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Biomedical subjects

E Freye

Publications and source records attributed to E Freye.

At least 55 records · Page 3Linked to original sources
PubMed1990

Does prostaglandin E1 and superoxide dismutase prevent ischaemic spinal cord injury after thoracic aortic cross-clamping?

The beneficial use of prostaglandin E1 (PGE1) and superoxide dismutase (SOD) on the tolerance to ischaemia of the spinal cord was evaluated following thoracic aortic cross-clamping in dogs. Aside from spinally evoked somatosensory potential (SEP) by means of a bipolar epidural catheter, postoperative evaluation of motor deficits was used to determine the efficiency of pharmacological protection when compared with controls. The animals were divided into four groups. Group I (n = 12) served as controls. The dogs of Group II (n = 12) were treated with PGE1 (100 ng/kg/min) during clamping and the first hour after declamping. In the third group (n = 12) SOD was given as an intra-arterial bolus (1 mg/kg) prior to declamping which was followed by a continuous perfusion (0.4 mg/kg/min) into the carotid artery for 25 min. In Group IV (n = 12) the dogs were treated with a combination of PGE1 and SOD in the same manner as in Groups 3 and 4. Results after pharmacological protection were significantly better than controls. In Group I all animals but one (92%) were paraplegic, as were five in Group II (42%) and eight in Group III (67%). In contrast no dog in Group IV developed paraplegia. There was a close correlation of SEP and postoperative recovery. The group with combination therapy (PGE1 plus SOD) was characterised by a loss of the evoked potential for a mean of 15 min, the PGE1 group for 45.8 min and the SOD group for 58.5 min. While the control group was characterised by a loss of 72.7 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Alprostadil↗
PubMed1989

Somatosensory-evoked potentials during block of surgical stimulation with propofol.

The effect of propofol on somatosensory evoked potentials was assessed during different intra-operative stimuli in prolonged (greater than 2 h) abdominal operations. SSEP were used to evaluate the extent of block of sensory nerve conduction at the following stages: preinduction; during steady state anaesthesia; during traction of the mesentery; 10 min after anaesthesia. Propofol 100 micrograms kg-1 min-1 and nitrous oxide in oxygen anaesthesia induced a significant decrease in amplitude of the SSEP; noxious stimulation resulted in an increase in afferent nerve transmission and a concomitant increase of amplitude of the late evoked potential. After operation, impulse transmission recovered rapidly and the amplitude was similar to control at 10 min after anaesthesia.

Abdomen↗
PubMed1989

[The central nervous system arousing effects of ketamine are decreased by addition of midazolam. A post-anesthesia study of patients following maxillary surgery with spontaneous respiration].

The present study was done in order to investigate the central nervous activity in patients (n = 15) after maxillo-facial surgery, 5 and 90 minutes post ketamine-midazolam-anesthesia. The combination of a benzodiazepine with ketamine was thought to be beneficial to reduce the usual excitatory effects after ketamine postoperatively. In order to demonstrate these benefits EEG-power spectra as well somatosensory-evoked potentials were derived (Neurotrac). Additionally, the central nervous effects were correlated with blood pressure changes. 5 minutes post ketamine-midazolam-anesthesia EEG-power spectra showed a marked depression in the alpha, theta and delta power band when compared to the control-awake situation. However, power in the beta domain (13-30 Hz) was significantly elevated. 90 minutes post anesthesia the high power values returned back to control. In no instance were there any signs of theta-paroxysms which can be taken as an index for central excitation. In the evoked potential a significant increase in amplitude of the early N20 and late N50 peak was evident. This correlated with an increase in systolic blood pressure. 90 minutes post anesthesia only the late N50 peak still remained elevated suggesting some residual excitatory effects in the thalamo-cortical projection area to be present. The latter may reflect an increase in activity in the associative cortical areas of the cerebral cortex. In general however, the additional administration of midazolam resulted in a marked reduction in excitatory central nervous effects when compared to the well known excitation after sole ketamine injection. Thus, the beneficial venture of the two separate classes of anesthetics is advocated for clinical practice.

Adolescent↗
PubMed1988

An open comparison of propofol and enflurane for prolonged abdominal operations.

Anaesthesia in 15 patients scheduled for prolonged abdominal surgery was induced with hexobarbitone and maintained with nitrous oxide and enflurane, while in a further 15 patients propofol was used for induction and maintenance. Three patients in the latter group required additional fentanyl but cardiovascular responses were otherwise similar in the two groups. Return of consciousness, response to verbal command, ability to answer questions and adequate spontaneous ventilation was more rapid in the propofol patients. EEG power spectra also returned to baseline more rapidly in the propofol group.

Abdomen↗
PubMed1988

[The agonist-antagonist nalbuphine prolongs gastro-cecal transit time and induces short-term pain following neuroleptanesthesia using fentanyl. A comparative study using a placebo].

Little is known about the effects of mixed opioid analgesics on gastrointestinal propulsion. In 20 patients, nalbuphine (0.1 mg/kg) was given after routine neuroleptanesthesia consisting of 70 micrograms/kg droperidol, 7 micrograms/kg fentanyl, and N2O/O2 (3:1) ventilation, to study its effect on gastrointestinal motility in the postoperative period. For comparison, another group of patients (n = 20) undergoing similar interventions received placebo (0.9% NaCl) at the end of the procedure. Gastrointestinal transit time was determined by measuring the exhaled H2 concentration following gastric lactulose administration. As lactulose is degraded only in the cecum, resulting in the release of hydrogen, the arrival of the polysaccharide at the terminal ileum could thus be determined. Compared to placebo, gastrointestinal transit was significantly longer in patients after nalbuphine (mean transit time 270 min vs 380 min). Pain estimation by visual analogue scale (VAS 0-10) suggested an antagonistic effect at the 10th and 20th min postoperatively, as pain scores in the nalbuphine group were higher when compared to placebo (3.5 vs 1.8 and 2.5 vs 1.4). There was a similar pain score in both groups (1.3 vs 1.4) 30 min after drug administration. However, there was significantly better pain relief after nalbuphine (0.7 vs 1.4 and 0.7 vs 1.1) in the late postoperative period (120th and 240th min). When given after potent opioids, it must be borne in mind that the antagonistic effect of nalbuphine is initially apparent. The agonistic potency of the compound will come into effect around the 30th min post-injection. Delayed gastrointestinal transit after nalbuphine is explained by agonist-like effects on peripheral opioid receptors in the gut.

Adult↗
PubMed1988

[Postoperative reversal of loss of vigilance following midazolam with the use of the antagonist flumazenil (Ro 15-1788). A comparative study with a placebo and the use of EEG-power spectra].

Midazolam, a benzodiazepine with the purportedly shortest half-life of all these compounds, is advocated for the induction of general anesthesia. It is still debatable, however, whether a long-lasting hangover may result in depression of vigilance postoperatively. After midazolam induction (0.18 mg/kg) and enflurane/nitrous oxide/oxygen anesthesia, ten patients received flumazenil (0.8 mg/70 kg) in the postoperative period while another ten received placebo in a double-blind fashion. Continuous recording of EEg activity was performed using the Lifescan monitor, computing the power in the various EEG frequency domains. Additionally, patients were scored with regard to orientation in space and time and their collaboration and comprehension of verbal commands. Compared to placebo, flumazenil induced power in the alpha domain, accompanied by a drop of power in the delta and theta bands. While the increase in alpha activity resolved after 30 min, beta activity increased significantly, an effect that lasted up to the 180th postoperative minute. As with the finding of higher power in the fast-frequency domains, flumazenil patients scored higher with regard to collaboration and comprehension as well as orientation in space and time. 1. When used for induction, midazolam may result in significant depression of vigilance even 120 min after operation. 2. Flumazenil is a specific antagonist with a rapid onset of action. 3. Flumazenil is an antagonist specifically directed to reverse the side-effects of benzodiazepines in a manner similar to naloxone, which is used in opioid overdose.

Adult↗
PubMed1986

The benzodiazepine (+)-tifluadom (KC-6128), but not its optical isomer (KC-5911) induces opioid kappa receptor-related EEG power spectra and evoked potential changes.

Tifluadom, a benzodiazepine with purported opioid receptor-related analgesic properties, was studied in regard to its acute effects on power spectra of the EEG to demonstrate vigilance changes. Additionally, somatosensory-evoked potentials (SEP) were derived to evaluate its effect on the propagation of impulses in sensory nerve fibers. In order to demonstrate stereospecificity, the two enantiomers of tifluadom (KC-5911 and KC-6128) were given in graded doses (20, 40, 80, 160 micrograms/kg i.v.) to awake, unrestrained and trained dogs at 10-min intervals. KC-6128, but not its optical counterpart KC-5911, induced synchronization of the EEG at 20 micrograms/kg with an increase of power (pW) in the delta (1-4 Hz; +300%), theta (4-8 Hz; +450%), and alpha (8-13 Hz +90%) bands. This was accompanied by a reduction of power in the fast beta domain (13-30 Hz; -95%). Vigilance changes were reflected in the beta/delta quotient which dropped from 3.7 (control) to 0.8 (20 micrograms/kg) and to 0.3 (40 micrograms/kg). A further increase in the dose resulted in saturation. At the highest dose (160 micrograms/kg) there was an additional reduction of the beta/delta quotient to 0.1. In order to unmask the receptor population, possibly mediating the observed changes, a benzodiazepine antagonist and opioid antagonists were given. Ro 15-1788 (240 micrograms/kg) had no effect and naloxone (20 micrograms/kg) induced a short term (5 min) arousal. Only the kappa antagonist Mr 2266 (20 micrograms/kg) induced a reversal of the beta/delta quotient back to 5.5. KC-5911 induced an insignificant drop in the beta/delta quotient which was reversed by Ro 15-1788.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Opioids with different affinity for subreceptors induce different effects on early and late sensory evoked potentials (SEP) in man.

Amplitude changes of event-related sensory potentials (SEP's) present objective measurements for the evaluation of pain perception in man. Alfentanil, an opioid with dominant binding to the mu-receptor was given in graded doses (5-, 10- micrograms/kg) to volunteers. Nalbuphine, an opioid with reported kappa-agonist activity, was given in graded doses (100-, 500-, 1000- micrograms/kg) to another group i.v. Both groups were also exposed to progressively increased electrical stimulations (mA) in order to determine tolerance threshold before and after drug administration. In the alfentanil group (n = 5) there was a dose- related decrease of the amplitude of the early N20-peak. The late N100-peak was not, however, affected. This correlated closely (r = 0.87) with a naloxone-reversible increase of tolerance to electrical current. In the nalbuphine group (n = 15), there was a dose-related, naloxone non-reversible reduction of amplitude of the late N100-peak which showed a good correlation (r = 0.9) with an increase in current threshold. As the early evoked potentials are primarily generated in the pontine-thalamic region, it is suggested that the mode of action of alfentanil resembles that of a blockade of sensory impulses. The latter takes place before impulses are transmitted to more rostrally located CNS structures which are responsible for pain identification. The late evoked potential affected by nalbuphine indicates an activity on thalamo-cortical projection sites which are involved in subjects' cognitive activities. Kappa-ligands, therefore, seem to exert a different mode of action than mu-opioids, which results in a modulation of the negative emotional response associated with pain, rather than an attenuation of pain impulses.

Adult↗
PubMed1986

[Tifluadom, a benzodiazepine with opioid-like activity: study of its central mechanism of action in conscious dogs].

A derivative of the 1,4-benzodiazepine series with reported opioid activity was evaluated in regard to its effect on central nervous activity in the awake canine. Additionally a possible benzodiazepine- or opioid-receptor interaction was evaluated by using specific antagonists. In 10 experiments increasing doses of tifluadom (5, 10, 20, 40, 80 micrograms/kg) modified somato-sensory-evoked potentials (SEP) inducing a dose-related latency change (40-80 micrograms/kg) and a suppression (80 micrograms/kg) of the P50-peak. Both effects are interpreted as a modification of stimuli reaching the somatosensory cortex. EEG-spectral analysis was characterized by a dose-related decrease of power in the higher frequency range (13-40 Hz) accompanied by an increase of power in the lower band (0.5-3.5 Hz). This effect was paralleled by deep sedation. The specific benzodiazepine antagonist Ro 15-1788 (240 micrograms/kg) was ineffective in reversing central nervous EEG- and SEP-changes. Naloxone (20 micrograms/kg) induced a short-term (5 min) arousal and a partial reversal of SEP-changes. The specific opioid-kappa-antagonist Mr 2266 (20 micrograms/kg) however, induced a long lasting return of power spectra and SEP-changes back to control. This results suggest that tifluadom, although being structurally a benzodiazepine, interacts with an opioid sub-receptor of the kappa-type, which is known to induce sedation and supraspinal analgesia without respiratory depression.

Animals↗
PubMed1986

[Alfentanil as the last dose (on top) in neuroleptanesthesia with fentanyl. Pharmacokinetics and pharmacodynamics with reference to the cortical effect].

Due to its predictable duration of action, its low volume of distribution in the organism (muscle, fat tissue, skin) and a corresponding low terminal elimination half life (t 1/2 beta), alfentanil seems suitable for use as the last dose of opioid given during NLA. In order to compare the efficacy of this regimen, patients (n = 10) during routine-NLA (induction 0.3 mg/kg etomidate, 140 micrograms/kg droperidol, 5 micrograms/kg fentanyl with a maintenance dose of 2 micrograms/kg when necessary and mechanical N2 O/O2 = 2:1 ventilation) received alfentanil (20 micrograms/kg) as the last opioid, while another set of patients (n = 5) received fentanyl (1.5 micrograms/kg). For recording of vigilance continuous EEG power spectra were derived (position Fpz--C3), and in addition minute volume was monitored postoperatively. After the last dose of the opioid, alfentanil--and fentanyl--blood plasma levels were determined every 10 min over a period of 100 min Vigilance, i.e. the sensitivity of the organism in responding to a stimulus, was significantly higher in the "on-top"-alfentanil group. This was derived from the high power in fast frequency domains, beta (greater than 460%) and alpha (greater than 34%) compared to routine NLA in the post op. period. No significance was observed among both groups in regard to postop. respiratory minute volumes and fentanyl plasma levels. There was no correlation between power in the various frequency bands (delta, theta, alpha and beta), postoperative respiratory minute volumes and corresponding plasma levels of fentanyl. Due to a higher state of postoperative vigilance, alfentanil is considered a suitable alternative as the last opioid during narcotic anaesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Alfentanil↗
PubMed1986

[Lung compliance in man is impaired by the rapid injection of alfentanyl].

To demonstrate opioid-induced muscular rigidity, compliance was measured in patients after induction of anaesthesia with etomidate (0.3 mg/kg) and N2O/O2 (2:1) ventilation. Alfentanil was given subsequently to two groups of patients: either as a bolus injection (n = 15) over 3 s, or as a slow injection (n = 15) over 30 s. Significant reduction of compliance (max. 30%) was observed after rapid injection in the following 4 min. This effect was promptly reversed by succinylcholine (25 mg i.v.). The slow injection of the opioid over 30 s, was followed by a small insignificant reduction in compliance. Alfentanil is increasingly used for short-term anaesthesia where no muscle relaxants are administered. Thus slow injection of the opioid is advised in order not to impair adequate ventilation.

Adult↗
PubMed1985

Pharmacokinetic data analysis of alfentanil after multiple injections and etomidate-infusion in patients undergoing orthopedic surgery.

The pharmacokinetics of Alfentanil, a new short acting analgesic, and Etomidate, a very short acting hypnotic compound, were studied in patients undergoing orthopedic surgery. Anesthesia was induced by bolus i.v. injection of Alfentanil and Etomidate, whereas the maintenance was performed by continuous infusion of Etomidate and repetitive i.v. injections of Alfentanil. The kinetics of the analgesic can be described by a two-compartment model; the elimination half-life has a mean value of 64.8 +/- 38.5 min. No cumulation of the drug was seen in spite of multiple injections. Concerning Etomidate it is not clear whether one or two compartments are needed. The mean elimination half-life is 29.4 +/- 6.2 min. The results suggest a possible shortening of the half-life of Etomidate in the presence of Alfentanil.

Adult↗
PubMed1985

Reversal of fentanyl related respiratory depression with nalbuphine. Effects on the CO2-response curve in man.

Due to the short duration of action of naloxone, late respiratory impairment may be anticipated when given for the reversal of opioid anesthesia. Nalbuphine, a mixed agonist-antagonist chemically related to naloxone has a longer duration of action. It therefore was considered to be of clinical interest in reversing fentanyl anesthesia related depression of respiratory drive. In an open study 15 patients (mean age 40 years) undergoing orthopedic surgery received nalbuphine (0.1 mg/kg) after fentanyl (median dose 1.4 mg over a mean length of operation time of 95 min) - N2O/O2-anesthesia. 5, 15, 30, 45 and 60 min after nalbuphine, the ventilatory response to CO2-stimulation (rebreathing technique), was assessed and compared to control pre-anesthetic values. Nalbuphine reversed total apnoea due to fentanyl anesthesia. The slope of the CO2-response curve (sensitivity of the respiratory center to CO2) was -8% below control at the 5th and +13.5% and +22.6% at the 30th respectively 45th minute post nalbuphine. The ventilatory response to an increased end-tidal pCO2 of 60 mm Hg (level of response of the respiratory center to CO2) remained below control (-23.5% to -21%) over the following 60 minutes. A return of respiratory depression was not observed as the slope of the CO2-response curve remained above control values. From this study it was concluded that nalbuphine seemed to be a suitable compound for the reversal of opioid-anesthesia induced respiratory depression.

Adult↗
PubMed1985

[Somatosensory evoked potentials (SEP) by isoflurane and enflurane in cardiosurgical interventions].

In the order to gain further insight into the sensory nervous pathways during enflurane- and isoflurane anaesthesia, two different concentrations (1 and 2 vol.%) of the anaesthetics were given to patients during extracorporeal circulation in normothermia and normocarbia, while somatosensory-evoked potentials (SEP) were recorded. As SEP-changes either reflect a change in functional integrity of the sensory nervous pathways (amplitude suppression) and a change in the speed of conduction (latency changes), the central effects of the volatile anaesthetics could be more fully evaluated. Isoflurane as well as enflurane induced a concentration-related change in latency especially of the late N100-component. However, in contrast to isoflurane administration the isomer enflurane in the high concentration range (2 vol.%) induced an increase of amplitudes of the early N20 and late N100-peak. Such an increase in amplitudes is interpreted as a disinhibition of medullary inhibitory centres, a possible premonitory sign of epileptogenic cortical activity, which already had been observed by various investigators.

Afferent Pathways↗