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A Doenicke

Publications and source records attributed to A Doenicke.

At least 19 recordsLinked to original sources
PubMed1992

Does etomidate cause haemolysis?

Etomidate is currently presented as a solution with propylene glycol as solvent. This organic solvent has an extremely high osmolality and is probably responsible for some of the side effects of this drug. In order to detect haemolysis, an indication for cell damage, we have measured serum haptoglobin concentrations in 12 healthy male volunteers after administration of etomidate 0.3 mg kg-1. Six subjects received etomidate in propylene glycol (EtoPG) with an osmolality of 4965 mosmol kg-1 and six received etomidate in lipid emulsion (EtoLip, 400 mosmol kg-1). Haptoglobin concentrations in the EtoPG group decreased by 44% and 43% from baseline values at 2 and 4 h after administration, respectively, and were significantly smaller than after administration of EtoLip. After 24 h, haptoglobin concentrations had not reached baseline values.

Adult↗
PubMed1992

Onset and recovery of rocuronium (Org 9426) and vecuronium under enflurane anaesthesia.

We have studied the onset, duration of action and recovery index of twice the ED90 of rocuronium (Org 9426) (0.6 mg kg-1) and of vecuronium (0.08 mg kg-1) in patients during enflurane anaesthesia. Rocuronium had a significantly shorter mean onset time of 1.8 (SD 0.4) min, compared with vecuronium 3.4 (0.8) min. Clinical duration (time for the first twitch in the train-of-four to recover to 25% of control) was similar for both drugs (29 (10) min vs 31 (12) min). Spontaneous recovery times (TOF ratio 70%) did not differ significantly between rocuronium (47 (10) min) and vecuronium (44 (11) min).

Adolescent↗
PubMed1992

Osmolalities of propylene glycol-containing drug formulations for parenteral use. Should propylene glycol be used as a solvent?

Propylene glycol (PG) is a widely used vehicle for water-insoluble drugs. Injection of drugs formulated with this solvent often results in pain, thrombosis, or thrombophlebitis that can be reduced by premedication with local anesthetics or opioids. Because osmolality and pH that are unphysiologic may cause these adverse effects, we assessed the contribution of PG to the osmolality of parenteral drug formulations. Osmolality of PG measured in distilled water showed that PG content and osmolality were directly related: 2% wt/vol PG, 264 mOsm/L; 100% PG, 15, 200 mOsm/L. The osmolalities of commercially available preparations of drugs dissolved in PG ranged from 365 mOsm/L (2% PG content) to 12,800 mOsm/L (83.46% PG), with most above 1000 mOsm/L. Replacement of PG by a solvent with lower osmolality in Germany has effectively reduced the incidence of side effects for one drug. Until PG can be replaced in drugs, we recommend diluting drugs in a large volume of saline solution; this may help to minimize the undesirable effects of this solvent.

Anesthesiology↗
PubMed1992

[Histamine release during induction of combination anesthesia using nalbuphine or fentanyl. Modulation of the reaction by premedication with promethazine/pethidine].

In a controlled clinical trial in patients admitted for general surgery (mainly abdominal and thyroid), histamine release following nalbuphine 1 mg/kg i.v. versus fentanyl 5 micrograms/kg i.v. was studied in the course of an otherwise routine induction with promethazine/pethidine as premedication 30 min before the opioids and alcuronium-flunitrazepam-thiopental 5 min later. Succinylcholine was given before intubation and further analgesia was obtained by repeated administration of either nalbuphine or fentanyl. Plasma histamine levels were measured by a specific fluorometric assay, heart rate and blood pressure were measured for assessing hemodynamics, and clinical signs of anaphylactoid reactions such as skin eruptions and arrhythmias were registered. RESULTS. Nalbuphine and fentanyl both released histamine with an incidence of more than 40%. In addition, nalbuphine potentiated the histamine release evoked by the sequential administration of alcuronium-flunitrazepam-thiopental in one complex of application. The incidence of histamine release in the nalbuphine group was 6/13 = 46%, in the fentanyl group only 1/11 = 9% (chi2 test, P less than 0.05). Furthermore, this study showed high histamine levels after succinylcholine and intubation in a relation to time of administration that suggested histamine release as a stress response to intubation. Finally, the incidence of histamine release after a second injection of the opioids was still 30%. A direct correlation between plasma histamine levels, hemodynamic changes, and skin reactions could not be shown. A detailed causality analysis with histamine release as a contributory determinant showed histamine release less detrimental to hemodynamic stability than the opposite, which had been expected. However, the promethazine administered 30 min before induction of anaesthesia had strong H1- and H2-receptor antagonistic activity and was given with optimum timing for H1- and H2-prophylaxis. CONCLUSION. The study demonstrated that histamine release during anaesthesia and surgery depends strongly on the time sequence of drugs and measures used. Histamine release is not predictable from studies in human volunteers alone; studies in patients have to be added. Histamine release is not always detrimental. H3-receptor-mediated effects after H1- and H2-prophylaxis may help patients to counteract the effects of a series of vasoactive drugs given during induction of anaesthesia.

Adult↗
PubMed1992

[The action of S-(+)-ketamine on serum catecholamine and cortisol. A comparison with ketamine racemate].

The S(+)-isomer of ketamine has about twice the anaesthetic potency of the commercially available racemic mixture of ketamine. It is assumed that the known side-effects of ketamine are significantly reduced when administering half the usual dose with the same pharmacodynamic effect [17, 25]. The aim of the present study was to determine the haemodynamic effects, the catecholamine and cortisol plasma levels after administration of equally potent doses of S-(+)-Ketamine and racemic mixture of ketamine. In addition, the effect of premedication with i.v. midazolam was assessed. METHOD. After approval by the ethics committee and written informed consent, 30 healthy male volunteers were randomly allocated to three groups (n = 10). Group 1 received 2 mg/kg ketamine racemate, group 2 1 mg/kg S-(+)-Ketamine, and group 3 1 mg/kg S-(+)-Ketamine 5 min after i.v.-premedication with 0.1 mg/kg midazolam. Non-invasive blood pressure (BP) and heart rate (HR) were continuously recorded. Blood samples were drawn 7 min before, and 2, 4, 8, 16, 32, 64 and 128 min after drug administration. Plasma epinephrine and norepinephrine (NE) levels were determined by HPLC and cortisol plasma levels by RIA. Data were analysed with the Kruskal-Wallis test (P < or = 0.05) for differences between groups. RESULTS. HR and BP showed a significant rise after injection of racemate and isomer, without any significant differences between groups. This was also seen for norepinephrine and cortical plasma levels. Epinephrine levels, however, differed between groups, showing a significant rise after racemate compared to isomer. Premedication with midazolam, in contrast, blunted major haemodynamic and hormonal changes. DISCUSSION. The haemodynamic changes did not differ between the racemate and isomer group despite a reduced isomer dose. HR and BP rise were similar, although epinephrine levels were significantly lower after isomer than racemate. Hence we assume that the increase in the haemodynamic parameters were mainly caused by NE. Midazolam apparently prevented the centrally mediated sympathetic stimulation caused by ketamine and its isomers. Therefore, i.v. premedication with midazolam should be applied when racemate or isomer is used, especially in high-risk cardiac patients.

Adult↗
PubMed1992

[Ketamine racemate or S-(+)-ketamine and midazolam. The effect on vigilance, efficacy and subjective findings].

Ketamine is a racemic mixture containing equal amounts of optical isomers that have almost identical pharmacokinetic properties but different pharmacodynamic effects. The S-(+)-isomer of ketamine has about twice the anaesthetic and analgesic potency of the racemic ketamine preparation and is judged to induce less psychic emergence reactions and to be followed by a more rapid recovery of vigilance. The present study was designed to assess whether the S-(+)-isomer of ketamine is superior to the racemic mixture in cardiovascular characteristics, emergence reactions and cognitive functions, and whether side effects may be reduced or prevented by administration of midazolam prior to injection of S-(+)-ketamine. METHODS. Following ethics committee approval and informed consent, 30 volunteers were randomly allocated in this double-blind study to three groups of 10 each. Group 1 received 2 mg/kg bw racemic ketamine, group 2, 1 mg/kg bw S-(+)-ketamine and group 3, 1 mg/kg bw S-(+)-ketamine after premedication with 0.1 mg/kg midazolam i.v. Cardiovascular changes, state of vigilance, cognitive performance, subjective mood and acceptance of anaesthesia were assessed by means of haemodynamic routine monitoring, electroencephalography (EEG), psychometric tests and interview. RESULTS. The increases in mean arterial pressure and heart rate following the injection of racemic ketamine and S-(+)-ketamine were identical and the differences from baseline values significant after both. Premedication with midazolam ensured stable haemodynamics after injection of S-(+)-ketamine. EEG analysis displayed the characteristic changes well known from ketamine anaesthesia for both racemic and S-(+)-ketamine. The vigilosomnoscript showed an identical profile of vigilance up to 30 min after injection of both drugs. The vigilance status after 125 min was less impaired by S-(+)-ketamine than by racemic ketamine. Psychological assessment showed a prompter recovery of visual attentiveness and sensorimotor performance in the S-(+)-ketamine group. Subjective mood was judged by the volunteers to be significantly better after S-(+)-ketamine, and volunteers found S-(+)-ketamine to be more acceptable than racemic ketamine. The frequency of dreams was the same after both drugs. No unpleasant dreams were reported after S-(+)-ketamine, but one of the volunteers who received racemic ketamine had uncomfortable dreams. Midazolam prevented any unpleasant emergence sequelae. On the other hand, the cognitive performance could not be restored to the baseline values until at least 240 min after injection of S-(+)-ketamine, because of the sedative effects of midazolam. DISCUSSION. These results suggest that S-(+)-ketamine offers the advantages of faster recovery of cognitive performance, greater acceptance by the volunteers and identical depth of anaesthesia after injection of half the dose compared with racemic ketamine. The clinical use of S-(+)-ketamine therefore seems to be justified. Premedication with benzodiazepines, e.g. midazolam, is essential. The dose to be administered, however, should be carefully selected in order not to abolish the positive effect of S-(+)-ketamine on vigilance by the sedative effects of the benzodiazepine.

Adult↗
PubMed1992

[Anesthesiologic efficacy of propanidid as a liposome dispersion. An experimental study with rats].

BACKGROUND: Propanidid, an ultra-short-acting i.v. anaesthetic agent, was widely used in the 1960s. Reports of anaphylactoid reactions in patients associated with release of histamine following administration of the drug, however, led to withdrawal of this useful anaesthetic. Since the adverse side effects of the former solution could be attributed to the solvent cremophor, attempts have recently been made to produce a propanidid solution without addition of the solvent. We report on comparative investigations employing a new liposomal solution (B. Braun, Melsungen, FRG) and the conventional cremophor preparation with regard to anaesthetic properties, haemodynamic side effects, and electroencephalographic effects (EEG). METHODS: Sprague-Dawley rats (n = 46) were implanted with venous and arterial lines and epidural EEG electrodes during chloral-hydrate anaesthesia. The following day, arterial blood pressure (ABP), heart rate (HR), and EEG were monitored in awake animals and then after induction of anaesthesia by a bolus of the respective propanidid preparation, followed by an infusion period of 15 min in six different experimental groups. Animals of groups L-60, L-90, L-120, or C-60, C-90, or C-120 groups received 60, 90, or 120 mg.100 g-1.h-1 of the liposomal (L) or cremophor (C) preparation. During anaesthesia, the corneal reflex and nociception to tail-clamping were also tested. At termination of the infusion, blood samples were drawn for determination of plasma propanidid concentrations. RESULTS: Both preparations were similarly effective in induction and maintenance of anaesthesia in a dose-dependent manner; both similarly lowered ABP and HR. The corneal reflex and nociceptive responses to tail clamping were also comparably suppressed. However, whereas the liposomal preparation was well tolerated at higher dose levels, the cremophor preparation caused considerable dose-dependent mortality of 11%, 86%, and 86% in animals in groups C-60, C-90, and C-120, respectively. Both preparations were found to induce a burst-suppression pattern in the EEG associated with clonic seizures, with a lower incidence with the liposomal preparation (22% and 50% in groups L-90 and L-120) as compared to the cremophor preparation (100% and 89% in groups C-90 and C-120). A remarkable variability in propanidid plasma concentrations was found at the end of the infusion period, although no differences were observed between both preparations. Discontinuation of infusion of propanidid resulted in rapid awakening (less than 5 min), irrespective of whether the liposomal or conventional preparation was employed. CONCLUSION: The present findings demonstrate largely identical anaesthetic potencies of a new liposomal solution as compared to the conventional cremophor preparation of propanidid. The liposomal preparation, however, was superior as far as tolerance and incidence of clonic seizures was concerned. The present findings should prompt further studies on the suitability of liposomal propanidid as a short-acting anaesthetic agent in patients.

Anesthesia, Intravenous↗
PubMed1991

Controlled clinical trials and cross-sectional studies with plasma histamine measurements and histamine receptor antagonists: solving the problem of preoperative H1- + H2-prophylaxis by asking new questions?

The problem of a preoperative histamine H1- + H2 - prophylaxis was tackled by a group of new studies including randomized controlled clinical trials and cross-sectional studies with plasma histamine measurements and administration of H1- + H2 - antagonists to a control group. The first study demonstrated serial histamine release in the induction of anaesthesia up to 4 times in a single patient. Basal plasma histamine levels in resting subjects fell below 100 pg/ml during the time necessary for preparation of the surgical patient. Hence, spikes of elevated plasma histamine concentrations corresponded to histamine release. Although this histamine release very often was less than 1 ng/ml plasma histamine, it created systemic reactions after atracurium. The cut-off point of 1 ng/ml for such anaphylactoid reactions does no longer exist, also lower plasma levels are of patho-physiological significance. The clinical signs of histamine release in the induction of anaesthesia vary from drug to drug. Sometimes tachycardia and hypertension produce the highest likelihood ratio, sometimes tachy- and bradycardia, but no changes in blood pressure as in the case of atracurium. It is concluded that the reasons why histamine release in anaesthesia and surgery is so much underreported and under-estimated include the present paradigms about plasma histamine levels and the "classical picture" of histamine release. Both are no longer valid and need a re-assessment.

Adolescent↗
PubMed1991

[The neuromuscular blocking effects of ORG 9426].

ORG 9426 is a new non-depolarizing steroidal muscle relaxant with a short onset time and intermediate duration of action. Its ED90 ist estimated to be between 0.25 and 0.36 mg/kg. The present study investigated the onset time, duration of action and time to spontaneous recovery after 0.3 and 0.9 mg/kg ORG 9426, respectively (i.e. about single or triple ED90). METHODS. Following the consent of the ethics committee and informed patient consent, two groups of 18 patients (ASA I or II) were formed, each scheduled for general or ORL surgery. After premedication with lormetazepam, anesthesia was induced with midazolam (0.07 mg/kg) and etomidate (0.3 mg/kg) and maintained with N2O/O2 at a 65:35 ratio, enflurane (0.8-1.5%) and supplements of fentanyl as needed. The ulnar nerve was stimulated with supramaximal 2 Hz Train-of-four (TOF) every 20 s. Neuromuscular twitch response was registered with EMG. Muscle relaxation was achieved by administration of ORG 9426 0.3 (group 1) and 0.9 mg/kg (group 2), respectively. The following parameters were measured: onset time (time interval from injection to maximal or total block), T125/75 (time for T1 to reach 25% or 75% of control), TOF70 (time for TOF ratio to reach 70% of control), heart rate and blood pressure. RESULTS. (mean +/- SD). At a dosage of 0.3 mg/kg, the onset time was 3.1 +/- 0.8 min and the maximum blockade was 87 +/- 9%. A dosage of 0.9 mg/kg led to complete paralysis (100%) in all patients within 1.2 +/- 0.3 min. The time for recovery of T1 to 25 and 75% of baseline was 18 +/- 7 and 26 +/- 8 min in group 1, in group 2 46 +/- 11 and 53 +/- 17 min, respectively. TOF70 (i.e., time to adequate spontaneous recovery of neuromuscular function) was achieved after 30 +/- 10 and 63 +/- 14 min, respectively. CONCLUSIONS. At a dosage of 0.3 mg/kg, ORG 9426 has an onset time of about 3 min and a duration of activity of nearly half an hour. Its neuromuscular effects are similar to a single ED90 dose of vecuronium. In contrast to a previous study, we observed a much shorter onset time of 70 s following the administration of 0.9 mg/kg. The clinical duration of action and spontaneous recovery of neuromuscular function, however, were significantly prolonged to more than 1 h. The hemodynamic parameters showed only slight alterations.

Adult↗
PubMed1991

[The pharmacokinetics of lormetazepam following cimetidine].

Cimetidine delays the elimination from plasma of those benzodiazepines that are subject to oxidative drug metabolism. An open-label cross-over study was conducted to discover whether cimetidine also changes the plasma level profile of lormetazepam. METHODS. Ten volunteers (5 female, 5 male) took part in the study. After oral administration of 1 mg lormetazepam alone followed by a 6-day washout phase, the subjects received five 200-mg cimetidine tablets at intervals of 6 h (Table 1). The subjects took another 1-mg dose of lormetazepam p.o. together with the last tablet of cimetidine. Blood was sampled at specified intervals after both lormetazepam administrations, and the concentration of the drug in the plasma was determined by means of a specific radioimmunoassay. RESULTS. Cimetidine had no influence on the plasma levels of lormetazepam (Fig. 1). The drug concentrations increased quickly after both treatments regardless of sex and reached their highest values 1-2 h after oral ingestion. half-lives of 30-40 min were determined for the beta-phase and 8-10 h for the terminal elimination phase (Table 2). DISCUSSION. Lormetazepam, over 90% of which is excreted in humans as lormetazepam glucuronide, like oxazepam and lorazepam, does not obviously interact with cimetidine. All other benzodiazepines, which have to undergo oxidation before excretion, interact with drugs that inhibit the microsomal (cytochrome-P-450-dependent) enzyme system. CONCLUSION. In this study, no influence of simultaneous administration of cimetidine--a well-known inhibitor of P-450 dependent drug metabolism--on the pharmacokinetics of lormetazepam in either men or women was observed. This is in agreement with theoretical considerations: due to a 3-hydroxy group, lormetazepam does not require oxidation (hydroxylation) before it is metabolized into a water-soluble form capable of being excreted from the body. Cimetidine is therefore unlikely to potentiate the sedative effect of lormetazepam.

Anti-Anxiety Agents↗
PubMed1990

[Beta activation following the intravenous administration of benzodiazepines and the specific antagonist flumazenil (Ro 15-1788)].

In a prospective randomized study involving 32 male subjects aged 18 to 38, the effects of flunitrazepam (0.25 to 2 mg/70 kg), lormetazepam (0.5 to 4 mg/70 kg), midazolam (1.5 to 12 mg/70 kg) and diazepam (4 to 32 mg/70 kg) on the beta-activity (13 to 20/s) were investigated. Each subject received four benzodiazepine injections of increasing dosage. The doses were selected so that the lowest had only a slight effect on the test person's condition, while the highest resulted in deep sedation. The increase in beta-activity started off with a latency of 30 to 60 s; it was proportional to the dosage and reached its maximum between the 2. and 3. minutes. The subsequent decrease in beta-activity could be represented by an exponential function. The effect could be cancelled temporarily by administering repeated doses of the specific antagonist, flumazenil (0.1, 0.3 and 0.9 mg/70 kg). The method is suited for describing pharmacodynamic processes, determining equipotential doses of benzodiazepines and detecting the interaction between benzodiazepines and specific antagonists.

Adult↗
PubMed1990

[The effect of propofol-ketamine anesthesia on hemodynamics and analgesia in comparison with propofol-fentanyl].

Propofol (Diprivan), a modern intravenous hypnotic, produces a reduction in both cardiac index (CI) and mean arterial pressure (MAP). Ketamine (Ketanest), a potent analgesic, in contrast, causes an increase in MAP and CI. The aim of the present study was to investigate whether the combination of propofol and ketamine can give better hemodynamic stability during the induction and maintenance of general anesthesia than propofol used with fentanyl, whose cardiodepressant actions may cumulate. METHODS. For induction of general anesthesia 10 patients (ASA I and II) each received 3-5 boluses of propofol (0.5 mg.kg-1 during 35 s until predetermined level of anesthesia was reached (stage D2/E0 according to [20]) followed by a continuous propofol infusion (0.120 mg.kg-1.min). Fentanyl 0.1 mg was administered to each patient in group A for induction of anesthesia and again if evident pain was present. In group B ketamine was given following a pharmacokinetic model based on computer-simulated calculation. After an initial bolus of 38 mg injected within 2 min further doses of 42 mg, 35 mg, 32 mg and 28 mg ketamine were administered over 30 min at a time. Signs of evident pain were treated by means of supplementary doses of 0.5 mg.kg-1. RESULTS. In both groups a moderate drop of MAP was observed after the induction of general anesthesia. Two patients in each group showed a distinct decrease in MAP (-32%). The heart rate dropped slightly (-9%) in group A, but did not change in group B. Following intubation the MAP rose by less in group A (+8%) than in group B (+21%). After the beginning of the operation the group treated with propofol/fentanyl showed major hemodynamic changes; in particular, bradycardia with less than 40 bpm was observed in more patients than in the propofol/ketamine group. Postoperatively, fewer patients in group B required rescue doses of analgesics (1 of 10) than these in group A (7 of 10), though vigilance was better in group B. DISCUSSION. The dose of ketamine administered during the induction of general anesthesia may have been not high enough to neutralize the cardiodepressant effect of propofol. But during the maintenance of anesthesia there was in fact better hemodynamic stability in group B than in group A as a result of the neutralization of opposing actions. Fentanyl even intensified the fall in MAP after propofol. Patients in group B showed better vigilance as well as better pain relief postoperatively. The population of the fentanyl group was obviously more deeply sedated and analgesia was still inadequate. In our study general intravenous anesthesia with propofol and ketamine offered the advantages of better analgesia, a higher state of vigilance and the absence of respiratory depression during the postoperative phase compared with the combination of propofol and fentanyl.

Analgesia↗
PubMed1990

[Etomidate using a new solubilizer. Experimental clinical studies on venous tolerance and bioavailability].

Pain following intravenous injection as well as thrombophlebitis are substantial side effects of etomidate that have been reported from the first clinical study (1972-1973) onwards. Investigations of our own and by Gran et al. have pointed out that injectable etomidate with intralipid as a solvent removes side effects without impairing the good hypnotic action. The idea of using a lipid emulsion as a solvent was presented a few years later, inducing two further studies. METHOD. Both pharmacodynamic (continuous EEG registration) and pharmacokinetic [determination (HPLC) of plasma levels of the active substance] investigations were carried out on volunteers. At random 16 volunteers received etomidate in propylene glycol or etomidate in lipid emulsion for general anesthesia. A dose of 0.3 mg kg-1 was given over 60 s. In a clinical study 100 patients were divided into two independent groups of 50 each. They received either the commercially available etomidate in 35% propylene glycol (group I) or the new formulation containing 20 mg etomidate in 10 ml of a lipid-emulsion (Lipofundin MCT 20%) (group II). A dose of 0.3 mg kg-1 etomidate was given. RESULTS. There was a higher concentration of etomidate for 8 min after injection in lipid emulsion compared with etomidate in propylene glycol. The plasma concentration of etomidate (200 ng/ml) correlates with C2 corresponding to the light sleep stage after etomidate in propylene glycol, but with D0 according to the deep sleep stage after etomidate in lipid emulsion. At lower plasma concentrations, the hypnotic action of etomidate in propylene glycol is stronger than the effect of the lipid emulsion. This result means that it is possible that a part of the etomidate remains in the lipid particles. In the clinical study the anesthetic induction time was nearly identical in both groups; blood pressure and heart rate were stable. Following etomidate in propylene glycol, 36% of the patients complained of a painful injection. On the first postoperative day, 9 of 47 patients showed signs of phlebitis and three others thrombosis. On the 7th day a venous reaction was evident in 22% of these patients; 2 patients had developed phlebitis, 5 thrombosis and 4 thrombophlebitis. After etomidate in lipid emulsion, there were no signs of local irritation. The same results have been obtained in the study with volunteers. CONCLUSION. Two unpleasant side effects of etomidate, pain on injection and postoperative thrombophlebitis, were abolished by the solvent "lipid emulsion".

Adult↗
PubMed1987

[Processes of perioperative risk from the viewpoint of the anesthesiologist].

Nearly all of the pharmaceutical preparations that are used for anesthesia can release histamine. H1 and H2 receptor blockades are recommended for the following groups of patients at risk: 1) Patients who show hypersensitivity to i.v. administered medications and radiological contrast media. 2) Patients with risk factors in their case histories, e.g., atopy, previous cardiac and/or pulmonary damage, and an age of over 70 years. 3) Conditions with a pathological increase in the plasma histamine level. Such conditions include (a) polytrauma, chronic kidney insufficiency, patients under radium irradiation treatment; (b) the exploration phase during a surgical procedure, more frequent blood transfusions, extracorporeal circulation, and Palacos implantation. 4) Chymopapain for chemonucleolysis.

Anaphylaxis↗
PubMed1985

[Histamine liberation induced by anesthetics or their solvents: specific or non-specific?].

Histamine release is a frequent event in the perioperative period. The reasons for its occurrence are complex; they include pseudoallergic and allergic phenomena--and probably a mixture of both. Some drugs and solvents seem to modulate histamine release induced by other drugs. Thus the terms "specific and nonspecific" or "selective and nonselective" histamine release which have their well appreciated place in experimental immunology and pharmacology should be avoided in describing histamine release responses in clinical conditions. The clinical relevance of histamine release in the perioperative period is considerable and can be compared with that of perioperative thrombosis and thromboembolism. Far too many drugs and anaesthetic and surgical procedures give increased plasma histamine levels; premedication with H1- + H2-histamine receptor antagonists is therefore recommended in patients who have a history of hypersensitivity reactions to intravenous agents; a history of atopy, who are to be given the same drug a few days later, undergo surgery with a high risk of histamine release, are more than 70 years old or are poor risk patients with perioperative cardiac, respiratory or liver failure and shock.

Anesthetics↗