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C Werner

Publications and source records attributed to C Werner.

At least 109 records · Page 6Linked to original sources
PubMed1998

The effects of sevoflurane on cerebral blood flow autoregulation in rats.

UNLABELLED: In this study, we investigated the effect of sevoflurane on cerebral blood flow (CBF) autoregulation in rats. Twenty-four male Sprague-Dawley rats were randomly assigned to receive one of the following anesthetic treatments. In Group 1 (n = 8, control) anesthesia was maintained using fentanyl (25 microg x kg(-1) x h(-1)) and N2O/O2 (fraction of inspired oxygen 0.33). In Group 2 (n = 8) and Group 3 (n = 8), anesthesia was maintained using 2% sevoflurane (1 minimum alveolar anesthetic concentration [MAC]) and 2 MAC sevoflurane (4 vol%) in O2/air (fraction of inspired oxygen 0.33), respectively. Cortical CBF autoregulation was measured during graded hemorrhage within the mean arterial pressure (MAP) range of 100-30 mm Hg using laser Doppler flowmetry. CBF was constant with fentanyl/ N2O (Group 1) and 1 MAC sevoflurane (Group 2) within the MAP range of 100-40 mm Hg. In Group 3 (2 MAC sevoflurane), CBF decreased as a linear function of hemorrhagic hypotension. These results indicate that CBF autoregulation was intact during 1 MAC sevoflurane. In contrast, CBF autoregulation was impaired with 2 MAC sevoflurane. This is probably related to a reduction of baseline cerebrovascular tone with higher concentrations of sevoflurane, which results in a decreased capacity of autoregulatory cerebrovascular dilation during hemorrhage. IMPLICATIONS: The purpose of the present study was to investigate the effect of sevoflurane on cerebral blood flow autoregulation in rats. Cerebral blood flow autoregulation was intact with 1 minimum alveolar anesthetic concentration sevoflurane but was impaired with 2 minimum alveolar anesthetic concentration sevoflurane.

Anesthetics, Inhalation↗
PubMed1998

Hypercapnia prevents jugular bulb desaturation during rewarming from hypothermic cardiopulmonary bypass.

UNLABELLED: BACKGROUND. The rewarming period of hypothermic cardiopulmonary bypass (CPB) is associated with reduced jugular bulb venous oxygen saturation (SjO2). This study investigates the effects of normocapnia vs. hypercapnia on changes in SjO2 during rewarming from hypothermic CPB for coronary artery bypass graft in patients classified as American Society of Anesthesiologists physical status 111. METHODS: Anesthesia was induced and maintained with fentanyl, midazolam, and continuous infusion of etomidate. Hypothermic CPB (27 degrees C) was managed according to alpha-stat conditions. The SjO2 percentage was measured using a fiberoptic catheter placed in the right jugular bulb via the right internal jugular vein. Data were recorded before and during the rewarming period. Patients were assigned to a normocapnic (PaCO2: 36-40 mmHg, n = 10) or hypercapnic (PaCO2: 45-50 mmHg, n = 10) PaCO2 regimen during rewarming. RESULTS: The maximum reduction of SjO2 occurred during rewarming with the jugular bulb temperature at 35-36 degrees C. In contrast, SjO2 did not change during rewarming from hypothermia in hypercapnic patients. CONCLUSIONS: These results show that mild hypercapnia prevents the desaturation of SjO2 seen with the normocapnic group during the rewarming period from hypothermic CPB. These data suggest that mild hypercapnia during rewarming from CPB is associated with a better balance between cerebral oxygen supply and demand.

Aged↗
PubMed1998

Monitoring of the central nervous system.

Clinical studies have shown a close relationship between variables such as hypoxia, increased intracranial pressure, arterial hypotension, or seizures and neurological outcome. This indicates the need for monitoring techniques of the central nervous system including measurements of cerebral blood flow, cerebral oxygenation and neuronal function. Semiquantitative changes in cerebral blood flow can be measured continuously using transcranial Doppler sonography. Measurements of jugular venous oxygen saturation or tissue oxygenation reflect the balance between cerebral oxygen delivery and cerebral oxygen demand. Near-infrared spectroscopy appears to be a technology with potential for non-invasive measurements of cerebral oxygen saturation and mitochondrial oxygen availability. The current technology is, however, of limited clinical utility. Brain electrical monitoring techniques such as electroencephalogram and evoked potentials are sensitive and specific to detect changes in neuronal function caused by cerebral ischaemia. Electroencephalogram and evoked potential measurements of depth of anaesthesia and specific electroencephalogram patterns for pharmacodynamic quantification of drug effects may gear the dosage of anaesthetics according to the anaesthetic effect.

Journal Article↗
PubMed1998

Correlation of transcranial Doppler sonography mean flow velocity with cerebral blood flow in patients with intracranial pathology.

Several studies suggest that relative changes in cerebral blood flow (CBF) may be assessed via transcranial Doppler sonography (TCD). The present study investigates the correlation between changes in TCD-mean flow velocity (Vm) and changes in CBF in patients with a variety of types of intracranial pathology undergoing cerebrovascular reactivity tests. After informed consent was obtained, 32 patients presenting with stenoses of brain-supplying arteries (n = 13), cerebral vascular malformations (n = 6), surgical decompression for subarachnoid hemorrhage (n = 2), brain edema after closed head injury (n = 8), or hepatic encephalopathy (n = 3) were studied. The patients were divided into two groups for different reactivity tests. Patients in group 1 (awake or sedated, n = 18) received a 1-g dose of acetazolamide intravenously. In group 2 (n = 14), mechanical ventilation was adjusted to produce a 20% decrease in arterial CO2 tension compared with baseline. Regional CBF was measured using xenon-enhanced computed tomography (Xe-CT). Xe-CT scans at the levels of the basal ganglia and the lateral ventricles were performed during a 4.5-min xenon wash-in period. Bilateral flow velocity was measured in the middle cerebral artery using a 2-MHz pulsed TCD system. Mean arterial blood pressure, heart rate, and end-tidal CO2 were continuously recorded during the procedure. After baseline measurements and either alteration of CO2 or application of acetazolamide, the cerebrovascular reactivity was assessed at 20 min by a second measurement of CBF, TCD, and all other physiologic variables. The correlation coefficient for relative changes of MCA territory CBF versus Vm and for the overall population was r = 0.82. In groups 1 and 2, the r values were 0.39 and 0.5, respectively. Correlation coefficients did not exceed r = 0.4 in any subgroup-classification based on diagnosis. The close correlation between changes in CBF and Vm (r = 0.82) in patients with heterogeneous intracranial pathology seems to show that TCD is a measure of CBF. However, in groups 1 and 2 and in subgroups formed of patients classified according to diagnoses, data dispersion suggests that the actual correlation is weaker. Relation of changes in Vm to those in CBF may depend on the underlying diagnosis. These data indicate that the correlation between Vm and CBF may vary with intracranial pathology.

Acetazolamide↗
PubMed1998

Blood compatible polymers in intensive care units: state of the art and current aspects of biomaterials research.

The use of artificial organs in cases of acute renal failure, acute respiratory distress syndrome (ARDS) and multiorgan dysfunction syndrome (MODS) has lead to a significant reduction of mortality. However, the interaction between body and biomaterials results in the activation of the coagulation system and in the induction of systemic inflammatory response syndrome. The necessary anticoagulation may be contraindicated and may even further increase the risk for the patient. This article evaluates the currently applied polymeric materials used in intensive care units (ICU) and gives a possible outlook into future developments. It is emphasized that systematic interdisciplinary research of physicians and biomaterial scientists is essential for the successful development of new polymers with improved biocompatibility. For this purpose a brief overview of analytical techniques for surface characterization is given, and future developments to a fully biocompatible polymer are described.

Artificial Organs↗
PubMed1997

Degradation of the polyamine alkaloid aphelandrine by endophytic fungi isolated from Aphelandra tetragona.

Members of the genus Aphelandra (Acanthaceae) produce rare macrocyclic polyamine alkaloids which consist of spermine acylated with two units of 3-(4-hydroxyphenyl)prop-2-enoic acid. Endophytic fungi were isolated from roots and shoots of Aphelandra tetragona and tested for their ability to metabolize the main alkaloid aphelandrine, which accumulates exclusively in the roots of the plants. Several endophytes were able to metabolize aphelandrine but only root endophytes belonging to the Nectriaceae were good metabolizers. In addition, the endophytes were grown on an agar medium containing putrescine, spermidine, or spermine as the sole nitrogen source. All fungi were able to grow on putrescine, but only the good aphelandrine metabolizers grew well on spermidine or spermine. Acremonium sp. 15, one of the most active metabolizers, grew also on a medium containing aphelandrine as sole nitrogen source. A number of strains thought to be conspecific with Acremonium sp. 15 were also tested for their ability to metabolize aphelandrine. The ability of the endophytes to metabolize aphelandrine suggests an ecological adaptation of the symbionts to their host. The possibility of using the aphelandrine metabolism as a taxonomic character is briefly discussed.

Alkaloids↗
PubMed1997

[Ketamine racemate and S-(+)-ketamine. Cerebrovascular effects and neuroprotection following focal ischemia].

The phencyclidine derivative ketamine is a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist with the thalamo-neocortical projection system as the primary site of action. Racemic ketamine consists of the enantiomers S(+)-ketamine and R(-)-ketamine. Racemic ketamine has never been considered an adequate anaesthetic agent in neurosurgical patients since it produces regionally specific stimulation of cerebral metabolism (CMRO2) and increases cerebral blood flow (CBF) and intracranial pressure (ICP). However, recent experiments suggest that both tracemic ketamine and S(+)-ketamine may reduce infarct size in animal models of incomplete cerebral ischaemia and brain injury. This experimental protective effect appears to be related to decreases in Ca++ influx and maintenance of brain tissue magnesium levels due to NMDA and quisqualate receptor blockade by ketamine. Studies in dogs have shown that racemic ketamine (2.0 mg/kg) increases CBF in the presence of the cerebral vasodilator N2O. In contrast, studies in rats without background anaesthesia showed increases in CBF after racemic ketamine (100 mg/kg i.p.). This suggests that the cerebrovascular effects of racemic ketamine are related to the pre-existing cerebrovascular tone induced by background anaesthetics. Cerebrovascular CO2 reactivity was maintained regardless of the baseline cerebrovascular resistance. There are several mechanisms by which racemic ketamine may increase CBF. It induces dose-dependent respiratory depression with consequent mild hypercapnia in spontaneously ventilating subjects. This produces vasodilation due to the intact cerebrovascular CO2 reactivity. Racemic ketamine also induces regional neuroexcitation, which leads to stimulation of cerebral glucose consumption in the limbic, extrapyramidal, auditory, and sensory-motor systems. This regional neuroexcitation with increased CMRO2 produces increases in CBF that can be blocked by infusion of barbiturates or benzodiazepines. However, increases in CBF with racemic ketamine (1 mg/kg) may also occur during normocapnia and without changes in CMRO2. This effect is related to some additional direct cerebral vasodilating potency of racemic ketamine based on a mechanism involving blockade of Ca++ channels. The effects of racemic ketamine on CBF autoregulation have not been investigated systematically. However, studies in rats have shown that CBF autoregulation was maintained with low- and high-dose S(+)-ketamine. Infusion of racemic ketamine alters intracranial volume and ICP. Studies in spontaneously ventilating pigs with and without intracranial hypertension have shown that racemic ketamine (0.5-5.0 mg/kg) produces increases in PaCO2 and ICP. In contrast, identical experiments with mechanical ventilation and controlled PaCO2 showed no changes in ICP following racemic ketamine infusion. This implies that increases in ICP are related to inadequate ventilation with consecutive hypercapnia and increases in intracranial blood volume. However, mechanical ventilation may not be sufficient to control ICP following racemic ketamine. Experiments in mechanically ventilated dogs indicate that racemic ketamine (2 mg/kg) increases cerebral blood volume and ICP even in the presence of normoventilation, a response that is reversible by hyperventilation or the administration of diazepam. Studies in patients have shown that racemic ketamine (2.0 mg/kg) reduces CBF in the presence of cerebral vasodilators like halothane or N2O. In contrast, studies in unanaesthetised humans showed increases in CBF after racemic ketamine (2-3 mg/kg). This observation is consistent with animal studies and suggests that the cerebrovascular effects of racemic ketamine are related to the pre-existing cerebrovascular tone induced by background anaesthetics. Studies in humans with and without intracranial pathology confirm the data from animal experiments. (ABSTRACT TRUNCATED)

Animals↗
PubMed1997

[Remifentanil].

Explore the source record for details and available documents.

Anesthesia, Intravenous↗
PubMed1997

[From the racemate to the eutomer: (S)-ketamine. Renaissance of a substance?].

The pharmacological profile of ketamine: Until recently, clinically available ketamine was a racemic mixture containing equal amounts of two enantiomers, (S)- and (R)-ketamine. The pharmacological profile of racemic ketamine is characterized by the so called dissociative anesthetic state and profound sympathomimetic properties. Among the different sites of action, N-methyl-D-aspartate (NMDA)-receptor antagonism is considered to be the most important neuropharmacological mechanism of ketamine. Effects on opiate receptors, monoaminergic and cholinergic transmitters, and local anesthetic effects are obvious as well. Following intravenous administration, a rapid onset of action is seen within 1 min, lasting for about 10 min. The anaesthetic state is terminated due to redistribution, followed by hepatic and renal elimination with a half-life period of 2-3 h. For alternative administration, the intramuscular and oral route is also appropriate. The most important adverse effects are hallucinations and excessive increases in blood pressure and heart rate. These reactions can be attenuated or avoided by combining of ketamine with sedative or hypnotic drugs like midazolam and/or propofol. During controlled ventilation, increases in intracranial pressure are unlikely to occur. The special pharmacological profile of (S)-ketamine: In general, the pharmacological properties of (S)-ketamine are comparable to the racemic compound. On the different sites of action, qualitatively comparable effects were found, but significant quantitative differences also became obvious. When compared with (R)-ketamine and the racmic mixture, the analgesic and anesthetic potency of (S)-ketamine is threefold or twofold higher. Thus, a 50% reduction of dosage is possible to achieve comparable clinical results. Because of the faster elimination of (S)-ketamine, better control of anesthesia will be provided. In summary, the pharmacokinetic improvements of (S)-ketamine are characterized by a reduced drug load, along with more rapid recovery. The clinical use of (S)-ketamine: The clinical use of (S)-ketamine depends on its analgesic and sympathomimetic properties, whereas the anaesthetic potency remains in the background. In clinical anesthesiology, (S)-ketamine, especially in combination with midazolam and/or propofol, can be used for short procedures with preserved spontaneous ventilation, for induction of anesthesia in patients with shock or asthmatic disorders, and for induction and maintenance of anesthesia in caesarean sections. Additional indications are repeated anesthesia, for example, in burn patients, analgesia during delivery and diagnostic procedures and intramuscular administration in uncooperative patients. The value of (S)-ketamine as an analgesic component for total intravenous anesthesia has not been defined yet. In comparison with opioides, the advantages are related to improved hemodynamic stability and reduced postoperative respiratory depression. When (S)-ketamine, especially in combination with midazolam, is used for analgosedation in intensive care medicine, a reduction of exogenous catecholamine demand can be expected. Moreover, the effects on intestinal motility are superior to opioids. In combination with midazolam and propofol, excellent control of analgosedation was found, making both combinations suitable for situations in which repeated neurological assessment of patients is necessary. In emergency and disaster medicine, (S)-ketamine is of outstanding importance because of its minimal logistic requirements, the chance for intramuscular administration and the broad range of use for analgesia, anaesthesia and analgosedation as well. Further perspectives of (S)-ketamine may be the treatment of chronic pain and the assumed neuroprotective action of the substance.

Anesthesia, General↗
PubMed1997

Haemodynamic changes and skeletal muscle oxygen tension during complete blood exchange with ultrapurified polymerized bovine haemoglobin.

OBJECTIVE: The study investigates the effect of continuous blood exchange with ultrapurified, polymerized bovine haemoglobin (UPBH) in comparison to hetastarch on haemodynamics, oxygen transport and skeletal muscle oxygen tension in a canine model. DESIGN: Sixteen anaesthetized beagle dogs underwent haemodilution with lactated Ringer's to a starting haematocrit of 20% followed by progressive blood exchange with 6% hetastarch 200,000/0.5 (HES, group 1) or UPBH (haemoglobin 13 +/- 1 g.dl-1, molecular weight (MW) 32-500,000, group 2) to haematocrit target levels of 15%, 10% and 5% or less. MEASUREMENTS AND RESULTS: Besides haemodynamics, skeletal muscle tissue oxygen tension (tPO2) was measured using a polarographic needle probe. In HES-treated animals, heart rate, cardiac output and blood flow were higher while systemic vascular resistance, systemic and regional arterio-venous oxygen difference (avDO2) and oxygen extraction ratios were lower when compared to the UPBH group. In spite of a higher final haematocrit of 5% in group 1, in comparison to group 2 with 2%, final muscular oxygen uptake (4.7 +/- 4 vs 10.1 +/- 2 ml.min-1) and mean tPO2 (11.8 +/- 2.3 vs 51.1 +/- 2.9 mm Hg) were lower in group 1 than in group 2. While tPO2 histograms were continuously shifted to lower oxygen tensions during progressive haemodilution with HES, UPBH-exchanged animals showed tPO2 histograms shifted to higher values than baseline. CONCLUSION: In spite of vasoconstriction, UPBH provided more haemodynamic stability and enhanced skeletal muscle tPO2 during progressive blood exchange when compared to HES.

Analysis of Variance↗
PubMed1997

Microwave CO2 plasma-initiated vapour phase graft polymerization of acrylic acid onto polytetrafluoroethylene for immobilization of human thrombomodulin.

The functionalization of polytetrafluoroethylene (PTFE) for human thrombomodulin (hTM) binding has been achieved by CO2 plasma activation and subsequent vapour phase graft polymerization of acrylic acid (AA). The PTFE surfaces after CO2 plasma treatment, AA grafting and hTM immobilization were characterized by attenuated total reflection Fourier transform infrared (ATR-FTIR) spectroscopy, X-ray photoelectron spectroscopy (XPS) and electron spin resonance (ESR) spectroscopy, as well as by zeta potential and wetting measurements to quantitatively control each step of modification. The activity of immobilized hTM was estimated by the protein C activation test.

Acrylates↗
PubMed1997

Immobilization of human thrombomodulin onto PTFE.

Human thrombomodulin (hTM) is an endothelial cell-surface glycoprotein and has effective anticoagulant properties. This protein was immobilized onto polytetrafluorethylene (PTFE) surfaces to create biomaterials with enhanced haemocompatibility. The PTFE surface was functionalized by CO2 plasma activation and subsequent vapour-phase graft polymerization of acrylic acid. Surface characterization after plasma treatment, grafting and hTM immobilization was achieved by attenuated total reflection-Fourier transform-infrared spectroscopy, X-ray photoelectron spectroscopy, zeta potential and wetting measurements. The activity of immobilized hTM was estimated using the protein C activation test.

Journal Article↗
PubMed1997

Chronic terbutaline treatment desensitizes beta-adrenergic inhibition of lymphocyte activation in healthy volunteers.

1. A substantial body of evidence has accumulated that beta-adrenoceptor mediated increases in human lymphocyte cyclic AMP can inhibit activation of resting lymphocytes. The aim of this study was to determine whether this effect might desensitize during chronic beta-adrenoceptor agonist treatment. We assessed the effects of 2 weeks treatment with the beta 2-adrenoceptor agonist terbutaline (3 x 5 mg day-1 p.o.) on isoprenaline-induced inhibition of concanavalin A-evoked lymphocyte activation in nine healthy male volunteers. Lymphocyte activation was determined by [3H]-thymidine incorporation (as a measure of proliferation), and inositol phosphate formation was assessed in [3H]-myo-inositol prelabelled lymphocytes in the presence of 10 mM LiCl. 2. Terbutaline treatment caused a significant reduction in isoprenaline (1 nM-10 microM)-induced increases in lymphocyte cyclic AMP content; the maximal increase was 14 +/- 3 pmol/10(6) cells before and 7 +/- 2 pmol/10(6) cells (n = 9, P < 0.05) after terbutaline treatment. 3. The mitogen concanavalin A (Con A, 1-32 micrograms ml-1)-induced increase in inositol phosphate formation was significantly enhanced after terbutaline treatment (max. increase before treatment: 255 +/- 25% above basal; after treatment 453 +/- 16% above basal; n = 9, P < 0.001), while isoprenaline (1 nM-10 microM)-induced inhibition of Con A (16 micrograms ml-1)-evoked increases in inositol phosphate formation was significantly reduced after the terbutaline treatment (max. inhibition before treatment: 22 +/- 4%; after treatment 9 +/- 1%, n = 9, P < 0.01). 4. Con A (1.25-10 micrograms ml-1)-induced increases in [3H]-thymidine incorporation into the lymphocytes (as a measure of proliferation) was not affected by the terbutaline treatment. On the other hand, isoprenaline (1 nM-1 microM)-induced inhibition of Con A (5 micrograms ml-1)-evoked lymphocyte proliferation (max. inhibition: 33 +/- 7%, n = 9) was almost completely abolished after the terbutaline treatment. 5. We conclude that chronic treatment with terbutaline desensitizes lymphocyte beta 2-adrenoceptors and, therefore, the inhibitory effect of cyclic AMP on lymphocyte activation.

Adrenergic beta-Agonists↗