Biomedical subjects

E Hartung

Publications and source records attributed to E Hartung.

At least 55 records · Page 3Linked to original sources

PubMed1991

[Fulminant malignant hyperthermia during the 6th general anesthesia using volatile anesthetics].

We report on the fulminant crisis of malignant hyperthermia occurring in a 30-year-old female during kidney transplantation. In the past, she had been anaesthetised repeatedly without complications. Anaesthesia was induced with thiopental and vecuronium and continued with isoflurane/N2O/O2. After an initially normal course of anaesthesia, the patient developed symptoms of a fulminant malignant hyperthermia (MH) including excessive increase in end expiratory CO2, hyperkalaemia, tachycardia and hyperpyrexia. The patient was saved by the timely administration of dantrolene. A surgical revision required the next day because of bleeding was done under dantrolene cover and took an uncomplicated course. The patient was extubated 7.5 hours after the second intervention and transferred to a normal ward after 4 days. A subsequently performed in vitro contracture test clearly revealed susceptibility to malignant hyperthermia.

Adult↗

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↗

PubMed1988

Capillary rarefaction characteristic of the skeletal muscle of hypertensive patients.

There is evidence that the rarefaction of the capillary bed is typical for the skeletal muscle of spontaneously hypertensive rats. We were therefore interested to learn whether there is also a rarefaction in skeletal muscle of human hypertensives. The number of capillaries was morphometrically analysed and counted in the quadriceps and the pectoralis major muscles of human normotensives (n = 12) and hypertensives (n = 15). The clinical diagnosis and certain pathological criteria, such as blood pressure (with or without antihypertensive therapy), heart weight, left ventricular wall thickness, the state of kidney arterioles and brain, and heart vessels, were used to classify the patients into two groups. The dissected tissue samples were prepared according to the GMA method and the capillary numbers per area were counted using light microscopy (250 x). The quadriceps muscle had a capillary density (per 2.5 mm2) of 442 +/- 51 in normotensives and 277 +/- 41 in hypertensive patients; in the pectoralis major muscle we counted 477 +/- 30 in controls and 232 +/- 28 in hypertensives. The rarefaction in the quadriceps muscle ranged by about 37%, in the pectoralis major muscle by about 51%. It is suggested that the reduction of the capillary surface area caused by the capillary rarefaction reduces the transcapillary fluid exchange and in that way prevents an overperfusion of the terminal vascular bed.

Capillaries↗

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↗

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↗

PubMed1984

Acute effects of shock-type vibration transmitted to the hand-arm system.

The aim of the project was to find out whether shock-type vibration of hand-tools compared to non-impulsive vibration has stronger acute effects on the hand-arm system and therefore needs a stricter evaluation from the occupational health point of view in comparison with the requirements of the Draft International Standard ISO-DIS 5349. Under laboratory conditions, subjects were exposed to simulated vibration of hand-tools (grinder, chain saw, hammer-drill, pneumatic hammer, rivet hammer and nailer). The following evaluation criteria were used: biomechanical transmissibility of the hand-arm system (wrist, elbow joint, shoulder joint); muscle-activity (m. flexor carpi ulnaris, m. biceps, m. triceps); peripheral circulation (skin temperature) and subjective perception (comparison of intensity of standard and test vibrations). The results show no significant difference in acute effects on the hand-arm system between impulsive and non-impulsive type vibrations of the hand-tools tested with respect to the chosen vibration level, short-time exposure (up to 8 min) and evaluation criteria. In summary, therefore, it may be concluded that for the evaluation of shock-type vibration of the hand-tools tested, it is justified to use the existing Draft International Standard ISO-DIS 5349.

Adult↗

PubMed1984

[Somatosensory evoked potentials under alfentanyl].

Somatosensory evoked potentials (SEP) at present seem to be the most reliable and accurate method for the investigation of compounds modulating pain sensation. Besides detecting changes in the duration and the potency of action of analgesics, their possible site of action in the sensory pathways may be derived by this method. In ten trials using two trained canines the efficacy and the duration of action of a new and short acting opioid, alfentanil was evaluated on SEP using cumulative doses (3, 30, 60, 120 micrograms/kg). Concomitantly arterial blood gases were analyzed for possible respiratory depressant effects. The results demonstrate that alfentanil induces a short lasting suppression of the N100 peak as well as a latency change of the N140 peak to N220, the latter lasting for more than 80 min. These effects saturate at doses higher than 30 micrograms/kg. The significant change in arterial blood gases - a fall in PaO2 and an increase in PaCO2 - are most prominent with 30 micrograms/kg and 120 micrograms/kg, respectively. It is of short duration and correlates with the suppression of the N100 peak. The latency changes seem to correlate with a marked sedatory effect. Due to the differential effects induced by the opioid, an interaction with different opioid subreceptor sites is postulated.

Alfentanil↗

PubMed1984

Nalbuphine reverses fentanyl-related EEG-changes in man.

Nalbuphine, chemically related to naloxone however, with mixed agonist-antagonist activity, was considered to be of clinical interest in reversing opioid anesthesia. In an open-end study 15 patients (mean age 40 years) undergoing orthopedic surgery received nalbuphine (0.1 mg/kg) after fentanyl (total dose 17.4 micrograms/kg over a mean of 95 min). In order to establish the state of vigilance, continuous EEG-recording of the posterior region of the cortex (P3-O1) was done with the aid of power spectral analysis using fast Fourier transformation (FFT). Additionally blood pressure and heart rate were measured. The observed effects were compared with the awake unpremedicated preoperative state. In the EEG nalbuphine reversed the anesthesia-related increase in power in the delta (0.25-4 Hz) and decrease in alpha (8-12 Hz), beta 3 (20-25 Hz) and beta 4 (25-32 Hz) domain. After the 45th minute delta significantly increased while power in the beta-band unsignificantly dropped. Power in the alpha-band remained elevated throughout the whole postoperative period. In regard to blood pressure measurements nalbuphine induced an increase in systolic, diastolic pressure and heart rate 15% above control. These parameters declined towards the 30th minute; only heart rate reached predrug values at the 45th minute. With the aid of EEG-power spectral analysis it was demonstrated that nalbuphine seems a valuable tool for the reversal of opioid-induced cortical depression.

Adult↗

PubMed1983

Naloxone reverses the hypnotic effect and the depressed baroreceptor reflex of halothane anaesthesia in the dog.

In order to evaluate the effect of an opioid antagonist on depressed intrinsic central vaso-motor drive (carotid sinus reflex) and high voltage slow delta waves in the EEG associated with halothane, naloxone was injected intravenously in a bolus of 100 or 200 micrograms.kg-1 on different days in the anaesthetized dog (0.64 Vol% halothane in oxygen). Only the 200 micrograms.kg-1 dose of naloxone reversed the halothane-induced depression of the blood pressure and heart rate response to clamping of both exteriorized common carotid arteries. The EEG changed from high voltage slow waves to low voltage fast waves, inducing a reduction of power in the delta band in spectral analysis. This effect was most pronounced during the 20th minute post naloxone injection. Naloxone did not reverse the halothane-related hypotension and bradycardia. Because of the late "cortical arousal" reaction during halothane-anaesthesia and the high dose necessary, naloxone appears to exert its action through a generalized increase in CNS excitation. An antagonisation of halothane-induced release of opiate-like peptides therefore is less likely.

Anesthesia, Inhalation↗

PubMed1983

Tifluadom (KC 5103) induces suppression and latency changes on somatosensory evoked potentials which are reversed by opioid antagonists.

Suppression of evoked potentials of the EEG are indicators of analgesia. Tifluadom induces latency changes which are reversed by the kappa-antagonist Mr 2266. Naloxone reverses peak suppression which indicates an additional interaction with the my-opioid-receptor. The specific benzodiazepine antagonist Ro 15-1788 is not effective in reversing peak-changes. Therefore nociceptive stimuli are modulated by tifluadom not only through the interaction with kappa- but also with my-opioid-receptors.

Animals↗

PubMed1983

Prevention of late fentanyl-induced respiratory depression after the injection of opiate antagonists naltrexone and S-20682: comparison with naloxone.

Compared with naloxone, two opiate antagonists (naltrexone and S-20682) were tested in the intact dog in order to reverse respiratory depression, induced by fentanyl 50 micrograms kg-1 i.v. Respiratory rate and arterial blood-gases were measured at 5, 30, 60, 120, 180 and 240 min after the additional i.v. injection of the antagonist (1 microgram kg-1). Only S-20682, but not naloxone or naltrexone, prevented late (240 min) fentanyl-induced depression of respiratory drive. A late respiratory depression coincided with an increase in amplitudes and a reduction of frequency in electrical cortical activity (EEG). Naltrexone exhibited an antagonistic effect of duration twice (60 min) that of naloxone.

Animals↗

PubMed1983

Effects of three narcotic antagonists (naltrexone, diprenorphine, and S-20682) on blood pressure, heart rate and electrical cortical activity.

Three narcotic antagonist drugs (EN-1639 or naltrexone, M-5050 or diprenorphine and the 6-oxo analogue of oxilorphan, S-20682) were evaluated in increasing doses (1-80 micrograms/kg) in the unanaesthetised dog for possible effects on blood pressure, heart rate, respiratory rate, arterial blood gases, and convulsive EEG changes. Compared to the control-awake situation, diprenorphine and S-20682 induced hypotension (maximum fall 15%), bradycardia (maximum 12%) and bradypnoea (maximum 25%). These effects were not increased at doses higher than 20 micrograms/kg. Despite the induced bradypnoea, there were no significant changes in arterial pO2 and pCO2. Simultaneously, with the cardio-respiratory changes, EEG activity shifted from high frequency, low amplitudes of the awake state, to low frequency, high amplitudes of a sleep-like state. Convulsive EEG changes were never recorded with any of the tested compounds. It is suggested that the observed cardiovascular changes are due to a reduced state of vigilance, since auditory stimuli induced an arousal reaction with a reversal of the depressed variables. In contrast, naltrexone induced only bradycardia in the observed dose range (maximum 25%). There were no effects on blood pressure, respiratory rate, arterial blood gases and EEG.

Animals↗

PubMed1983

Bremazocine: an opiate that induces sedation and analgesia without respiratory depression.

The benzomorphan analogue bremazocine has been shown to be a potent analgesic with a low dependence liability and with no respiratory depressant effects in preliminary pharmacologic screening. As this compound may prove to be of potential interest to anesthesiologists, it was tested in the conscious dog in increasing doses (1, 5, 10, 20, and 40 micrograms/kg) while blood pressure, heart rate, respiratory rate, arterial blood-gas tensions, electrical cortical activity, and somatosensory-evoked potentials (SS-EVP) were recorded. Bremazocine had no significant cardiovascular or respiratory effects. Power spectral analysis of the EEG showed a dose-related increase of power in the theta to delta band. SS-EVP was characterized by a decrease in amplitude of the P45 and P70 waves and an increase in the latency of the P 100 peak. EEG and peak latency changes could be reversed by the kappa-specific antagonist Mr 2266 (20 micrograms/kg), but not by the classic opiate antagonist naloxone (20 micrograms/kg). It is suggested that kappa receptor sites distinct from those interacting with common opioids (mu) are responsible for the observed changes associated with bremazocine.

Analgesics↗

PubMed1983

Plasma levels of alfentanil and etomidate in patients and their relation to compressed power spectral analysis of the EEG.

In 22 patients alfentanil-etomidate anesthesia was used for orthopedic procedures using for the induction period 300 micrograms/kg of the hypnotic and 100 micrograms/kg of the opioid. Maintenance of anesthesia consisted of 20 micrograms/kg of alfentanil given every 15 min and 20 micrograms/kg/min of etomidate given over an infusion. The patients were intubated and mechanically ventilated with pure oxygen. In order to access the state of vigilance with respect to etomidate and alfentanil plasma levels, EEG power spectra were computed from electrical cortical activity of the occipital region (P3-O1); respectively venous blood samples were assayed by means of gas chromatography for alfentanil and etomidate plasma concentration. In the EEG power spectrum, anesthesia replaced the high dominant alpha-peaks of the control-awake period by a disharmonious pattern over the whole frequency range (0.5-16.0 Hz). At the end of anesthesia vigilance recording indicated a correlation with plasma etomidate level. Once concentration had dropped below 100 ng/ml power spectra were characterized by a stable harmonious peak in the alpha-range (8.0-10.0 Hz). Plasma levels above 100 ng/ml induced a fluctuating pattern with peaks in the theta to delta band (0.5-8.0 Hz); the latter was characterized by drowsiness and a reduced respiratory drive. Opioid plasma levels above 100 ng/ml with etomidate levels below 80 ng/ml did not influence to the same extent. EEG power spectra seem to be a useful tool in pinpointing to a reduced state of vigilance. Such a state when present with opioid ingestion is often accompanied by respiratory depression.

Adult↗

PubMed1982

Perfusion of the fourth cerebral ventricle with the synthetic opioid peptide, FK 33-824, induces dose-related bradycardia and naloxone-reversible respiratory depression in the awake dog.

The importance of natural opioids in the central control of blood pressure, heart rate and respiratory function was evaluated with a synthetic analogue of Met-enkephalin, FK 33-824, which is more resistant to enzymatic degradation than the natural opioids. Increasing concentrations (20, 100, 200 and 400 micrograms/ml), perfused through the 4th cerebral ventricle of the conscious dog, induced a concentration-related depression of respiratory function - as reflected in arterial pCO2 and pO2 and heart rate. Naloxone (40 micrograms/ml) was able to reverse respiratory depression whereas bradycardia was naloxone-resistant even after massive (100 micrograms/kg) intravenous doses. Mean arterial blood pressure was not affected in the tested concentration range. Because respiration was reversed by naloxone, it is concluded that respiratory control is regulated by the mu-type opioid receptor. Heart rate, however, may be governed by the delta-type opioid receptor which is less susceptible to naloxone.

Animals↗