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P Conzen

Publications and source records attributed to P Conzen.

At least 37 records · Page 2Linked to original sources
PubMed1996

[Fluoride-induced nephrotoxicity: factor fiction?].

In the 1960s, the widespread use of the inhalational anaesthetic methoxyflurane was associated with a significant occurrence of postoperative renal dysfunction. This was attributed to hepatic biotransformation of methoxyflurane and subsequent release of inorganic fluoride ions into the circulation. Based upon the clinical experience with methoxyflurane, serum fluoride concentrations exceeding 50 mumol/l were considered to be nephrotoxic. Without further reevaluation, this 50 mumol/l threshold was subsequently applied to other fluorinated anaesthetics as well. Enflurane and even isoflurane may, when used during prolonged operations, also yield anorganic fluoride levels in excess of 50 mumol/l. Nevertheless, no cases of renal dysfunction attributable to prolonged use of these anesthetics have been reported. About 4% of the new inhalational anaesthetic sevoflurane is metabolized, and fluoride concentrations exceeding those after enflurane are frequently measured. Numerous studies have examined the nephrotoxic potential of sevoflurane degradation products. However, fluoride-related toxicity has been observed neither in animal nor in clinical studies, including prolonged administration and patients with pre-existing renal disease. New insights into the intrarenal metabolisation of volatile anaesthetics may well explain the absence of nephrotoxicity after sevoflurane. The threshold for fluoride nephrotoxicity of 50 mumol/l, still given in many medical text-books, can no longer be applied as an indicator of nephrotoxicity after isoflurane, enflurane or sevoflurane. Therefore, the elevated serum fluoride concentrations consistently recorded following anaesthesia with sevoflurane are devoid of clinical significance.

Anesthetics, Inhalation↗
PubMed1996

[Intraoperative awareness and auditory evoked potentials].

Midlatency auditory evoked potentials (MLAEP) are suppressed dose-dependently during anaesthesia with a variety of general anaesthetics. Therefore, MLAEP have been proposed to measure depth of anaesthesia and to indicate intraoperative awareness. Several studies give evidence of a close relationship between MLAEP and motor signs of wakefulness, intraoperative awareness, and explicit and implicit memory functions during general anaesthesia. Summarising these data, one may conclude that there is a close hierarchical relation between cognitive function, memory and wakefulness during anaesthesia, and MLAEP latencies. A short Nb latency below 45 ms is consistent with conscious awareness and unimpaired memory function with explicit recall and adequate response to commands. When Nb latency increases to 45-50 ms, it may be associated with conscious awareness. Patients still respond to commands, but memory formation is impaired and explicit recall is lost. A further increase of Nb latencies seems to be consistent with unconscious awareness, characterised by implicit memory of intraoperative events; 60 ms seems to be the threshold value for motor signs of wakefulness during anaesthesia. With a further increase of MLAEP latency during anaesthesia, conscious awareness and memory formation, explicit and implicit recall, response to commands, and spontaneous purposeful movements during anaesthesia are blocked. The new volatile anaesthetic sevoflurane leads to a dose-dependent increase in MLAEP peak latencies and a decrease in MLAEP amplitudes. At about 1.5 vol.% end-expiratory sevoflurane concentration, MLAEP are significantly suppressed and Nb latency is in the range of 68-80 ms. Therefore, from the present data and those from the literature, one may expect that sevoflurane at concentrations greater than 1.5 vol.% for general anaesthesia would be able to suppress awareness phenomena such as purposeful movements, auditory perception, intraoperative wakefulness and awareness, memory formation, and explicit and implicit recall of intraoperative events.

Anesthetics, Inhalation↗
PubMed1995

Does nitrous oxide affect coronary microcirculation? An intravital microscopic study in the canine heart.

The safe use of nitrous oxide, in particular in patients with coronary artery disease, has been questioned. This study was designed to determine whether nitrous oxide directly affects global coronary hemodynamic variables and coronary arteriolar microvessels in the absence of changes of myocardial oxygen consumption. In dogs the effects of nitrous oxide were evaluated during normotension (NT, intravenous [IV] piritramid, nitrogen/oxygen; and NT/N2O, IV piritramid, nitrous oxide/oxygen) and during hypotension (MAP 60 mm Hg) (HT, IV piritramid, halothane, nitrogen/oxygen; and HT/N2O, IV piritramid, halothane, nitrous oxide/oxygen). The diameter of coronary arteriolar microvessels (range, 20-450 microns) was assessed by intravital fluorescence microscopy. Myocardial blood flow was determined by radioactive microspheres. Systemic and coronary hemodynamics, as well as arteriolar microvessel diameters, were comparable between NT and NT/N2O. During HT, nitrous oxide (HT/N2O) affected neither systemic nor coronary hemodynamics. Moreover, there was no obvious difference in the diameters of coronary microvessels between HT and HT/N2O. In conclusion, nitrous oxide, whether at normotensive or hypotensive conditions, neither influences coronary arteriolar tone nor reduces or redistributes myocardial blood flow.

Animals↗
PubMed1995

Hemodynamic effects of anesthetic induction with eltanolone-fentanyl versus thiopental-fentanyl in coronary artery bypass patients.

We evaluated the hemodynamic profile of eltanolone and fentanyl versus thiopental and fentanyl anesthetic induction in patients with documented coronary artery disease. Fifty patients scheduled for coronary artery bypass grafting were randomly assigned to two treatment groups (25 patients each). Anesthesia was induced by eltanolone (0.5 mg/kg) or by thiopental (3 mg/kg). Each patient also received 3 micrograms/kg fentanyl and 0.1 mg/kg vecuronium. Heart rate, arterial, pulmonary arterial, central venous, and pulmonary capillary wedge pressures, and cardiac output were determined in the awake state, 2 min after induction of anesthesia, and at 1 and 5 min after intubation, which was performed 3 min after induction. Between-group statistics showed significantly (P < 0.05) lower mean arterial pressure and systemic vascular resistance for eltanolone-treated patients at all measuring points. Pulmonary capillary wedge pressure was lower at 1 min after intubation; left ventricular stroke work index was lower at 1 and 5 min after intubation in the eltanolone group. We conclude that the lower mean arterial pressure with eltanolone as compared to thiopental is a result of greater peripheral vasodilation.

Adult↗
PubMed1995

The effects of anesthesia with increasing end-expiratory concentrations of sevoflurane on midlatency auditory evoked potentials.

We studied midlatency auditory evoked potentials (MLAEP) during general anesthesia with increasing end-expiratory concentrations of sevoflurane in 12 patients scheduled for elective gynecologic surgery. After oral premedication with 20 mg clorazepate dipotassium, anesthesia was induced with etomidate (0.2 mg/kg intravenously [IV]). Vecuronium (0.1 mg/kg) was given for neuromuscular block, and controlled ventilation with sevoflurane in 100% O2 was instituted. Auditory evoked potentials were recorded in the awake state and during anesthesia with end-expiratory steady-state concentrations of 0.5, 1.0, 1.5, and 2.0 vol% of sevoflurane on vertex (positive) and mastoids on both sides (negative). Latencies of peaks V, Na, Pa, Nb, and P1 (ms) and amplitudes of Na/Pa, Pa/Nb, and Nb/P1 (microV) were measured. In the awake state, MLAEP had high peak-to-peak amplitudes and a periodic waveform. During general anesthesia with increasing end-expiratory concentrations of sevoflurane, the latency of the brainstem response V increased slightly. In contrast, MLAEP showed marked dose-dependent, statistically significant increases in the latencies of Na, Pa, Nb, and P1 and decreases in the amplitudes of Na/Pa, Pa/Nb, and Nb/P1. Under 2 vol% of sevoflurane, MLAEPs were severely attenuated or abolished. Based on these observations, > or = 1.5 vol% sevoflurane should suppress phenomena such as auditory perceptions, intraoperative wakefulness, and awareness.

Adult↗
PubMed1995

Inhalation anaesthesia at the extremes of age: geriatric anaesthesia.

No single anaesthetic technique is superior for all elderly patients, although the prognosis is improved if minor surgical procedures are performed with local anaesthesia rather than with general or major regional anaesthesia. If general anaesthesia is required, which specific inhalation anaesthetic can improve the prognosis of the geriatric patient? The low solubility of desflurane and its resistance to biodegradation would seem to recommend its use in the geriatric patient. However, these theoretical advantages remain to be adequately documented.

Aged↗
PubMed1994

Biological effects of shock waves: induction of arrhythmia in piglet hearts.

During lithotripsy by electrohydraulic or electromagnetic lithotripters, the application of extracorporeal shock waves has to be synchronized with the electrocardiogram to reduce the induction of arrhythmias. The relation between the refractory period of the cardiac cycle and arrhythmia induction by shock waves, and the underlying mechanism have so far not been examined. In this experiment, the cardiac response to shock waves administered at 20 kV by an electrohydraulic lithotripter was assessed in nine piglets. The focus was positioned 5, 10 and 15 cm caudal to the apex of the left ventricle, and in some piglets also at the apex. The interval following the R-wave was determined during which the heart was refractory to shock wave stimulation by either single discharges or shock-wave bursts, i.e., groups of discharges separated by 10 ms intervals. This mechanical refractory period was compared to its electrical counterpart, which was determined by transvenous intracardiac atrial stimulation. As a result, mechanical refractory periods following the R-wave were at 5 cm distance 60 ms for single discharges and 70 ms for bursts (medians; range 10-180 ms); both stimulation modes were highly correlated (r = 0.88). While a similar result was obtained with the focus positioned directly at the cardiac apex, at 10 cm distance from it, bursts elicited a cardiac response significantly more often (in nine vs. two piglets). At 15 cm distance, no response was obtained at all. Both mechanical and electrical atrial refractory periods were in a similar range.(ABSTRACT TRUNCATED AT 250 WORDS)

Acoustic Stimulation↗
PubMed1993

[Enzyme liberation and activation of the kallikrein-kinin system in experimental pancreatitis. Studies of portal vein blood, pancreatic lymph and peritoneal effusion].

The clinical course of acute pancreatitis is strongly influenced by secondary cardiac, pulmonary and renal damage. The aim of the present study was to gather information about the compartment promoting the systemic damage. Therefore the activity of lipase, phospholipase A and plasma pro-kallikrein and the concentration of tissue kallikrein and kininogen were measured in portal venous blood, pancreatic lymph and peritoneal exudate. Anaesthetized pigs were subjected to fluid resuscitation to keep systemic haemodynamic parameters constant. The pancreas was isolated in situ. The pigs were randomly assigned to a control group (n = 9) or one of the two pancreatitis groups (n = 10 each). Pancreatitis was induced by i.a. infusion of free fatty acid (FFS) or retrograde infusion of 5% sodium taurocholate intraductally (NaT). In both pancreatitis groups the activity of lipase and phospholipase A increased. The most pronounced changes were seen in the peritoneal exudate (phospholipase A activity 40 min after induction: control 10.0 U/l, NaT 72.2 U/l). In both pancreatitis groups there was evidence for activation of the tissue kallikrein kinin system in the form of an increase in the kallikrein concentration and a decrease in the kininogen concentration. Again the changes were most pronounced in the peritoneal exudate (tissue kallikrein 40 min after induction: control 14.7 ng/ml, NaT 452 ng/ml).

Acute Disease↗
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

[Complications caused by protamine. 1: Pharmacology and pathophysiology].

Protamine is a strongly alkaline polypeptide with a molecular weight of about 4500. Protamine solutions contain paraben compounds as antimicrobial agents. Rapid neutralization of heparin by protamine may cause an anaphylactoid reaction characterized by a non-immunogenic histamine release and by unknown mediators mechanisms. This response is associated with systemic peripheral vasodilation resulting in slight to moderate hypotension. Weak negative inotropic effects by mechanisms different from the reduction of ionized calcium concentrations may also contribute to systemic hypotension. Apart from these mostly slight reactions, severe reactions may occur with life-threatening systemic hypotension, bronchospasm and, in rare cases, death. They are caused by anaphylactic/anaphylactoid reactions resulting in catastrophic pulmonary vasoconstriction which induces right and eventually global ventricular failure. Sensitization to protamine (anaphylactic) and anaphylactoid reactions are the underlying mechanisms. The majority of anaphylactic/anaphylactoid reactions are associated with complement activation and the release of anaphylatoxins C3a and C5a. These activate the cyclo-oxygenase pathway of the arachidonic acid metabolism in yet unidentified cells, probably within the lung. As a result, thromboxane and prostaglandins are released. Thromboxane is the pivotal mediator responsible for the pulmonary vasoconstriction and, presumably, also for the bronchospasm during protamine reactions. The pronounced activation of polymorphonuclear leukocytes and the decrease in platelet counts may reflect a mere epiphenomenon. The degree of right ventricular afterload increase at which systemic hypotension requiring immediate therapy would occur depends mainly on the contractile state of the heart. Potential risk patients for severe protamine reactions are depot insulin-dependent diabetics and patients with prior exposure to protamine.

Anaphylaxis↗
PubMed1991

[Complications caused by protamine. 2. Therapy and prevention].

Treatment of reactions. The treatment of reactions to protamine is still symptomatic. Hypotension resulting from systemic vasodilation (anaphylactoid reaction) is treated by volume infusion, and alpha-stimulating catecholamines may be necessary. The combination of increased right ventricular afterload and systemic hypotension (anaphylactic/anaphylactoid reaction) requires primarily the improvement of coronary perfusion pressure and, thus, of O2 delivery to the right ventricular myocardium. To this end, catecholamines with alpha-stimulating action should be administered. Nitroglycerin is indicated when pulmonary hypertension persists in the presence of essentially normal systemic pressure. In the acute situation, steroids and antihistamines have no beneficial effect. Prevention of protamine reactions. For prevention of systemic hypotension by vasodilatation, protamine should be infused very slowly and not during hypovolemia. General prophylaxis using H1/H2 antagonists is not justified. Reliable preoperative identification of patients who would suffer an anaphylactic/anaphylactoid reaction to protamine, for example by skin tests or by measuring specific anti-protamine IgE or IgG antibodies, is not possible. This prevents individual prophylaxis in risk patients. In view of the low incidence of severe protamine reactions and the lack of better alternatives to the heparin/protamine regimen, general prevention is not indicated. For patients who are potentially at risk (insulin-dependent diabetics, prior protamine exposure), the side-effects of preventive measures must be weighed against their benefits. Only known sensitivity to protamine justifies certain preventive actions. In vascular surgery prostacyclin can be used instead of heparin/protamine or can be withheld (fading out of heparin action). Administration of steroids and/or antihistamines should be avoided. In cardiac surgery the use of hexadimethrine (if available) or total avoidance of protamine is paramount. Corticosteroids may be considered. Aortic administration of protamine and anticoagulation with ancrod are not recommended. The most promising compounds for rpharmacologic prevention of anaphylactic/anaphylactoid reactions in the future are thromboxane receptor antagonists.

Anaphylaxis↗
PubMed1990

[Pancreatic circulation in experimental biliary pancreatitis].

Measurements of pancreatic micro- and macrocirculation were performed to evaluate the pancreatitis-induced changes. Pigs were anesthetized and ventilated mechanically. Hypotension induced side-effects were avoided by adequate volume replacement. After laparatomy, splenectomy and gastroectomy the animals were enterotomized. Systemic hemodynamic parameters were monitored as well as pancreatic blood flow (Q), which was measured electromagnetically, and arterial and portal-venous blood gases. Pancreatic microcirculatory parameters were observed using fluorescence-videomicroscopy after i.v. administration of FITC dextran 150 and FITC labeled autologous erythrocytes. The pigs were randomly assigned to a control (n = 9) and a pancreatitis group (n = 10), the later being induced by the retrograde infusion of sodium-taurocholate. Systemic and pancreatic macrohemodynamic parameters remained constant in both groups, except for avdO2 and O2-consumption (O2-c) decreasing significantly in the pancreatitis group. At baseline 42% of all capillaries were perfused in both groups. In pancreatitis we detected focal areas with persistent stasis and areas which were continuously perfused. In these areas the portion of capillaries perfused by erythrocytes increased significantly to 67%. This was accompanied by an extravasation of FITC dextran. The finding of an unchanged Q beside reduced O2-c and avdO2 during pancreatitis is explained by the changes in pancreatic microcirculation. Focal stasis was observed beside areas showing typical signs of an acute inflammation: increased macromolecular permeability and capillary recruitment, e.g. oedema and hyperaemia.

Acute Disease↗