the plasma. CONCLUSIONS: Fenoterol inhalation improved oxygenation after 270 and 360 min, attenuated the release of TNF-alpha and IL-6, and diminished the lung edema and infiltration of polymorphonuclear leukocytes.

Hydrochloric acid aspiration increases right ventricular systolic pressure in rats.

BACKGROUND AND OBJECTIVE: Pulmonary aspiration of gastric acid is a serious complication during anaesthesia and may cause aspiration pneumonitis and adult respiratory distress syndrome. The development of pulmonary hypertension may aggravate the initial course of the aspiration pneumonitis. The authors hypothesized that acid aspiration induces an acute increase in right ventricular pressure in the rat heart. Additionally, it was hypothesized as a secondary study that endothelin levels would be increased in this rat model. METHODS: Male Sprague Dawley rats, anaesthetized with sevoflurane, underwent tracheostomy, and catheters were inserted into the carotid and right ventricle. Lung injury was induced by instillation of 0.4 ml kg(-1) 0.1 mol l(-1) HCl; a control group received the same volume of 0.9% NaCl. Rats were then ventilated for 6 hours. p(a)O2, mean arterial blood pressures and right ventricular systolic pressures were documented every 30 minutes, and arterial blood gases were measured at baseline, 30, 90, 180, 270 and 360 min. Wet/dry ratio was performed and additionally endothelin-1 levels were examined before and 180 and 360 min after aspiration. RESULTS: p(a)O2 values were lower, whereas right ventricular systolic pressures were significantly higher in the HCl group. Mortality rate was 50% after HCl aspiration, whereas 100% of the rats survived NaCl aspiration. Wet/dry ratio and endothelin-1 levels showed a significant increase after 180 and 360 min of HCl aspiration. CONCLUSION: Acid aspiration induces a significant increase in right ventricular systolic pressure and endothelin levels, and causes metabolic acidosis in this animal model.

[Implementation of a web based software for documentation and control of quality of an acute pain service]. / Die webbasierte Software im Akutschmerzdienst - Implementierung, Dokumentation und Qualitätskontrolle.

Providing an acute pain service means accumulation of a large amount of data. The alleviation of data collection, improvement of data quality and data analysis plays a pivotal role. The electronic medical record (EMR) is gaining more and more importance in this context and is continuously spreading in clinical practice. Up to now only a few commercial softwares are available that specifically fit to the needs of an acute pain service. Here we report the development and implementation of such a program (Schmerzvisite, Medlinq, Hamburg, Germany) in the acute pain service of a University Hospital.

The accuracy of jugular bulb venous monitoring in detecting cerebral ischemia in awake patients undergoing carotid endarterectomy.

To investigate the accuracy of jugular bulb venous monitoring in detecting cerebral ischemia, we performed ipsilateral jugular bulb venous monitoring in 48 patients undergoing carotid surgery under regional anesthesia. Cerebral ischemia was assumed when neurologic deterioration occurred. During carotid clamping, the maximal arterial-jugular venous oxygen content difference [AJDO2 (max)], the minimal jugular venous oxygen saturation [SjO2 (min)], the maximal arterial-jugular venous lactate content difference [AJDL (max)], the maximal lactate oxygen index [LOI (max)], and the maximal modified LOI [mLOI (max)] were determined. To quantify the selectivity of each parameter, we performed receiver operating characteristic analysis and determined the area under the curve. The cutoff points providing the highest accuracy and the corresponding sensitivity (Se) and specificity (Spec) were determined. Neurologic deterioration occurred in 12 patients. All parameters, except AJDO2 (max), showed significant ability to distinguish between ischemic and nonischemic patients. The area under the curve for AJDL (max) was 0.840, for SjO2 (min) 0.766, for LOI 0.745, for mLOI 0.748, and for AJDO2 (max) 0.672. We found cutoff points of > or =0.16 mmol/L for AJDL (max) (Se=67%; Spec=86%) and < or =55% for SjO2 (Se=75%; Spec=83%). In conclusion, the present investigation shows that AJDL, SjO2, LOI, and mLOI provide the ability to detect cerebral hypoperfusion. The highest accuracy was found for AJDL. Neither the calculation of LOI nor of mLOI showed improved results.

Early treatment with pentoxifylline reduces lung injury induced by acid aspiration in rats.

STUDY OBJECTIVES: To evaluate the effect of pentoxifylline treatment on gas exchange and mortality immediately after bilateral instillation of hydrochloric acid. DESIGN: Randomized, prospective, placebo-controlled trial. SETTING: Animal laboratory of a university hospital. SUBJECTS: Twenty-four, adult, male Sprague-Dawley rats. METHODS: Sevoflurane-anesthetized rats (n = 12 in each group) underwent tracheostomy and insertion of a cannula into a hind paw vein and the left carotid artery. All animals received volume-controlled mechanical ventilation (zero positive end-expiratory pressure; fraction of inspired oxygen, 0.21). Acute lung injury was induced by instillation of 0.4 mL/kg 0.1 mol/L hydrochloric acid. The animals were randomized into two groups. The pentoxifylline group (n = 12) received a bolus of 20 mg/kg IV pentoxifylline after aspiration, followed by a continuous infusion of 6 mg/kg/h. The placebo group (n = 12) received an equivalent volume of saline solution. Arterial blood samples were collected for blood gas analysis 15 min and 0 min prior to aspiration and 30, 90, 180, 270, and 360 min after aspiration. Hemodynamic parameters, temperature, and ECG were recorded simultaneously. The primary end point was 6 h after aspiration. All surviving rats were killed by IV administration of pentobarbital. To assess morphologic changes due to lung injury, all animals underwent CT in inspiratory hold at the end of the experiment. MEASUREMENTS AND RESULTS: No difference in baseline measurements was observed. In pentoxifylline-treated rats, Pao(2) was significantly increased (p < 0.05) at 30, 90, 180, 270, and 360 min. Mortality at 6 h was 17% in the pentoxifylline group vs 67% in the placebo group. Placebo-treated rats showed significant abnormalities in CT lung scans compared with the pentoxifylline group. CONCLUSIONS: Acid aspiration impairs gas exchange and induces hypotension. Pentoxifylline administration shortly after acid instillation results in significant alleviation of impaired oxygenation, stabilization of BP with higher heart rates, and improved survival after 6 h.

Endothelin-receptor gene-expression in rat endotoxemia.

OBJECTIVE: The reduced vascular response to endothelin-1 has focused interest onto the regulation of the endothelin-receptor subtypes ET(A) and ET(B) during severe sepsis. DESIGN AND SETTING: Prospective animal trial followed by a controlled cell culture study in the laboratory of the Department of Anesthesiology. SUBJECTS: Male Sprague-Dawley rats weighing 200-250 g, aortic vascular smooth muscle cell line A7r5. INTERVENTIONS: Rats were injected with lipopolysaccharide to induce severe experimental endotoxemia. ET(A)/ET(B) receptor gene expression was investigated by specific RNase protection assay, and abundance of tumor necrosis factor alpha was determined in the lung and kidney. Aortic vascular smooth muscle cells were incubated with the proinflammatory cytokines interleukin-1beta, tumor necrosis factor alpha, and interferon gamma or with the nitric oxide donor S-nitroso- N-acetylpenicillamine to investigate the regulation of ET(A) receptor gene expression during severe inflammation. MEASUREMENTS AND RESULTS: ET(A)/ET(B) receptor gene expression was markedly downregulated in the lung but was unchanged in the kidney during endotoxemia. ET(A) receptor gene expression was downregulated in aortic vascular smooth muscle cells by tumor necrosis factor alpha but not by interleukin 1beta, interferon gamma, or nitric oxide. In vivo there seems to be a correlation between the tissue concentration of tumor necrosis factor alpha and gene expression of ET(A) receptors in the lung and kidney. CONCLUSIONS: Our data show that sepsis causes downregulation of ET(A) receptors at the level of gene expression, and provide correlative evidence that this effect can be mediated by tumor necrosis factor alpha. This downregulation of ET(A) receptors possibly contributes to the attenuated vascular response to endothelin-1 in the pulmonary circulation.

Convective air warming is more effective than resistive heating in an experimental model with a water dummy.

Trauma patients with accidental hypothermia have adverse outcomes when compared with normothermic patients. Studies with a small number of mild hypothermic volunteers suggested that convective warming is more effective than warming with 12 volt resistive heating blankets. In a laboratory study, we compared the warming effectiveness of two electric blankets and convective air warming. The average speed of convective rewarming during anaesthesia in patients is approximately 0.6 degree C per hour. Accordingly, calibration of the dummy was performed with increasing amounts of water during convective warming until we reached a temperature gain of 0.6 degree C per hour. The following warming experiments were performed: 12 volt electric warming blanket (SH6012, Hella); 12 volt electric warming blanket (Thermamed, whole-body blanket); convective air warming (Warm Touch, Mallinckrodt, whole-body blanket). Each experiment was repeated four times. The temperature development was measured and recorded online. Convective warming increased the dummy temperature 0.6 degree C per hour, Thermamed 0.3 degree C per hour (P<0.001 versus convective warming) and two Hella blankets 0.2 degree C per hour (P<0.001 versus convective warming). Our laboratory investigation confirmed the superiority of convective warming over resistive heating. Efforts should be made to incorporate convective warming into the out-of-hospital treatment of trauma patients.

Accuracy of cerebral monitoring in detecting cerebral ischemia during carotid endarterectomy: a comparison of transcranial Doppler sonography, near-infrared spectroscopy, stump pressure, and somatosensory evoked potentials.

BACKGROUND: This study compares the accuracy of cerebral monitoring systems in detecting cerebral ischemia during carotid endarterectomy. METHODS: The authors compared transcranial Doppler sonography (TCD), near-infrared spectroscopy (NIRS), stump pressure (SP) measurement, and somatosensory evoked potentials (SEP) in 48 patients undergoing carotid surgery during regional anesthesia. Cerebral ischemia was assumed when neurologic deterioration occurred. During clamping, the minimum mean middle cerebral artery velocity (TCD(min)), its percentage change (TCD%), the minimum regional saturation of oxygen (NIRS(min)), its percentage change (NIRS%), the mean SP, and the changes of SEP amplitude were recorded. To analyze the corresponding sensitivity and specificity of each parameter, the authors performed receiver operating characteristic analysis. RESULTS: Neurologic deterioration occurred in 12 patients. SP and NIRS were successfully performed in all patients. TCD monitoring was not possible in 10 (21%); SEP was not possible in 2 patients (4%). All parameters provided the ability to distinguish between ischemic and nonischemic patients. TCD% and NIRS% showed significantly better discrimination than TCD(min) and NIRS(min) (P < 0.05). The highest area under the curve (AUC) was found for TCD% (AUC = 0.973), but there was no significant difference compared with NIRS% (AUC = 0.905) and SP (AUC = 0.925). The lowest AUC was found for SEP (AUC = 0.749), which was significantly lower than that for TCD%, NIRS%, and SP. CONCLUSIONS: TCD%, NIRS%, and SP measurement provide similar accuracy for the detection of cerebral ischemia during carotid surgery. Lower accuracy was found for SEP monitoring. Because of the high rate of technical difficulties (21%), TCD monitoring was the least practical of the investigated monitoring devices.

A new pumpless extracorporeal interventional lung assist in critical hypoxemia/hypercapnia.

OBJECTIVE: Pump-driven extracorporeal gas exchange systems have been advocated in patients suffering from severe acute respiratory distress syndrome who are at risk for life-threatening hypoxemia and/or hypercapnia. This requires extended technical and staff support. DESIGN: We report retrospectively our experience with a new pumpless extracorporeal interventional lung assist (iLA) establishing an arteriovenous shunt as the driving pressure. SETTING: University hospital. PATIENTS: Ninety patients with acute respiratory distress syndrome. INTERVENTIONS: Interventional lung assist was inserted in 90 patients with acute respiratory distress syndrome. MEASUREMENTS AND MAIN RESULTS: Oxygenation improvement, carbon dioxide elimination, hemodynamic variables, and the amount of vasopressor substitution were reported before, 2 hrs after, and 24 hrs after implementation of the system. Interventional lung assist led to an acute and moderate increase in arterial oxygenation (Pao2/Fio2 ratio 2 hrs after initiation of iLA [median and interquartile range], 82 mm Hg [64-103]) compared with pre-iLA (58 mm Hg [47-78], p < .05). Oxygenation continued to improve for 24 hrs after implementation (101 mm Hg [74-142], p < .05). Hypercapnia was promptly and markedly reversed by iLA within 2 hrs (Paco2, 36 mm Hg [30-44]) in comparison with before (60 mm Hg [48-80], p < .05], which allowed a less aggressive ventilation. For hemodynamic stability, all patients received continuous norepinephrine infusion. The incidence of complications was 24.4%, mostly due to ischemia in a lower limb. Thirty-seven of 90 patients survived, creating a lower mortality rate than expected from the Sequential Organ Failure Assessment score. CONCLUSIONS: Interventional lung assist might provide a sufficient rescue measure with easy handling properties and low cost in patients with severe acute respiratory distress syndrome and persistent hypoxia/hypercapnia.

The correlation of the Narcotrend Index and classical electroencephalographic parameters with endtidal desflurane concentrations and hemodynamic parameters in different age groups.

BACKGROUND: The Narcotrend Index (NI) for assessment of depth of anesthesia by analysis of the electroencephalogram (EEG), is potentially a pharmacodynamic measure of the effects of desflurane on the brain. METHODS: In this prospective study of 30 pediatric and adult patients (group 1: 3-6 years, n = 10; group 2: > 6 < 12 years; group 3: 12-40 years), undergoing ophthalmological surgery, we investigated the pharmacodynamic relationship between nonsteady state endtidal desflurane concentrations (eT(Des)), NI, classical EEG parameters (cEEG), heart rate (HR) and mean arterial pressure (MAP). The performance of the Narcotrend for differentiation between consciousness and unconsciousness was evaluated using prediction probability (P(K)). RESULTS: Spearman correlation analysis showed significant negative correlations (P < 0.001) between eT(Des) and NI (group 1: r = -0.93, group 2: r = -0.86, group 3: r = -0.66). Correlations between eT(Des) and MAP or HR were either only weak negative (r < -0.5) or not significant. Desflurane EC(50) (eT(Des) with half maximal effect on NI) was 7.18% for group 1, 7.34% for group 2, and 4.15% for group 3 (P < 0.001 Vs groups 1 and 2). Overall awake NI values (96.7 +/- 1.4) were significantly higher (P < 0.001) than at the moment of loss of consciousness (58.3 +/- 17.5), with no overlap (P(K) 1.0), whereas P(K) values for cEEG, MAP and HR were all <0.85. CONCLUSIONS: The pharmacodynamic relationship between eT(Des) and NI is age dependent with a significantly higher EC(50) in children than in adolescents and adults. The NI appears to be superior to cEEG, MAP and HR in differentiating consciousness from unconsciousness.

The correlation of the Narcotrend Index with endtidal sevoflurane concentrations and hemodynamic parameters in children.

BACKGROUND: The Narcotrend Index (NI) of anesthetic depth is potentially a pharmacodynamic measure of the effects of sevoflurane on the brain. METHODS: In this prospective observational study of 30 pediatric surgical patients (1-11 years), we investigated the correlation between nonsteady-state endtidal sevoflurane (eT(Sevo)), NI, mean arterial pressure (MAP), and heart rate (HR). The performance of the Narcotrend for differentiation between consciousness and unconsciousness was evaluated using prediction probability (P(K)). RESULTS: Spearman correlation analysis showed significant correlations (P < 0.01) between eT(Sevo) and NI (r = -0.85) and MAP (r = -0.43). P(K)-values for differentiation between consciousness and unconsciousness were 1.0 for NI and <0.85 for MAP and HR. During the surgical procedure, NI-values showed a constant rise with each 0.5% step of lowering eT(Sevo) (P < 0.03), whereas MAP remained unaltered and HR showed a constant decline (P < 0.03), except between 1.5 and 1%. CONCLUSIONS: In children, nonsteady-state eT(Sevo) concentrations are more closely related with NI than with MAP or HR. In this study, only NI reliably differentiated consciousness from unconsciousness.

Interhospital transport: transport of critically ill patients.

Primary emergency medicine systems in developed countries are well organized. Besides this primary system a secondary interhospital transport system has been developed in the past decade. The need for this system is expected to increase in the future following dramatic changes in the organization of the medical health system. This article outlines the current status of these secondary interhospital transfer systems, their components, possibilities, advantages or disadvantages, and the actual literature. Surprisingly, the available scientific data on these cost-intensive and highly developed systems are quite insufficient.

Cytokines down-regulate alpha1-adrenergic receptor expression during endotoxemia.

OBJECTIVE: The reduced pressure response to norepinephrine in septic patients has directed our interest to the regulation of alpha1-adrenergic receptors in vitro and in vivo during conditions mimicking acute sepsis. DESIGN: Prospective animal trial followed by a controlled cell culture study. SETTING: Laboratory of the Department of Anesthesiology. SUBJECTS: Male Sprague-Dawley rats weighing 200 to 250 g and a mesangial cell line. INTERVENTIONS: Experimental endotoxemia was induced in rats with lipopolysaccharide, and blood pressure dose-response studies with norepinephrine were performed. Alpha1-receptor gene expression was determined in various organs by a specific RNase protection assay, and tissue concentrations of the proinflammatory cytokines interleukin-1beta and tumor necrosis factor-alpha were measured. Rat renal mesangial cells were incubated with these cytokines or with nitric oxide donors to investigate the regulation of alpha1-adrenergic receptors during severe inflammation on a cellular level. MEASUREMENTS AND MAIN RESULTS: The pressor effect of norepinephrine was markedly diminished during endotoxemia. The animals showed down-regulated mRNA levels of alpha1A-, alpha1B- and alpha1D-receptors in all organs investigated, and the tissue concentrations of interleukin-1beta and tumor necrosis factor-alpha were highly increased during experimental endotoxemia. Incubation of cultured rat renal mesangial cells with the cytokines resulted in diminished alpha -receptor gene expression and [3H]prazosin binding capacity, whereas incubation of the cells with nitric oxide donors did not affect alpha1B-receptor expression. In line, blocking of cytokine-induced nitric oxide synthesis by coincubation of mesangial cells with N(G)-nitro-L-arginine methyl ester did not influence cytokine-induced down-regulation of alpha1B-receptors. CONCLUSIONS: Our data show that endotoxemia causes a systemic down-regulation of alpha1-receptors on the level of gene expression and suggest that this effect is likely mediated by proinflammatory cytokines in a synergistic but nitric oxide-independent fashion. We propose that this down-regulation of alpha1-adrenergic receptors contributes to the attenuated blood pressure response to norepinephrine and, therefore, to septic circulatory failure in patients.

Cytokine-mediated downregulation of vasopressin V(1A) receptors during acute endotoxemia in rats.

The reduced pressure response to vasopressin during acute sepsis has directed our interest to the regulation of vasopressin V(1A) receptors. Rats were injected with lipopolysaccharide for induction of experimental gram-negative sepsis. V(1A) receptor gene expression was downregulated in the liver, lung, kidney, and heart during endotoxemia. Inasmuch as the concentrations of proinflammatory cytokines such as interleukin-1beta, tumor necrosis factor-alpha, and interferon-gamma were highly increased during sepsis, the influence of these cytokines on V(1A) receptor expression was investigated in primary cultures of hepatocytes and in the aortic vascular smooth muscle cell line A7r5. V(1A) receptor expression was downregulated by the cytokines in a nitric oxide-independent manner. Blood pressure dose-response studies after injection of endotoxin showed a diminished responsiveness to the selective V(1) receptor agonist Phe(2),Ile(3),Orn(8)-vasopressin. Our data show that sepsis causes a downregulation of V(1A) receptors and suggest that this effect is likely mediated by proinflammatory cytokines. We propose that this downregulation of V(1A) receptors contributes to the attenuated responsiveness of blood pressure in response to vasopressin and, therefore, contributes to the circulatory failure in septic shock.

Evaluation of the Alaris Auditory Evoked Potential Index as an indicator of anesthetic depth in preschool children during induction of anesthesia with sevoflurane and remifentanil.

BACKGROUND: Autoregressive modeling with exogenous input of middle latency auditory evoked potentials (A-Line autoregressive index [AAI]) has been proposed for monitoring depth of anesthesia in adults. The aim of this study was to evaluate the performance of the AAI during induction of anesthesia with sevoflurane and remifentanil in pediatric patients. METHODS: Twenty preschool children were anesthetized with sevoflurane and remifentanil. AAI, heart rate, and mean arterial pressure were compared for their ability to distinguish between different hypnotic states before inhalation induction and during sevoflurane anesthesia with and without remifentanil infusion. The prediction probability was calculated for discrimination between the predefined case milestones Awake, Spontaneous Eye Closure, and insertion of a laryngeal mask airway during general anesthesia (Laryngeal Mask Insertion). RESULTS: The AAI (mean +/- SD) in Awake children was 79 +/- 10, declining to 59 +/- 22 at Spontaneous Eye Closure and 34 +/- 13 when anesthetized. AAI values significantly overlapped between anesthetic states. For the AAI, the prediction probabilities regarding the ability to discriminate the hypnotic state at the case milestones Awake versus Spontaneous Eye Closure and Awake versus Laryngeal Mask Insertion were 0.77 and 0.99, respectively. In terms of prediction probability values, heart rate and mean arterial pressure were not indicative for anesthetic states. Remifentanil did not influence the AAI. CONCLUSION: During induction of pediatric patients with sevoflurane, the AAI is of higher value in predicting anesthetic states than hemodynamic variables and reliably differentiates between the awake and anesthetized states. However, individual AAI values demonstrate significant variability and overlap between different clinical conditions.

Mild hyperthermia down-regulates receptor-dependent neutrophil function.

Mild hypothermia impairs resistance to infection and, reportedly, impairs phagocytosis and oxidative killing of unopsonized bacteria. We evaluated various functions at 33 degrees-41 degrees C in neutrophils taken from volunteers. Adhesion on endothelial cells was determined using light microscopy. Adhesion molecule expression and receptors, phagocytosis, and release of reactive oxidants were assessed using flow cytometric assays. Adhesion protein CD11b expression on resting neutrophils was temperature-independent. However, up-regulation of CD11b with tumor necrosis factor (TNF)-alpha was increased by hypothermia and decreased with hyperthermia. Neutrophil adhesion to either resting or activated endothelial cells was not temperature-dependent. Bacterial uptake was inversely related to temperature, more so with Escherichia coli than Staphylococcus aureus. Temperature dependence of phagocytosis occurred only wi thopsonized bacteria. Hypothermia slightly increased N-formyl-L-methionyl-L-leucyl-phenylalanine receptors on neutrophils: hyperthermia decreased expression, especially with TNF-alpha. N-formyl-L-methionyl-L-leucyl-phenylalanine-induced H2O2 production was inversely related to temperature, especially in the presence of TNF-alpha. Conversely, phorbol-13-myristate-12-acetate, an activator of protein kinase C, induced an extreme and homogenous release of reactive oxidants that increased with temperature. In contrast to nonreceptor-dependent phagocytosis and oxidative killing, several crucial receptor-dependent neutrophil activities show temperature-dependent regulation, with hypothermia increasing function. The temperature dependence of neutrophil function is thus more complicated than previously appreciated.

In vivo uptake and elimination of isoflurane by different membrane oxygenators during cardiopulmonary bypass.

BACKGROUND: Volatile anesthetics are frequently used during cardiopulmonary bypass (CPB) to maintain anesthesia. Uptake and elimination of the volatile agent are dependent on the composition of the oxygenator. This study was designed to evaluate whether the in vivo uptake and elimination of isoflurane differs between microporous membrane oxygenators containing a conventional polypropylene (PPL) membrane and oxygenators with a new poly-(4-methyl-1-pentene) (PMP) membrane measuring isoflurane concentrations in blood. METHODS: Twenty-four patients undergoing elective coronary bypass surgery with the aid of CPB were randomly allocated to one of four groups, using either one of two different PPL-membrane oxygenators for CPB or one of two different PMP-membrane oxygenators. During hypothermic CPB, 1% isoflurane in an oxygen-air mixture was added to the oxygenator gas inflow line (gas flow, 3 l/min) for 15 min. Isoflurane concentration was measured in blood and in exhaust gas at the outflow port of the oxygenator. Between-group comparisons were performed for the area under the curve (AUC) during uptake and elimination of the isoflurane blood concentrations, the maximum isoflurane blood concentration (C(max)), and the exhausted isoflurane concentration (F(E)). RESULTS: The uptake of isoflurane, expressed as AUC of isoflurane blood concentration and a function of F(E), was significantly reduced in PMP oxygenators compared to PPL oxygenators (P < 0.01). C(max) was between 8.5 and 13 times lower in the PMP-membrane oxygenator groups compared to the conventional PPL-membrane oxygenator groups (P < 0.01). CONCLUSIONS: The uptake of isoflurane into blood via PMP oxygenators during CPB is severely limited. This should be taken into consideration in cases using such devices.