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Biomedical subjects

Kai Taeger

Publications and source records attributed to Kai Taeger.

13 recordsLinked to original sources

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.

Adult↗

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.

Anesthesia, Inhalation↗

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.

Adolescent↗

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.

Animals↗

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.

Anesthesia, General↗

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.

Bedding and Linens↗

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.

Adult↗

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.

Animals↗

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.

Analysis of Variance↗

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.

Adult↗

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.

Journal Article↗

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.

Acute Disease↗