[Patch clamp studies on recombinant GABA A receptors using an ultra-quick application system].
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Anesthetics↗
Biomedical subjects
E Kochs
Publications and source records attributed to E Kochs.
Increasing isoflurane concentration may cause paradoxical increases in the EEG bispectral index in surgical patients.
We have studied the effects of increases in isoflurane concentration on the EEG bispectral index (BIS) in 70 patients anaesthetized with isoflurane-nitrous oxide-sufentanil for major abdominal surgery. During surgery, baseline BIS was recorded at 0.8% end-tidal isoflurane with nitrous oxide in oxygen (FIO2 0.35). After this, end-tidal isoflurane was increased to 1.6% for 15 min and decreased subsequently to 0.8% for 20 min to assess recovery. In 20 patients, BIS decreased from a mean value of 40 (SD 9) during baseline to 25 (10) at 1.6% isoflurane. In contrast, BIS did not change in 23 patients and increased in 27 patients from 35 (6) to 46 (8) as isoflurane was increased to 1.6%. In all patients, BIS recovered to baseline values at 0.8% isoflurane. The changes in BIS with increasing isoflurane concentration were not related to drugs or differences in physiological variables, which did not differ between groups. Patients with a decrease in BIS were significantly younger (38 (range 18-68) yr) than those with unchanged (55 (26-70) yr) or increased (60 (40-70) yr) BIS values (P < 0.001). It is possible that the paradoxical increase in BIS is related to continuous pre-burst EEG patterns consisting of high-frequency activity. This suggests that the use of BIS as a guide for isoflurane administration may be misleading in some patients undergoing surgical procedures.
Abdomen↗
Postoperative pain management and recovery after remifentanil-based anaesthesia with isoflurane or propofol for major abdominal surgery. Remifentanil Study Group.
We have assessed if recovery times after morphine or fentanyl, given before terminating remifentanil anaesthesia with isoflurane or propofol, are compromised. We studied patients undergoing elective, major abdominal surgery, allocated randomly to receive remifentanil and isoflurane (n = 277) or remifentanil and propofol (n = 274) anaesthesia. Twenty-five minutes before the end of surgery, patients received fentanyl 0.15 mg or morphine 15 mg in a randomized, double-blind manner followed by a second dose (fentanyl 0.05 mg, morphine 7 mg) for moderate or severe pain in recovery. Recovery was rapid and at an Aldrete score > or = 9 (median 12-15 min), 42-51% of patients reported none or mild pain. However, 26-35% of patients reported severe pain and > 90% required a second dose of opioid within 21-27 min after anaesthesia.
Abdomen↗
Effects of xenon on cerebral blood flow and autoregulation: an experimental study in pigs.
We have investigated the effects of xenon on regional cerebral blood flow (rCBF) and autoregulation in pigs sedated with propofol 4 mg kg-1 h-1. Balloon-tipped catheters were placed into the descending aorta and inferior vena cava of 15 Göttingen Minipigs for manipulation of arterial pressure and blood sampling. rCBF was measured using the sagittal sinus outflow technique. Xenon was adjusted randomly to end-tidal fractions (FE'Xe) of 0, 0.30, 0.50 and 0.70. After baseline measurements of heart rate (HR), mean arterial pressure (MAP), rCBF, sagittal sinus pressure (SSP) and calculation of regional cerebrovascular resistance (rCVR) at each respective FE'Xe, autoregulation was tested in the MAP range 60-120 mm Hg. Increasing FE'Xe had no effect on HR, MAP, rCBF or SSP. rCVR increased with increases in MAP, regardless of FE'Xe. Autoregulation was not impaired. We conclude that xenon inhalation had no effect on rCBF and autoregulation in our model, which could suggest that xenon is an adequate adjunct for neurosurgical anaesthesia.
Anesthetics, Inhalation↗
Dual action of isoflurane on the gamma-aminobutyric acid (GABA)-mediated currents through recombinant alpha(1)beta(2)gamma(2L)-GABA(A)-receptor channels.
Isoflurane (ISO) increased the agonist-induced chloride flux through the gamma-aminobutyric acid A receptor (GABA(A)R). This may reflect an anesthetic-induced increase in the apparent agonist affinity. A dual effect of anesthetics was postulated for both the nicotinic acetylcholine receptor (nAChR) and the GABA(A)R. We tested the hypothesis that, in addition to a blocking effect, ISO increases gamma-aminobutyric acid (GABA)-gated currents through recombinant GABA(A)R channels. HEK293 cells were transfected with rat cDNA for alpha(1),beta(2),gamma(2L) subunits. Currents elicited by 1 mM or 0. 01 mM GABA, respectively, alone, or with increasing concentrations of ISO, were recorded by using standard patch clamp techniques. ISO reduced the peak current elicited by 1 mM GABA. Currents induced by 0.01 mM GABA were potentiated by small ISO (twofold at 0.5 mM ISO) and inhibited by larger concentrations. Withdrawal of ISO and GABA induced rebound currents, suggesting an open-channel block by ISO. These currents increased with increasing concentrations of ISO. At large concentrations of ISO, the inhibitory effect predominated and was caused by, at least partly, an open-channel block. At small concentrations of ISO, potentiation of the GABA-gated currents was more prominent. This dual action of ISO indicates different binding sites at the GABA(A)R. The balance between potentiation and block depends on the concentrations of both ISO and GABA.
Anesthetics, Inhalation↗
Nitrous oxide and xenon increase the efficacy of GABA at recombinant mammalian GABA(A) receptors.
We investigated the interactions between recombinant gamma-aminobutyric acid receptor complex (GABA(A)R) and nitrous oxide (N(2)O) or xenon (Xe). Human embryonic kidney cells (HEK 293) were transfected with rat cDNA for alpha(1)beta(2)gamma(2L) or for alpha(1)beta(2) recombinant GABA(A)R subunits. Patch clamp techniques were used in the whole-cell mode to evaluate the effect of N(2)O and Xe on GABA-induced currents. A piezo-driven "liquid filament switch" was used for fast application. Both N(2)O (100%, 29.2 mM) and Xe (100%, 3.9 mM) reversibly increased GABA-induced currents through the alpha(1)ss(2)gamma(2L) and the alpha(1)beta(2) GABA(A)R channels. The potentiating effect of N(2)O or Xe on peak currents was prominent at small GABA concentrations (10(-7) to 10(-5) M). The addition of N(2)O or Xe increased the efficacy of GABA (10(-7) to 10(-3) M). Both N(2)O and Xe significantly decreased the risetime((10%-90%)) of the currents elicited by small GABA concentrations. At the concentrations used, neither N(2)O nor Xe had an intrinsic effect. We conclude that, similar to other anesthetics, both N(2)O and Xe increase the efficacy of GABA at the GABA(A)R and enhance inhibitory GABAergic synaptic transmission.
Anesthetics, Inhalation↗
Cerebral histopathology following portal venous infusion of bacteria in a chronic porcine model.
BACKGROUND: The aim of this study was to histologically investigate brain damage after prolonged periods of bacteremia in pigs. METHODS: Twenty-one pathogen-free Göttingen minipigs were anesthetized and instrumented with a femoral arterial, a pulmonary arterial, and through midline abdominal incision with a portal venous catheter. After craniotomy the superior sagittal sinus was cannulated. A lumbosacral spinal catheter was inserted for sampling of cerebrospinal fluid. Twelve hours after instrumentation, the animals were randomized in two groups: septic and control animals. The septic group received an infusion of 107 colony-forming units per kilogram of living Escherichia coli over 0.5 h through portal venous catheter each day. The control group received saline. Postoperative intensive care treatment included 4 days of controlled mechanical ventilation, sedation, and intravenous nutrition. The brains then were removed, fixed, and processed for histology. Each pathologic alteration found in the samples was assessed and given a severity code (0-3). RESULTS: Sham-operated animals showed no alterations caused by the instrumentation and the intensive care treatment. The septic group showed typical clinical signs of sepsis. Vasopressor support and mechanical ventilation prevented systemic hypotension and hypoxemia. High serum and cerebrospinal fluid levels of interleukin-6 and tumor necrosis factor-alpha were detected. The septic group showed severe histologic abnormalities of the brain including perivascular edema, spongiform degeneration, hyperemia, and purpura. Damage of neurons was seen including eosinophilic cytoplasm, shrunken nuclei, and disintegration of the nuclear membrane. CONCLUSIONS: Abdominal sepsis induced severe brain damage that was not related to systemic hypoxia or ischemia. High cerebrospinal fluid levels of tumor necrosis factor-alpha and interleukin-6 were related to an inflammatory process in the brain resulting in cerebral edema and death of neurons.
Animals↗
S(+)-ketamine up-regulates neuronal regeneration associated proteins following glutamate injury in cultured rat hippocampal neurons.
In previous studies, racemic ketamine improved neurological outcome after experimental brain injury and S(+)-ketamine demonstrated neuroprotective effects in neurons after damage in vitro. We compared the expression of regeneration-associated proteins in rat hippocampal neurons after glutamate injury and treatment with S(+)-ketamine versus racemic ketamine. Following an 8 minute exposure to 100 microM glutamate, neurons were maintained untreated or in the presence of S(+)-ketamine or racemic ketamine (10(-4) M, 10(-5) M, 10(-6) M) for one week. Growth-associated protein-43 (GAP-43) and synaptosomal-associated protein-25 (SNAP-25) was analyzed by Western Blotting, the mitochondrial transmembrane potential (MTP) by fluorescence imaging, and [3H]2-deoxy-D-glucose ([3H]2-DG) uptake by scintillation spectrometry. Seven days after exposure, GAP-43 decreased to 15% and SNAP-25 to 30% in the glutamate-injured, untreated neurons. The MTP declined to 50% and [3H]2-DG to 30%. Both S(+)-ketamine and racemic ketamine at 10(-4) M and 10(-5) M minimized the decline in MTP, almost maintaining it at control value. Additionally, S(+)-ketamine and racemic ketamine decreased the reduction in [3H]2-DG. S(+)-ketamine at 10(-4) M and 10(-5) M and racemic ketamine at 10(-4) M reduced the decline in SNAP-25 to 60% of controls (P < .05). However, S(+)-ketamine at 10(-4) M and 10(-5) M only reversed the decrease in GAP-43 to 50% and 40% of controls, respectively (P < .05). We conclude that the synthesis of a growth-associated protein related to plasticity and repair in the adult nervous system is increased by S(+)-ketamine but is not increased by racemic ketamine.
Animals↗
[Rapid sequence induction with succinylcholine: an option to reduce side effects].
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Anesthesia, Inhalation↗
[When the patient wakes up during surgery. Help for anesthesia victims. Interview by Dr. Brigitte Moreano].
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Anesthesia, General↗
Isoflurane induces dose-dependent changes of thalamic somatosensory information transfer.
In spite of several reports about suppressive effects of volatile anesthetics on somatosensation, their neuronal mechanisms are largely unknown. The present study investigates somatosensory impulse transmission at the thalamic level in rats under varied concentrations of isoflurane by recordings of neuronal responses to mechanical stimulation of the body surface. Single-unit recordings of thalamo-cortical relay neurons (TCNs, third order neurons; n=28) and presumed trigemino-thalamic fibers (TTFs, second order neurons; n=7) were performed in the ventral posteromedial nucleus. Functional response characteristics were quantified following defined tactile stimulation (trapezoidal or vibratory deflection of sinus hairs or fur) applied to the neuronal receptive fields. End-tidal isoflurane concentration was increased in steps of 0.2% between 0.6% (baseline) and 2.0%. The response activity in all TCNs studied was suppressed in a dose-dependent manner (2.0% isoflurane decreased responses to 3. 5+/-1.1% of baseline; mean+/-S.E.M.); the response activity in TTFs was much less affected (decrease to 55.0+/-8.2%). Suppression of ongoing activity, however, was similar for both, TCNs and TTFs. Furthermore, in TCNs, the response characteristics changed with increasing isoflurane between 1.0% and 1.8%: tonic and sustained responses were converted to phasic on-responses. In contrast, the tonic and sustained response characteristics of TTFs were preserved even at higher isoflurane concentrations. The results indicate that isoflurane attenuates the output of somatosensory signals in the specific nucleus of the rat's thalamus, while its input is only marginally affected. The observed changes of thalamic neuronal response characteristics, at least in part, may cause the loss in sensory discrimination observed during general anesthesia.
Anesthetics, Inhalation↗
Cerebral blood flow velocity and carbon dioxide vasoreactivity during gamma-hydroxybutyrate/fentanyl anaesthesia in non-neurosurgical patients.
In this study the effects of gamma-hydroxybutyrate/fentanyl on cerebral blood flow velocity (CBFV) (as measured in the middle cerebral artery by transcranial Doppler ultrasonography) and on cerebrovascular carbon dioxide reactivity were investigated. Mean CBFV (Vmean) and haemodynamic responses were recorded in 12 non-neurosurgical patients before, during and after induction of general anaesthesia with gamma-hydroxybutyrate (GHB) (20 min constant rate infusion of 100 mg kg-1). Two patients were excluded, one because of bradycardia and the other because of severe myoclonia. During the infusion of GHB, normocapnia was maintained by manually assisting ventilation as necessary. The infusion of GHB did not affect Vmean [awake: 57 +/- 12 cm s-1 (mean +/- SD); 22.5 min: 62 +/- 15 cm s-1, NS difference] or mean arterial blood pressure (MAP) (awake: 97 +/- 12 mmHg; 22.5 min: 89 +/- 10 mmHg, NS). This suggests that cerebral blood flow velocity is unaltered by an anaesthetic dose of GHB. Twenty-five minutes after the start of GHB, fentanyl 3 micrograms kg-1 and vecuronium 0.1 mg kg-1 were given, the trachea was intubated and the lungs were mechanically ventilated to maintain end-tidal PCO2 of 4.6 +/- 0.4 kPa (30 min). At 30 min after the start of the GHB infusion, Vmean and MAP decreased to 38 +/- 10 cm s-1 and 76 +/- 12 mmHg (both P < 0.05 vs 22.5 min) respectively. After adjusting the ventilation to achieve hypocapnia (40 min: end-tidal PCO2 3.5 +/- 0.2 mmHg), Vmean decreased to 29 +/- 7 cm s-1, while MAP did not change. This allowed the relative vasoreactivity (percentage change in Vmean/0.133 kPa change in the end-tidal PCO2 from normocapnia to hypocapnia) to be estimated as 2.7 +/- 1.6% 0.133 kPa-1. This suggests that cerebrovascular response to CO2 during gamma-hydroxybutyrate/fentanyl anaesthesia is maintained.
Adolescent↗
[Lactate: a marker for tissue hypoxia].
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Biomarkers↗
[Prophylaxis against obstetric acid aspiration syndrome in the German Federal Republic in 1997. A review based on results of a federal survey].
A survey of all German hospitals providing obstetric anesthesia was performed in 1997 (n = 1061, recovery rate 82%; comprising about 700,000 deliveries and 115,000 cesareans, resp.) concerning the routine prophylactic measures for acid aspiration syndrome (AAS) in pregnant patients and before obstetric procedures (i.e., prevention of aspiration by positioning, Sellick's manoeuvre, reduction of intragastric volume, or reduction of gastric content acidity). In pregnant patients, any prophylaxis of AAS is performed in 36%. Of the patients expecting delivery in the labour ward, only 7% receive pharmacological AAS treatment. Before scheduled (urgent, non-emergency) cesarean section in general anesthesia, 93% (94%) of patients receive prophylactic treatment, either pharmacological or non-pharmacological. Before regional anesthesia, the corresponding numbers are 52% for both scheduled or urgent CS.
Adult↗
[Visceral resorption of intra-abdominal insufflated carbon dioxide in swine].
OBJECTIVES: Total intraperitoneal carbon dioxide (CO2) resorption from CO2-pneumoperitoneum increases in relation to intraabdominal pressure (IAP) up to an upper limit of 10 to 15 mmHg. The purpose of this prospective study was to evaluate the visceral fraction of CO2 resorption in comparison to total intraperitoneal CO2 resorption in pigs to address possible reasons for this upper limit. METHODS: 16 pigs were chronically instrumented. Via midline laparotomy, a transit-time ultrasound flow probe was placed around the portal vein for continuous recording of the portal venous blood flow and a catheter was inserted into the portal vein via lienal vein. After complete recovery (7-10 days), animals were anesthetized with propofol and fentanyl and a pulmonary artery, a hepatic venous, an arterial, and an intraabdominal insufflation catheter were inserted. Mechanical ventilation (O2/air; FiO2 = 0.4) was adjusted to maintain endtidal CO2 at 34 to 36 mmHg using an Engstrøm Elvira ventilator. After an equilibration period of 3h, CO2, (n = 8) or air (n = 8) was insufflated. IAP was increased in steps of 4 mmHg and maintained constant at each respective IAP-level for 20 min. Blood gas analyses were assessed from portal venous, hepatic venous, central venous, and arterial probes at each IAP-level. Total intraperitoneal CO2 resorption was calculated from parameters derived from indirect calorimetry, the portal venous fraction from blood gas values and the portal venous blood flow following Fick's principle. Data were analyzed using Friedman's test. RESULTS: Total CO2 resorption increased continuously with rising IAP. Highest values were measured at IAP = 16 mmHg with 84 (74-93) ml/min. A further increase of IAP resulted in a significant decrease of total CO2 resorption. The visceral fraction of intraperitoneal CO2 resorption increased up to 28 (17-36) ml/min at IAP = 12 mmHg. Portal venous blood flow was also elevated or unchanged up to this IAP. At IAP = 20 mmHg or IAP = 24 mmHg portal venous blood flow decreased (79% of baseline) and in consequence portal venous calculated fraction of intraperitoneal carbon dioxide resorption decreased to 14 (8-20) ml/min. 20 min after desufflation, intraabdominal CO2 resorption was completed. With air insufflation, all parameters of CO2 balance were unchanged. DISCUSSION: The IAP dependent increase in CO2 resorption is limited due to an IAP related occlusion of the peritoneal capillaries and the limited expansion of peritoneal diffusion area. In this model, it was possible to show that visceral fraction is about one third of the total intraperitoneal carbon dioxide resorption and that this fraction depends on portal venous blood flow. Thus, a decrease in total CO2 resorption may indicate a reduction in portal venous blood flow.
Abdomen↗
[Septic encephalopathy].
Impaired mental function, from clouding of consciousness to deep coma is often seen in patients with systemic inflammation. Diagnosis of this syndrome which is called "septic encephalopathy" is dependent on exclusion of other causes. The underlying mechanisms have only been defined in parts. The appearance of cerebral symptoms during an infection increases mortality. Primary symptoms of septic encephalopathy appear early, before other septic organ manifestations become apparent. The most sensible parameter for diagnosis of septic encephalopathy in comatose patients or under sedation is the EEG. It shows general alterations which increase parallelly to the severity of septic encephalopathy. Septic encephalopathy has to be considered a multifactorial event. In an early stage of the development of septic encephalopathy, bacteremia induces overproduction of cytokines and other mediators. This causes metabolic dysregulation with effects on the cerebral protein-, glucose and neurotransmitter metabolism. In addition, cytokines damage the blood-brain-barrier and exert direct cytotoxic effects. This results in histologic detectable neuronal damage. Further effects of the cytokine expression are perivascular edema and hemorrhage. The loss of metabolic regulation of the brain perfusion and local cerebral ischemia additionally contribute to the etiology of septic encephalopathy. A specific therapy is not yet known.
Brain Diseases↗
[Translaryngeal tracheostomy in Bechterew's disease and Guillain-Barre syndrome].
Recently, the Translaryngeal Tracheostomy (TLT) has been developed by Fantoni [1,2]. This new technique has been suggested for long-term ventilated intensive care patients as an alternative to other minimal invasive tracheostomy techniques like the Percutaneous Dilatational Tracheostomy described by Ciaglia [3] or Griggs [4]. In comparison to these techniques, the main advantage of the TLT seems to be the access to the airway from inside the trachea to outside. This procedure minimizes the risk of luxations of parts of the tracheal wall into the tracheal lumen resulting in obstructive ventilatory problems. The often discussed risk of stomal infections associated with this technique due to a possible bacterial contamination of the mouth seems not to be clinically relevant. In the past minimal invasive tracheostomy techniques have only been recommended for patients with normal anatomical conditions and without any special risk factors. The present case report describes the successful performance of a TLT in a patient with a severe M. Bechterew and respiratory failure due to a Guillain-Barré-syndrome. This patient was at high risk for operative complications during a conventional surgical tracheostomy due to his underlying diseases.
Aged↗
[Neuromuscular recovery following mivacurium is predictable in patients with severe systemic disease prognoses].
OBJECTIVES: Fast recovery from mivacurium-induced neuromuscular blockade is impaired in patients with decreased plasma cholinesterase activity which is often associated with dysfunction of different organs. Nevertheless, predictability of neuromuscular recovery may be given. Thus, this study evaluates parameters to predict individual neuromuscular recovery in patients with uncommon diseases. METHODS: 84 male or female patients (18-70 years of age) were allocated to one of two groups according to their ASA risk profile (without severe systemic diseases: ASA 1 and 2; with severe systemic diseases: ASA 3 and 4). Plasma cholinesterase activity (PChE) had been determined preoperatively. Anaesthesia was performed with propofol and fentanyl. Neuromuscular transmission was monitored by electromyography. The ulnar nerve was stimulated by train-of four stimuli and neuromuscular transmission was measured at the hypothenar. After mivacurium 0.1 mu mg/kg, an infusion of mivacurium was adjusted to maintain T1/T0 at approximately 5% for at least 60 min. Duration from application of the initial bolus until recovery to T1/T0 = 5% (dur 5), the mean mivacurium infusion rate (IR), infusion time, the early recovery time from cessation of infusion to T1/T0 = 25% (rec 25) and the final recovery time from T1/T0 = 25% to T4/T1 = 75% (final rec) was measured. Statistical analysis of data was performed using t-tests. (alpha = 0.05). Predictability of the recovery times (rec 25 and final rec) was tested by multiple linear least-squares regressions. Dependent variables were PChE, dur 5, IR, infusion time, and rec 25, respectively. To test for predictability of neuromuscular blockade by mivacurium with respect to severe systemic diseases, the ASA risk score was defined to be the second independent variable at each regression, the respective interaction was defined to be the third independent variable (variable 1 x group). Variables entered multiple regression analysis in a forward stepwise manner (F > 4.0). RESULTS: PChE was significantly lower in patients with severe systemic diseases (3.7 +/- 1.2 kU/l vs. 4.5 +/- 0.9 kU/l), dur 5 significantly prolonged (17.3 +/- 7.3 min vs. 11.0 +/- 3.0 min), IR significantly lower (4.6 +/- 2.6 micrograms/kg/min vs. 6.5 +/- 2.8 micrograms/kg/min), and rec 25 (8.7 +/- 4.0 min vs. 6.0 +/- 1.7 min) as well as final rec (23.0 +/- 16.3 min vs. 13.0 +/- 3.7 min) significantly prolonged compared to patients without severe systemic diseases. Both recovery intervals correlated significantly with PChE, dur 5, or IR, but not with the ASA risk score. Multiple regression analysis revealed a close correlation between rec 25 and final rec very closely (R2 = 0.875). Prolonged mivacurium infusion time and additionally high ASA risk score were correlated with a prolonged neuromuscular recovery (R2 = 0.130). DISCUSSION: Prolonged neuromuscular recovery could be predicted from a reduced PChE, a prolonged duration of action of the initial mivacurium bolus and a decreased mivacurium-infusion rate required to maintain a 95% neuromuscular blockade. Measurement of plasma cholinesterase and monitoring of mivacurium induced neuromuscular blockade can avoid resting neuromuscular blockade postoperatively despite of prolonged neuromuscular recovery.
Adolescent↗