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O Möllenberg

Publications and source records attributed to O Möllenberg.

12 recordsLinked to original sources
PubMed2000

High-dose S(+)-ketamine improves neurological outcome following incomplete cerebral ischemia in rats.

PURPOSE: To determine the effects of the non-competitive NMDA-receptor antagonist S(+)-ketamine on neurological outcome in a rat model of incomplete cerebral ischemia. METHODS: Thirty rats were anesthetized, intubated and mechanically ventilated with isoflurane, O2 30% and nitrous oxide 70%. Following surgery animals were randomly assigned to one of the following treatment groups: Rats in group 1 (n = 10,OFF control) received fentanyl (bolus: 10 microg x kg(-1) i.v.; infusion 25 microg x kg(-1) x h(-1)) and N2O 70% / O2. Rats in group 2 (n = 10) received O2 30% in air and low-dose S(+)-ketamine (infusion: 0.25 mg x kg(-1) x min(-1)). Rats in group 3 (n = 10) received O2 30% in air and high-dose S(+)-ketamine (infusion: 1.0 mg x kg(-1) min(-1)). Following 30 min equilibration period ischemia was induced by combined unilateral common carotid artery ligation and hemorrhagic hypotension to 35 mm Hg for 30 min. Plasma catecholamines were assayed before and at the end of ischemia. Neurological deficit was evaluated for three postischemic days. RESULTS: Neurological outcome was improved with high-dose S(+)-ketamine when compared to fentanyl / N2O -anesthetized controls (9 vs. 1 stroke related deaths, P<0.05). Increases in plasma catecholamine concentrations were higher in fentanyl / N2O -anesthetized (adrenaline baseline 105.5+/-92.1 pg x ml(-1), during ischemia 948+/-602.8 pg x ml(-1), P<0.05; noradrenaline baseline 407+/-120.2 pg x ml(-1), ischemia 1267+/-422.2 pg x ml(-1), P <0.05) than in high-dose S(+)-ketamine-treated animals (adrenaline baseline 71+/-79.5 pg x ml(-1), ischemia 237 +/-131.9; noradrenaline baseline 317.9+/-310.5 pg x ml(-1), ischemia 310.5+/-85.7 pg x ml(-1)). CONCLUSION: Neurological outcome is improved following incomplete cerebral ischemia with S(+)-ketamine. Decreases in neuronal injury may be related to suppression of sympathetic discharge.

Animals↗
PubMed2000

[The neuroprotective effect of the glutamate antagonist acamprosate following experimental cerebral ischemia. A study with the lipid peroxidase inhibitor u-101033e].

INTRODUCTION: This study investigates the effects of acamprosate, a glutamatergic modulator, and the lipid peroxidation inhibitor U-101033E on neurological outcome following incomplete cerebral ischemia and reperfusion in rats. MATERIAL AND METHODS: Twenty-seven male Sprague-Dawley rats were randomly assigned to one of the following treatment groups: 1 (n = 9, control, no drug treatment), 2 (n = 9, 2 x 200 mg/kg acamprosate i.p.), and 3 (n = 9, 2 x 0.3 mg/kg U-101033E i.v.). Background anesthesia was maintained using a combination of fentanyl and O2/N2O (FiO2 = 0.3). Ischemia was produced by combined unilateral common carotid artery ligation and hemorrhagic hypotension to a mean arterial blood pressure (MAP) of 35 mm Hg for 30 minutes. Functional neurological deficit was evaluated for the following 3 days after cerebral ischemia. RESULTS: At the third postischemic day, five control animals and five animals treated with U-101033E were dead for stroke-related reasons. Surviving animals presented severe neurological deficits. In contrast, acamprosate improved neurological outcome, with stroke-related death occurring in one animal only and a minor neurological deficit in the surviving rats. DISCUSSION: The present study demonstrates that acamprosate, in contrast to U-101033E, significantly reduces neurological deficits following transient hemispheric ischemia. The neuroprotective mechanisms of acamprosate may be related to its antiglutamatergic effect with consecutive reduction of transmembraneous Ca++ flux through NMDA-activated ion channels.

Acamprosate↗
PubMed1999

Desflurane and isoflurane improve neurological outcome after incomplete cerebral ischaemia in rats.

We have investigated the effects of isoflurane and desflurane on neurological outcome in a rat model of incomplete cerebral ischaemia. We studied 40 non-fasted male Sprague-Dawley rats, anaesthetized, intubated and ventilated mechanically with isoflurane and nitrous oxide in oxygen (FlO2 0.3). Arterial and venous catheters were inserted for measurement of arterial pressure, drug administration and blood sampling. A biparietal electroencephalogram (EEG) was recorded continuously using subdermal platinum electrodes. At completion of surgery, administration of isoflurane was discontinued (with the exception of those animals receiving isoflurane as treatment) and rats were allowed an equilibration period of 30 min according to the following procedure: group 1 (n = 10), 66% nitrous oxide in oxygen and fentanyl (bolus 10 micrograms kg-1 i.v. followed by infusion at a rate of 25 micrograms kg-1 h-1); group 2 (n = 10), 1.0 MAC of isoflurane in oxygen (FlO2 0.3) and air; groups 3 and 4 (n = 10 per group), 1.0 MAC or 1.5 MAC of desflurane in oxygen (FlO2 0.3) and air, respectively. Ischaemia was produced by combined unilateral common carotid artery ligation and haemorrhagic hypotension to 35 mm Hg for 30 min. Functional neurological deficit was evaluated for 3 days after cerebral ischaemia. At baseline, brain electrical activity was higher with fentanyl-nitrous oxide, 1.0 MAC of isoflurane and 1.0 MAC of desflurane (groups 1-3) compared with 1.5 MAC of desflurane (group 4). Neurological outcome was improved in isoflurane and desflurane anaesthetized animals (groups 2-4), regardless of the concentration used compared with fentanyl-nitrous oxide anaesthesia (group 1). The increase in plasma epinephrine and norepinephrine concentrations during ischaemia was significantly higher in fentanyl-nitrous oxide anaesthetized animals (group 1) compared with animals who received volatile anaesthetics (groups 2-4). These data suggest that cerebral protection produced by isoflurane and desflurane appears to be related to reduction in sympathetic activity rather than suppression of cerebral metabolic rate.

Anesthetics, Inhalation↗
PubMed1998

[Level concept of analgesic dosing in intensive care medicine with sufentanil].

OBJECTIVE: The efficacy of a 3-level regimen of analgesia and sedation was investigated in a clinical setting. Level 1 consisted of continuous administration of sufentanil, in level 2 continuous administration of midazolam and level 3 continuous administration of midazolam and clonidine was added according to patients' needs. METHODS: Sufentanil at 1 microgram/kg/h was given initially. Later it was adjusted to patients' requirements in accordance with the Ramsay score (group 1). Long-term intubated patients received in addition midazolam 0.05 mg/kg/h (group 2). If needed, clonidine 1 microgram/kg/h was added (group 3). Mean drug requirements were investigated during controlled ventilation and during assisted ventilation with spontaneous breathing > 25% of total minute ventilation. In group 1 arterial paCO2 was measured to estimate drug-induced respiratory depression. Values given are median and ranges. RESULTS: With the 3-level-regimen of analgesia and sedation a Ramsay score of 2-3 was achieved in all intensive-care patients. In group 1 (n = 109; 36.7%) paCO2 values were similar at all times. Patients on controlled ventilation needed sufentanil 0.6 (0.075-2.5) microgram/kg/h, on assisted ventilation 0.4 (0.05-2.5) microgram/kg/h. Patients of group 2 (n = 113; 38.1%) had on controlled ventilation a higher requirement of sufentanil 1.2 (0.09-2.7) micrograms/kg/h, in addition Midazolam 0.05 (0.002-0.56) mg/kg/h was given. On assisted ventilation with spontaneous breathing > 25% sufentanil 0.9 (0.05-2.6) microgram/kg/h plus midazolam 0.04 (0.002-0.38) mg/kg/h was sufficient. Group 3 (n = 75; 25.2%) had on controlled ventilation a higher requirement of sufentanil with 1.5 (0.09-4.0) micrograms/kg/h and midazolam 0.05 (0.005-0.52) mg/kg/h, in addition clonidine 1.1 (0.12-2.88) micrograms/kg/h was given. On assisted ventilation with spontaneous breathing > 25% requirement of sufentanil with 1.1 (0.15-2.6) micrograms/kg/h and of midazolam with 0.05 (0.002-0.22) mg/kg/h was slightly lower, whereas more clonidine was needed with 1.3 (0.12-2.88) micrograms/kg/h. CONCLUSION: Continuous infusion of sufentanil only for analgesia and sedation is suitable for intensive-care patients with a short stay in the ICU. Respiratory depression during spontaneous breathing is not significant. The supplementary administration of midazolam and clonidine according to the presented regimen was shown to be of advantage for patients with a longer stay in ICU.

Alfentanil↗
PubMed1997

[Electroconvulsive therapy--anesthesiological procedures].

Electroconvulsive therapy (ECT) utilises the electrical induction of a generalised seizure for treating severe mental disorders. The treatment, developed in 1938, is neglected especially in Germany. This is partly due to the original application in non-anaesthetised patients resulting in many atraumatic side effects. Since the beginning of the sixties, "modified" ECT under anaesthesia with neuromuscular blockade has become worldwide standard. Controlled studies showed that in major depression ECT is at least equal to pharmacotherapy with relatively few adverse side effects. ECT is an effective alternative in patients resistant to pharmacotherapy. The development of modern ECT devices with improved kinds of impulses has reduced the incidence of cognitive side effects in recent years. Due to a variety of centrally acting co-medications and circulatory effects during ECT, these patients are quite a challenge to the anaesthesiologist. Common hypnotic agents obstruct the generation of convulsions. Therefore, therapeutic outcome is directly influenced by the quality of the anaesthetic management. This review is intended to familiarise with the ECT and to provide hints for an optimised selection, setup and practice of anaesthetic treatment.

Anesthesia, General↗
PubMed1997

[Effect of S-(+)-ketamine on autoregulation of cerebral blood flow].

PURPOSE: The present study investigates the effects of S-(+)-ketamine on cerebral blood flow (CBF) autoregulation in rats. METHODS: Following IRB approval, 24 nonfasted male Sprague-Dawley rats were anesthetised with isoflurane, intubated and mechanically ventilated. Catheters were inserted into the right femoral artery, both femoral veins, and into the right jugular vein for drug administration, measurement of mean arterial blood pressure (MAP), and blood sampling. Cortical cerebral blood flow was measured using laser-Doppler-flowmetry (PF 403, Perimed). At the end of surgery isoflurane was discontinued and all animals were randomly assigned to one of the following anaesthetic treatments. In group 1 (n = 8, control), anaesthesia was maintained using fentanyl (10 micrograms/kg i.v. bolus, followed by 25 micrograms/kg/h i.v.) and N2O/O2 (FiO2: 0.3). In group 2 (n = 8) and group 3 (n = 8) animals received 0.5 mg/kg/min S-(+)-ketamine i.v. or 1.0 mg/kg/min S-(+)-ketamine i.v. and O2/air (FiO2: 0.3), respectively. CBF was tested by graded haemorrhage. Arterial blood gases, arterial pH, and pericranial temperature were controlled over time. RESULTS: CBF autoregulation was maintained under low and high doses of S-(+)-ketamine compared to fentanyl/N2O-anaesthetised controls. However, low-dose S-(+)-ketamine shifted the autoregulatory curve towards higher MAP values. CONCLUSIONS: The present study indicates that autoregulatory cerebrovascular dilation is preserved with low and high doses of S-(+)-ketamine. Differences in the lower limit of CBF autoregulation may be consistent with an increased sympathetic tone induced by low doses of S-(+)-ketamine.

Anesthetics, Dissociative↗
PubMed1996

Analgesic efficacy of low-dose ketamine. Somatosensory-evoked responses in relation to subjective pain ratings.

BACKGROUND: Low-dose ketamine has been shown to exert analgesic effects. Whether ketamine-induced pain relief may be quantitated by somatosensory evoked cerebral potentials has not been established. METHODS: Thirty healthy volunteers were assigned randomly to one of three groups. Subjects of group 1 (n = 10, control) were given saline as placebo. In groups 2 (n = 10) and 3 (n = 10), intravenous ketamine (0.25 mg. kg-1 and 0.50 mg. kg-1, respectively) was administered. The following variables were recorded at baseline and for 50 min after drug administration: electroencephalographic (EEG) data, somatosensory-evoked late cortical responses (SEP) elicited by intracutaneous stimulation of the fingertip (2-3 fold pain threshold), heart rate, mean arterial blood pressure, and end-tidal PETCO2 via a tight-fitting mask. Electroencephalographic spectral power in selected frequency bands and frequency percentiles were calculated from the spontaneous EEG segment preceding each somatosensory stimulus. Somatosensory-evoked late cortical response parameters were calculated from the respective poststimulus EEG segments. After recording of each EEG response, subjects were asked to rate the individual pain sensation. RESULTS: In group 1, all variables did not change over time. Ketamine administration resulted in dose-dependent decreases in alpha-activity and increases in theta power (group 2: 190%, group 3: 440%). Electroencephalographic changes were not related to changes in pain perception. For the first 30 min after ketamine injection, a dose-dependent decrease of the long-latency N150-P250 somatosensory-evoked late cortical response component was observed (group 2: 15-20%; group 3: 25-30%). Subjective pain ratings were also different between groups, with a higher degree of pain relief in group 3 for the first 30 min. At the end of the observation period, pain relief and the N150-P250 amplitude were comparable in both ketamine groups. CONCLUSIONS: These data indicate that pain relief induced by low-dose ketamine is dose-dependent for the first 30 min after bolus injection. Changes in pain perception may be quantitated by somatosensory-evoked cortical responses. Also, EEG changes are not specific for changes in nociception, but the increase in theta power may reflect the hypnotic effect of low-dose ketamine.

Adult↗
PubMed1995

Sevoflurane improves neurological outcome after incomplete cerebral ischaemia in rats.

We have studied the effects of sevoflurane on neurological outcome in a rat model of incomplete cerebral ischaemia. After institutional approval, 30 non-fasted male Sprague-Dawley rats (455-555 g) were anaesthetized, the trachea intubated and the lungs ventilated mechanically with isoflurane and 30% oxygen in air. Catheters were inserted into the right femoral artery, both femoral veins and into the right jugular vein for measurement of arterial pressure, drug administration and blood sampling. At completion of surgery, isoflurane was discontinued and the rats were allowed an equilibration period of 30 min according to the following regimens: group 1 (n = 10) received 70% nitrous oxide in oxygen and fentanyl (bolus 10 micrograms kg-1 i.v.; infusion 25 micrograms kg-1 h-1); group 2 (n = 10) received 1.98 vol% sevoflurane in oxygen and air (FIO2 0.3); group 3 (n = 10) received 1.98 vol% sevoflurane in oxygen and air (FIO2 0.3) and 40% glucose (6 ml kg-1 i.p.) 30 min before ischaemia. Ischaemia was produced by combined unilateral common carotid artery ligation and haemorrhagic hypotension to 35 mm Hg for 30 min. Temperature, arterial blood-gas variables and arterial pH were maintained within the physiological range. Plasma glucose concentration was measured before, during and after ischaemia. Neurological deficit was evaluated for 3 days after ischaemia. Neurological outcome was better in sevoflurane anaesthetized animals, regardless of the plasma glucose concentration, compared with nitrous oxide-fentanyl controls. This indicates that differences in plasma glucose concentrations do not account for the cerebral protection seen with sevoflurane.

Anesthetics↗
PubMed1991

Concurrent increases in brain electrical activity and intracranial blood flow velocity during low-dose ketamine anaesthesia.

The purpose of the present study was to assess the effects of low-dose ketamine on spontaneous brain electrical activity (EEG) and intracranial blood flow velocity. Twenty healthy volunteers were divided into two groups: Group I (n = 10) received 0.25 mg.kg-1 ketamine iv; Group II (n = 10) received 0.5 mg.kg-1 ketamine iv. Mean arterial blood pressure (MAP), heart rate (HR), end-tidal PCO2 (PETCO2), and arterial oxygen saturation (SaO2) were measured. The EEG was recorded from temporo-occipital recording sites over both hemispheres. Blood flow velocity in the middle cerebral artery was measured using a transcranial Doppler ultrasound system. All variables were evaluated at baseline and for 60 min following ketamine. Administration of ketamine resulted in increases of MAP and HR in both groups to a similar degree. The PETCO2 and SaO2 did not change in either group over time. Ketamine caused a dose-dependent, transient shift in the EEG to synchronous high-voltage slow waves with an increase in total power (Group I: 301 +/- 38%; Group II: 104 +/- 28%). These changes were associated with dose-dependent increases in mean blood flow velocity (Group I: 35 +/- 7%; Group II: 68 +/- 10%). Our data suggest that increases in intracranial blood flow velocity are closely correlated to increases in neuronal activity and are not secondary to changes in systemic haemodynamic variables.

Adult↗