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Biomedical subjects

K Engelhard

Publications and source records attributed to K Engelhard.

At least 19 recordsLinked to original sources
PubMed2006

Prostate biopsy in the supine position in a standard 1.5-T scanner under real time MR-imaging control using a MR-compatible endorectal biopsy device.

Thirty-seven consecutive patients with elevated PSA levels and negative tumor prostate biopsies underwent a MR-guided prostate biopsy in a 1.5-T scanner in the supine position. After localization of suspected tumor areas using an endorectal coil and two body-phased array coils, the biopsy device was positioned without any repositioning of the patient. The biopsy device consisted of a mount, a ball joint, a positioning stage and an insertion stage with a needle guide, which was filled with a MR-visible fluid to control positioning of the needle using a balanced steady-state free precession sequence (TrueFISP) and a high-resolution turbo spin echo (T2-TSE) sequence. Core biopsies were taken manually in the magnet. The biopsy needle could be correctly positioned in all cases. Suspected lesions with a diameter > or =10 mm could be successfully punctured. Four to nine (mean = 6) biopsies were taken per patient. In 14 patients, prostate cancer was confirmed at histology. Twenty-four biopsies positive for cancer were performed in 14 patients. A correct correlation was found between the site of biopsy and histology. MR-guided prostate biopsy can be effective in increasing primary positive tumor biopsy results in patients with a history of negative tumor TRUS-guided prostate biopsies.

Adenocarcinoma↗
PubMed2005

[Postoperative cognitive dysfunction].

Postoperative cognitive dysfunction is a severe and life-threatening complication after an operation. The mobilisation of the patient is difficult and, therefore, the stay of the patient in the hospital is extended and the resulting immobilisation is associated with further complications (e.g. decubitus, pneumonia, or thrombosis). The genesis of the postoperative cognitive dysfunction has different causes and the highest risk factors are the age of the patient and the character and the duration of the operation. Preexisting diseases, like diabetes mellitus, heart failure, depression or alcohol excess are high risk factors as well as the use of anticholinergic drugs. A specific therapy for this cognitive dysfunction is unknown and, therefore, preventive measures should be used in patients with a preexisting high risk.

Anesthesia↗
PubMed2005

Long-term effects of hypothermia on neuronal cell death and the concentration of apoptotic proteins after incomplete cerebral ischemia and reperfusion in rats.

BACKGROUND: The present study investigates the long-term effects of postischemic hypothermia on neuronal cell damage and concentration changes of apoptotic proteins after cerebral ischemia. METHODS: Sixty-four Sprague-Dawley rats were anesthetized, intubated and ventilated with 2.0 Vol% isoflurane and 70% N2O/O2. After preparation the animals were randomly assigned to the following groups: group 1 (n = 32, fentanyl-N2O/normothermia 37.5 degrees C), and group 2 (n = 32, fentanyl-N2O/hypothermia 34.0 degrees C. Ischemia (45 min) was induced by common carotid artery occlusion plus hemorrhagic hypotension (MAP = 40 mmHg). Arterial blood gases and pH were maintained constant. After 1, 3, 7, or 28 days (each n = 8) the brains were removed, frozen and cut. Neuronal damage was assessed by analyzing Bax, Bcl-2, p53, and Mdm-2 proteins, activated caspases-3-positive and eosinophilic cells. A third group (n = 8) of untreated animals served as naive controls. RESULTS: In hypothermic animals, Bax concentration was decreased by 50-70% over time compared to normothermia. On days 1 and 3, Bcl-2 was increased by 50% with hypothermia. The amount of activated caspase-3-positive cells in the ischemic hemisphere was 0.5% in the hypothermic and 1-2% in the normothermic animals. Of the hippocampal cells, 10-25% were eosinophilic in both groups over time. CONCLUSION: The present data show that hypothermia prevents an ischemia-induced increase of the pro-apoptotic protein Bax for as long as 28 days and increases the concentration of the antiapoptotic protein Bcl-2 up to 3 days compared to normothermic animals. Therefore, after cerebral ischemia, hypothermia has the sustained neuroprotective potential to shift apoptosis-related proteins towards neuronal cell survival.

Animals↗
PubMed2004

Sevoflurane and propofol influence the expression of apoptosis-regulating proteins after cerebral ischaemia and reperfusion in rats.

BACKGROUND AND OBJECTIVE: Sevoflurane and propofol reduce the extent of necrosis and improve neurological outcome in rodent models of cerebral ischaemia and reperfusion. However, the effects of these anaesthetics on programmed cell death (apoptosis) are unclear. The present study investigates whether sevoflurane and propofol affect the expression of apoptosis-regulating proteins after cerebral ischaemia in rats. METHODS: Thirty-two fasted male Sprague-Dawley rats were tracheally intubated and the lungs were ventilated (isoflurane and N2O/O2 anaesthesia). After surgical preparation, the animals were randomly assigned to one of the following groups: control (n = 8): fentanyl intravenous (10 microg kg(-1) bolus and 25 microg kg(-1) h(-1) infusion) with N2O/O2; sevoflurane (n = 8): 2.0% sevoflurane (end-tidal concentration) and O2/air; propofol (n = 8): 0.8-1.0 mg kg(-1) min(-1) propofol intravenous and O2/air; sham-operated (n = 8): 25 microg kg(-1) h(-1) fentanyl intravenous and N2O/O2, no cerebral ischaemia. Ischaemia (30 min) was induced by unilateral common carotid artery occlusion plus haemorrhagic hypotension to a mean arterial pressure of 30-35 mmHg. Four hours after cerebral ischaemia the brains were removed and the expression of apoptosis-regulating proteins (Bax, Bcl-2, p53, Mdm-2) was determined using immunofluorescence and Western-blot analyses. RESULTS: The expression of the pro-apoptotic protein Bax was greater in control animals than in sevoflurane or propofol anaesthetized rats and than in sham-operated animals. The concentrations of Bcl-2, p53 and Mdm-2 were not changed 4 h after cerebral ischaemia. CONCLUSIONS: In addition to the anti-necrotic effects of sevoflurane and propofol, these anaesthetics also reduce the concentration of the apoptosis-inducing protein Bax as early as 4 h after ischaemia.

Anesthetics, Inhalation↗
PubMed2004

Effect of remifentanil on intracranial pressure and cerebral blood flow velocity in patients with head trauma.

BACKGROUND: Remifentanil, an ultra-short-acting opioid, is used as an on-top analgesic in head trauma patients during transient painful procedures, e.g. endotracheal suctioning, physiotherapy, on the intensive care unit. However, previous studies have shown that opioids may increase intracranial pressure and decrease cerebral blood flow. METHODS: The present study investigates the effect of remifentanil on mean arterial blood pressure, intracranial pressure measured with intraparenchymal or epidural probes, and on cerebral blood flow velocity assessed by transcranial Doppler flowmetry in 20 head trauma patients sedated with propofol and sufentanil. Ventilation was adjusted for a target PaCO2 of 4.7-5.1 kPa. After baseline measurements a bolus of remifentanil (0.5 microg x kg(-1) i.v.) was administrated followed by a continuous infusion of remifentanil (0.25 microg x kg(-1) x min(-1) i.v.) for 20 min. RESULTS: There was no change in mean arterial blood pressure, intracranial pressure, and cerebral blood flow velocity in response to remifentanil infusion over time. Statistical analysis was performed using the Wilcoxon Signed Rank test. CONCLUSIONS: These data suggest that remifentanil can be used for on-top analgesia in head trauma patients without adverse effects on cerebrovascular haemodynamics, cerebral perfusion pressure or intracranial pressure.

Analgesics, Opioid↗
PubMed2003

Comparison of whole-body MRI with automatic moving table technique and bone scintigraphy for screening for bone metastases in patients with breast cancer.

The aim of this study was presentation of a whole-body MRI technique with a moving table as a screening tool for bone metastases in patients with breast cancer. Twenty-two patients with breast carcinoma underwent both a planar whole-body bone scintigraphy and whole-body MRI at 1.5 T. The MRI images were acquired with a moving table at six different anatomical positions within a measurement time of 20 min. Coronal images were acquired using a short-tau inversion recovery sequence, accomplished by an axial T2-weighted turbo-spin-echo sequence through the head, and a T1-weighted opposed-phase sagittal 2D fast low-angle shot sequence covering the whole spine. The MRI findings indicating bone metastases were compared with findings from bone scintigraphy. Metastatic lesions were confirmed by follow-up examinations over 1 year. Twelve patients showed bone metastases. Whole-body MRI was superior to bone scintigraphy in predicting lesion origin with a sensitivity of 92% (bone scintigraphy 83%), a specificity of 90% (scintigraphy 80%) and an accuracy of 91% (scintigraphy 82%). The MRI showed additional findings such as metastases of the lung and liver. Whole-body MRI with moving table technique may be an effective method of total body screening for bone in selected patients with breast carcinoma and a high risk of distant metastases, although with the higher costs of MRI bone scintigraphy must still be considered as the first method for screening patients with breast cancer.

Aged↗
PubMed2001

S(+)-ketamine/propofol maintain dynamic cerebrovascular autoregulation in humans.

PURPOSE: This study investigates the effects of S(+)-ketamine and propofol in comparison to sevoflurane on dynamic cerebrovascular autoregulation in humans. METHODS: Twenty-four patients were randomly assigned to one of the following anesthetic protocols: group I (n=12): 2.5 mg.kg(-1)*hr(-1) S(+)-ketamine, 1.5-2.5 microg*mL(-1) propofol-target plasma concentration; group II (n=12): 2.0 MAC (4.0 %) sevoflurane. Patients were intubated and ventilated with O(2)/air (PaO(2)=0.33). Following 40 min of equilibration dynamic cerebrovascular autoregulation was measured and expressed as the autoregulatory index (ARI), describing the duration of cerebral hemodynamic recovery in relation to changes in mean arterial blood pressure. STATISTICS: Mann-Whitney U test (statistical significance was assumed when P <0.05). RESULTS: Dynamic cerebrovascular autoregulation was intact in all patients with S(+)-ketamine/propofol anesthesia as indicated by an ARI of 5.4 +/- 1.1. In contrast, dynamic cerebrovascular autoregulation was significantly delayed with 2.0 MAC sevoflurane (ARI=2.6 +/- 0.7) CONCLUSION: Dynamic cerebrovascular autoregulation is maintained with S(+)-ketamine/propofol-based total iv anesthesia. In contrast, 2.0 MAC sevoflurane delayed dynamic cerebrovascular autoregulation. This supports the use of S(+)-ketamine in combination with propofol in neurosurgical patients based on its neuroprotective potential along with maintained cerebrovascular physiology.

Adult↗
PubMed2001

Effects of remifentanil/propofol in comparison with isoflurane on dynamic cerebrovascular autoregulation in humans.

BACKGROUND: This study investigates the effects of remifentanil and propofol in comparison to isoflurane on dynamic cerebrovascular autoregulation in humans. METHODS: In 16 awake patients dynamic cerebrovascular autoregulation was measured using transcranial Doppler sonography (TCD). Thereafter patients were intubated, ventilated with O2/air (FiO2=0.33) and randomly assigned to one of the following anesthetic protocols: group 1 (n=8): 0.5 microg x kg(-1) x min(-1) remifentanil combined with a propofol-target plasma concentration of 1.5 microg x ml(-1) group 2 (n=8): 1.8 % isoflurane (1.5 MAC). Following 20 min of equilibration the autoregulatory challenge was repeated. Arterial blood gases and body temperature were maintained constant over time. STATISTICS: Mann-Whitney U-test and Wilcoxon signed-rank test. RESULTS: Dynamic autoregulation was intact in all patients prior to induction of anesthesia expressed by an autoregulatory index (ARI) of 5.4+/-1.21 (mean+/-SD, group 1) and 5.9+/-0.98 (mean+/-SD, group 2). With remifentanil/propofol anesthesia dynamic autoregulation was similar to the awake state (group 1: ARI=4.9+/-0.88). In contrast, autoregulatory response was delayed with 1.5 MAC isoflurane (group 2, ARI=2.1+/-0.92) (P<0.05). CONCLUSION: These data show that dynamic cerebrovascular autoregulation is maintained with remifentanil-based total intravenous anesthesia. This is consistent with the view that narcotics (and hypnotics) do not alter the physiologic cerebrovascular responses to changes in MAP. In contrast, 1.5 MAC isoflurane delays cerebrovascular autoregulation compared to the awake state.

Adult↗
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↗
PubMed2000

Combination of signal intensity measurements of lesions in the peripheral zone of prostate with MRI and serum PSA level for differentiating benign disease from prostate cancer.

The aim of this study was to predict the benign or malignant nature of a prostatic lesion by defining a threshold value of signal intensity ratio and a limiting value of serum prostate-specific antigen (PSA) in patients with elevated PSA level. Twenty-six patients with elevated PSA level and no hypoechogenic lesions at endosonography underwent MR imaging using an endorectal body phased-array coil at 1.5 T (Siemens Magnetom Symphony). A T2-weighted turbo-spin-echo (TSE) pulse sequence was applied in a transverse orientation. Two radiologists evaluated the images. In the presence of a pathological finding they defined regions of interest (ROI) in the suspicious pathological area of the peripheral zone and in muscle for reference. The quotient of the two ROIs was calculated and then correlated with the actual PSA level. Diagnosis was confirmed by prostate biopsy. Ten of 12 patients with quotients smaller than 4 showed cancer at histology. Nine of 12 men with cancer proven by biopsy had PSA levels higher than 10 ng/ml. A significant difference (p < 0.001) was found between the quotients of cancer and quotients of chronic prostatitis, fibrosis, or glandular atrophy. The accuracy of tumor differentiation of the method was 77%. Measurement of signal intensity quotients in the peripheral zone of the prostate in combination with knowledge of defined limits of PSA levels the technique could be helpful in detecting additional cancer areas for prostate biopsy. False-negative tumor results of standard sextant biopsy can be reduced. In men with high PSA values the method has a role in differentiating between patients who require prostate biopsy and those of clinical observation.

Adult↗
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

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↗
PubMed1997

High-resolution MRI of pancreatic masses with a new circularly polarized body phased-array coil.

A total of 18 patients with clinical suspicion of a pancreatic tumor underwent dynamic contrast-enhanced CT and MRI examinations. A fat-suppressed T1-weighted 2D fast-low-angle-shot (FLASH) sequence and a T2-weighted spin-echo (SE) sequence were applied in a transverse orientation using a circularly polarized (CP) body phased-array coil. The FLASH sequence was repeated after Gd-DTPA administration. The highest spatial resolution was 1.37 x 1.37 x 3.00 mm3. In two cases a half Fourier single-shot turbo-SE sequence (HASTE) was additionally applied. In a comparison between CT and MRI, pancreatic masses could be demonstrated and characterized with excellent image quality. The fat-saturated 2D FLASH sequence yielded the highest contrast-to-noise ratios after Gd-DTPA administration between pancreas and inflammatory or neoplastic lesion. One non-contour deforming carcinoma could be detected only with MRI and was only retrospectively visible on CT with an element of uncertainty. Magnetic resonance imaging using a CP body phased-array coil and fat-suppressed T1- and T2-weighted FLASH, SE, and turbo-SE sequences offers diagnostic possibilities in improved imaging of the pancreas.

Aged↗
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

[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

[Reliability and interobserver concordance in detection of prostatic carcinoma with magnetic resonance tomography].

PURPOSE: To determine the reliability and the measuring agreement between two radiologists in the identification of relevant structures of prostate anatomy in patients with prostate carcinoma. PATIENTS AND METHOD: 15 patients with prostate carcinoma proved by histology underwent MR Imaging on 1.5 Tesla MR-system (Siemens Erlangen). T1- and T2-weighted sequences were used in the depiction of important anatomic structures for diagnosing prostate cancer. 5 sequences of every patient were evaluated for 5 times by each reader. Reliability was proved by the intraclass correlation coefficient and the measuring agreement was proved by Cohen's cappa test. RESULTS: Only the T2-weighted sequence was of sufficient sensitivity to reach a moderate reliability (r1 = 0.74) and a moderate measurement agreement between the two readers (kappa = 0.5). CONCLUSION: For the evaluation of MR images in staging prostate carcinoma, besides the validity and the measuring agreement, the reliability of the radiologist is the important factor.

Analysis of Variance↗