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Biomedical subjects

P Hans

Publications and source records attributed to P Hans.

At least 73 records · Page 4Linked to original sources
PubMed1998

Emergence from target-controlled anesthesia with propofol and sufentanil in patients undergoing intracranial surgery.

The study was designed to characterise the emergence from target-controlled anesthesia assessed by the recovery of spontaneous breathing, eye opening to command, and extubation in 18 adult patients undergoing intracranial surgery. Total intravenous anesthesia was induced and maintained with propofol and sufentanil. Target plasma concentration of propofol ranged between 3.0 and 5.5 micrograms.ml-1 and infusion was stopped after head dressing. The initial target plasma sufentanil concentration of 0.50 ng.ml-1 was decreased to 0.15 ng.ml-1 after craniotomy; sufentanil infusion was discontinued at the dura closure. The time from the end of surgery (head dressing) to recovery of spontaneous breathing was 8.3 +/- 6.5 min, and the time to eye opening and extubation was 14.7 +/- 10.0 min. At the end of surgery, the calculated plasma propofol concentration was 3.42 +/- 0.26 micrograms.ml-1. It significantly decreased to 2.11 +/- 0.51 micrograms.ml-1 at recovery of spontaneous breathing and to 1.81 +/- 0.41 micrograms.ml-1 at eye opening and extubation. The calculated plasma sufentanil concentration was 0.108 +/- 0.019 ng.ml-1 at the end of surgery but did not change significantly between recovery of spontaneous breathing (0.089 +/- 0.013 ng.ml-1), eye opening and extubation (0.087 +/- 0.013 ng.ml-1). The calculated plasma propofol concentrations recorded at emergence were not correlated with patient age, total dose of propofol, and duration of infusion; corresponding calculated sufentanil concentrations were not correlated with age and total dose of sufentanil. An inverse relationship (p < 0.05) was found between the duration of sufentanil infusion and the calculated sufentanil concentrations at emergence. No correlation was observed between calculated concentrations of propofol and sufentanil at emergence.

Adolescent↗
PubMed1998

Hemodynamic effects of epinephrine associated to an epidural clonidine-bupivacaïne mixture during combined lumbar epidural and general anesthesia.

Clonidine or epinephrine are frequently combined to epidural local anesthetics to strengthen sensory block and prolong analgesia. Both drugs impair the hemodynamic profile of central neural blockade but the effects of their combination on arterial pressure and heart rate are not known and were examined in this double-blind prospective randomised study. Forty four patients scheduled for lumbar disc surgery were allocated to two groups. Epidural anesthesia was obtained by administration of 150 micrograms clonidine in 15 ml bupivacaine 0.25% solution without (group C) or with (group C + E) 37.5 micrograms epinephrine. Systolic, mean, diastolic arterial pressure and heart rate were measured throughout the study. Combined epidural and general anesthesia induced a significant decrease in arterial pressure and heart rate in both groups. SAP and MAP decreased significantly less in the patients receiving epinephrine. Low dose epidural epinephrine decreases arterial pressure instability during combined epidural and general anesthesia.

Adolescent↗
PubMed1997

[Post-traumatic intracranial hypertension and biochemical disorders: cases and consequences].

Increased intracranial pressure is a risk factor which may result in secondary brain damage, and affect neurological outcome in head injured patients. In case of diffuse brain lesions, elevated intracranial pressure is characterised by two important features. First, it results from vasogenic or cellular oedema, or from an increase in cerebral blood volume. Second, it is strongly associated to biochemical disorders. The latter may be considered as a direct consequence of the initial traumatic impact, mediating factors of the secondary neurological lesion and the biochemical result of cerebral ischaemia. They contribute to increased intracranial pressure and ischaemia by inducing physiological disorders and cell lesions. They also reflect the degree of cerebral ischaemia. Cerebral acidosis, free radicals and excitatory amicoacids are the main biochemical disorders implicated in this vicious circle leading to neuronal death.

Acidosis, Lactic↗
PubMed1997

Predictive accuracy of continuous propofol infusions in neurosurgical patients: comparison of pharmacokinetic models.

The performance of 10 pharmacokinetic models in predicting blood propofol concentrations was evaluated in patients during neurosurgical anesthesia. Eight patients-ASA category I or II, aged 49 +/- 18-years, weighing 71 +/- 20 kg, and scheduled for routine neurosurgery-were anesthetized with propofol and sufentanil using Ohmeda pumps controlled with a personal computer. Sufentanil was administered as a bolus of 0.3 microgram.kg-1, 5 min before induction of anesthesia, and infused at a constant rate of 0.5 microgram.kg-1.h-1 throughout the study. At induction, propofol was administered as a bolus of 1.5 mg.kg-1 followed by a continuous infusion of 6 mg.kg-1.h-1. During surgery, the propofol infusion rate was deliberately increased by 2 mg.kg-1.h-1 every 15 min up to 12 mg.kg-1.h-1. Arterial blood samples were drawn at the end of each infusion step for measurement of propofol concentrations by high-performance liquid chromatography. Measured propofol concentrations were compared with theoretical concentrations derived from 10 published pharmacokinetic models designed in different clinical settings. Each model has been assessed by calculating the median of the performance error, the median of the absolute performance error, and their 10th and 90th percentiles. Models designed for certain categories, such as children, young, or elderly patients who received propofol as a bolus injection, showed a bad predictive accuracy. The models of Gepts et al. (Anesth Analg 1987; 66:1256-1263, Anaesthesia 1988; 43(suppl):8-13), Tackley et al. (Br J Anaesth 1989;62:46-53), and Cockshott (Postgrad Med J 1985;61:55), derived from healthy patients receiving continuous propofol infusions, provided the best agreement between expected and measured propofol concentrations; they showed bias and inaccuracy lower than 17%. In conclusion, the accurate prediction of blood propofol concentrations from different continuous infusion rates in ASA I or II patients requires the selection of appropriate pharmacokinetic models derived from similar categories of patients and using a similar technique of propofol administration. However, in clinical practice, the selection of a specific set among the appropriate models is balanced by the interindividual variability in blood propofol concentrations adjusted to clinical effects.

Adult↗
PubMed1997

Increase in antioxidant capacity of plasma during propofol anesthesia.

We have examined the effect of total intravenous anesthesia (TIVA) using a continuous propofol infusion on the antioxidant capacity of plasma in 18 neurosurgical patients who required cerebrospinal fluid shunting. Patients were premedicated with hydroxyzine, alprazolam, and atropine. Anesthesia was induced intravenously with propofol 1.5 mg kg-1 and sufentanil 0.15-0.3 microgram kg-1. Tracheal intubation was facilitated with atracurium 0.5 mg kg-1. Anesthesia was maintained with a continuous propofol infusion at an increasing rate from 6 to 12 mg kg-1 h-1 under controlled ventilation (FiO2 = 0.4 in air). In all patients, arterial blood samples were drawn before induction of anesthesia and during surgery for measurement of blood propofol concentration and plasma antioxidant capacity, which was assessed as the ability to inhibit lipid peroxidation. Lipid peroxidation was induced in vitro by exposing a linoleic acid microemulsion to hemoglobin-generated oxoferryl radicals, and assessed by ultraweak chemiluminescence in the absence (control) and the presence of the plasma samples. The antioxidant capacity of plasma, measured by the inhibition of light emission and expressed as a percentage of control, increased significantly from 39.8 +/- 2% (mean +/- SEM) to 44.7 +/- 2.4% during anesthesia (Wilcoxon test, p < 0.001). No correlation was observed between this increased resistance to lipid peroxidation and blood propofol concentrations (Spearman test, r = 0.07, NS). We conclude that the capacity of plasma to inhibit lipid peroxidation increases in patients during TIVA maintained with a continuous propofol infusion.

Anesthesia, Intravenous↗
PubMed1997

Elevated plasma alpha 1-acid glycoprotein levels: lack of connection to resistance to vecuronium blockade induced by anticonvulsant therapy.

This study was designed to investigate the relationships among anticonvulsant therapy, plasma alpha 1-acid glycoprotein (AAG) levels, and resistance to vecuronium blockade. Thirty-one patients scheduled for routine neurosurgery were included in the study. The patients were treated (TG; n = 20) with phenytoin (n = 15) and/or carbamazepine (n = 4) and/or phenobarbital (n = 3) for > or = 6 days or were left untreated (UG; n = 11, control group). TG patients were further assigned to one of two subgroups according to the plasma anticonvulsant level measured the day before surgery and found to be within (TGW, n = 10) or below (TGB, n = 10) the therapeutic range. Finally, the 31 patients were divided into two more groups according to their plasma AAG levels: higher than (HAAG, n = 17) or within (NAAG, n = 14) the normal range (25-94 mg dl-1). Anesthesia was induced and maintained with propofol and sufentanil. Muscle relaxation was obtained with vecuronium 0.1 mg kg-1. A train-of-four (TOF) stimulation mode at 2 Hz was applied to the ulnar nerve every 15 s, and neuromuscular transmission was assessed using a TOF-Guard accelograph monitor. Plasma AAG concentrations (means +/- SEM) were 103.7 +/- 7.6 mg dl-1 in TG, 80.7 +/- 6.7 mg dl-1 in UG, 95.9 +/- 13.2 mg dl-1 in TGW, 111.6 +/- 7.6 mg dl-1 in TGB. 114.9 +/- 7.4 mg dl-1 in HAAG, and 71.4 +/- 3.8 mg dl-1 in NAAG groups. The differences in plasma AAG concentrations between UG and TG and between HAAG and NAAG groups were statistically significant. No significant relationship was found between plasma AAG levels and phenytoin concentrations (r = -0.26). The time (mean +/- SEM) to recovery of T1 to 25% of control was significantly shorter in TG (28.2 +/- 1.4 min) than in UG (42.2 +/- 3.1 min) but did not differ significantly according to the plasma anticonvulsant level (27.3 +/- 2.0 min in TGW; 29.1 +/- 1.9 min in TGB) and the plasma AAG level 31.7 +/- 1.9 min in HAAG; 35.3 +/- 3.3 min in NAAG). The time for the TOF ratio to recover to 25% yielded similar profiles and statistical significance levels: TG, 32.9 +/- 2.2 min; UG, 51.2 +/- 4.0 min; TGW, 35.0 +/- 3.9 min; TGB, 30.7 +/- 1.8 min; HAAG, 38.1 +/- 3.1 min; NAAG, 42.0 +/- 4.1 min. We conclude that anticonvulsant therapy induces an increase in plasma AAG independently of the plasma anticonvulsant level. However, duration and recovery of vecuronium blockade do not differ according to plasma AAG levels. Consequently, elevated AAG does not contribute to the resistance to vecuronium blockade induced by anticonvulsants.

Adult↗
PubMed1996

[Pharmacological therapeutic prospects of cerebral vasospasm].

New therapies of cerebral vasospasm aim to prevent the effects of subarachnoid haemorrhage. These effects result in red blood cell haemolysis and release of oxyhaemoglobin, free radicals formation and lipid peroxidations, imbalance in endothelial modulation of vasomotor tone and activation of the complement system. Low doses of fibrinolytic agents administered intrathecally accelerate the fibrinolysis of the clot and reduce the oxyhaemoglobin release. The tissue-type plasminogen activator has proven to be effective in preventing vasospasm, but the modalities of this therapy remain to be defined. Free radical reactions may be inhibited by free radical scavengers and inhibitors of lipid peroxidations. Tirilazad is a potent inhibitor of lipid peroxidations, which improves the patients' outcome and has gone to Phase III human trials. Superoxide dismutase and tropolone derivatives are currently evaluated in animal models. Vasomotor tone can be modified in experimental models either by blocking endothelin receptors (BQ-123), or by facilitating the release and enhancing the effect of nitric oxide using protein kinase C inhibitors, drugs that increase intracellular calcium (cyclopiazonic acid, LP-805) and free radicals scavengers (superoxide dismutase). These possibilities are being investigated. Finally, preliminary studies have demonstrated the efficacy of FUT-175, an inhibitor of the complement system, in the prevention of vasospasm. In the next years, these new therapies have to be validated by prospective and randomized clinical trials to propose guidelines for the management of patients at risk of cerebral vasospasm after aneurysmal rupture.

Antioxidants↗
PubMed1996

Effect of propofol on in vitro lipid peroxidation induced by different free radical generating systems: a comparison with vitamin E.

Propofol has been reported to have antioxidant properties and to inhibit lipid peroxidation. In this study, we examined the ability of propofol to inhibit lipid peroxidation induced by three free radical systems (hydroxyl, ferryl, and oxo-ferryl radicals), and we compared the effect of propofol with that of vitamin E, an endogenous antioxidant. Lipid peroxidation was induced by exposing a linoleic acid emulsion to either water gamma radiation, a ferrous iron-ascorbate solution, or human hemoglobin, generating the hydroxyl, ferryl, and oxo-ferryl radicals, respectively. Each experiment was performed in triplicate with and without propofol or vitamin E at concentrations between 10(-5) and 10(-4) M. Lipid peroxidation was quantified by gas chromatography measurement of the pentane released (nmoles) from lipid decomposition. In each condition, a significant dose-response relationship was found between the release of pentane and the concentration of either propofol or vitamin E. The antioxidant activities of both agents were similar but significantly higher against the hydroxyl than the ferryl and oxo-ferryl radicals. The study suggests that propofol could be beneficial as an anesthetic or sedative drug in patients presenting pathologies associated with free radical reactions.

Anesthetics, Intravenous↗
PubMed1996

Intraoperative localisation of the primary motor cortex using single electrical stimuli.

A new method of intraoperative localisation of the primary motor cortex is described, based on the application of single anodal electric pulses to the brain surface. Patients were anaesthetised with propofol infusion, and neuromuscular blockade was temporarily alleviated to allow recording of surface EMG responses (CMAPs) to the stimuli. Primary motor areas could be localised in 18/19 patients studied. In the other patient, no responses were elicited, as the operative field was posterior to the motor cortex. When compared with MEPs elicited in awake patients by magnetic stimuli, responses to intraoperative anodal stimulation were of small amplitude (usually less than 10% of MEPs) and their latency was some 1 to 2 ms longer. One month after the operation, only 1/19 patients was left with a slight muscle weakness, although seven showed preoperative motor deficit. The procedure proved easy and fast, needing no preliminary surgery or time consuming preparation. It did not induce any detectable side effects.

Brain Mapping↗
PubMed1996

Comparison of neuromuscular block of atracurium and rocuronium in adults.

We studied the time-course of action of atracurium 0.5 mg kg-1 and rocuronium 0.6 mg kg-1 in 24 healthy adult patients. Anesthesia was induced with thiopentone and sufentanil, and maintained with 50% nitrous oxide and 1% enflurane in oxygen. Neuromuscular transmission was monitored by stimulating the ulnar nerve at the wrist and measuring the acceleration of the thumb using the TOF-Guard accelerograph monitor. Supramaximal stimuli of 0.2 ms duration were applied in a single twitch stimulation mode at 1 Hz frequency until completion of block, and in train-of four (TOF) sequence at 2 Hz every 15 sec thereafter. Onset time was longer with atracurium (mean +/- SD:90 +/- 18 sec) than with rocuronium (49 +/- 6 sec). Clinical duration of action (Tl25) was longer with atracurium (52.3 +/- 7.2 min) than with rocuronium (40.0 +/- 6.4 min). Recovery index (Tl25-Tl75) and time for TOF ratio to recover to 0.75 were 17.8 +/- 4.2 and 73.9 +/- 8.8 min with atracurium, and 13.8 +/- 4.1 and 70.4 +/- 14.1 min with rocuronium. The differences between both groups were statistically significant except the difference in the time for TOF to return to 0.75.

Adult↗
PubMed1995

Effect of plasma anticonvulsant level on pipecuronium-induced neuromuscular blockade: preliminary results.

Patients receiving anticonvulsants are resistant to nondepolarizing muscle relaxants (NDMR). This study examines the effect of plasma anticonvulsant levels on pipecuronium-induced neuromuscular blockade. Twenty adult patients scheduled for neurosurgery were assigned to one of two groups. Group 0 (G0) consisted of 10 patients not on anticonvulsant therapy; group 1 (G1) included 10 patients treated either with phenytoin or carbamazepine. G1 patients were further divided into G1u (n = 4) and G1w (n = 6) subgroups, according to the plasma anticonvulsant level measured the day before surgery--under (G1u) or within (G1w) the therapeutic range. Neuromuscular transmission was monitored with a Biometer International A/S Accelograph. Anesthesia was induced and maintained using propofol and sufentanil. After calibration of the accelograph, a bolus of pipecuronium 0.08 mg/kg was given IV. The time from pipecuronium injection to the peak reduction of T1 was taken as the onset time. The time in min from pipecuronium injection to recovery of T1% (first accelograph response/baseline response) x 100 and TR% (fourth accelograph response/first accelograph response) x 100 were recorded at 25, 50, and 75% of baseline. The recovery index (RI) was taken as the time from 25 to 75% of baseline. The recovery index (RI) was taken as the time from 25 to 75% recovery of the baseline response. The onset time was not different in G0 (203 +/- 60.4 s), G1 (230.5 +/- 79.3 s), and G1u (181.8 +/- 60.4 s) but prolonged in G1w (279.2 +/- 67.7 s).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

[Hydrostatic pressure and neurosurgical pathology].

Hydrostatic pressure is a force applied by a liquid on the surface of an immersed body. Inside the circulatory system it depends on the weight of the blood column between the heart and a given level. In neurosurgical patients, the hydrostatic pressure plays an important role in cerebral perfusion, transcapillary fluid movements and venous air embolism. The mean arterial pressure (Pa), the CSF pressure (CSFP) and the pressure in the jugular vein (JVP) are the hydrostatic determiners of the cerebral perfusion pressure (CPP). The hydrostatic pressure gradient associated with head raising decreases Pa, cerebral venous pressure and JVP, decreases or increases intracranial pressure (ICP) and decreases CPP. The consequences of the resulting hypoperfusion depend on the status of autoregulation. When the skull is open, the pressure under the cerebral retractors determines the transmural pressure and cerebral perfusion. The transcapillary fluid movements depend on a permeability coefficient, a hydrostatic pressure gradient and an osmotic pressure gradient. In case of a rupture of blood brain barrier (BBB), the increase of Pa and the decrease of ICP (craniotomies) favour the development of vasogenic oedema. When the Pa stands higher than the upper limit of autoregulation, the hydrostatic capillary pressure increases. It results in a vasodilation, an increase of cerebral blood flow and oedema, the lesion of BBB being initiated by an increase of the amount and the activity of the pinocytotic vesicles in endothelial cells. The syndrome of BBB rupture at a normal CPP is the consequence of an increase in hydrostatic pressure in the dilated capillary territory and can make more difficult the surgical treatment of arterio-venous malformations.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood-Brain Barrier↗
PubMed1994

Propofol protects cultured rat hippocampal neurons against N-methyl-D-aspartate receptor-mediated glutamate toxicity.

The effect of propofol on the toxicity induced by glutamate (GLU), N-methyl-D-aspartate (NMDA), kainate (KA), and amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) was investigated on cultured fetal rat hippocampal neurons. The degree of neuronal injury was quantified by measuring the release of the neuron-specific enolase (NSE) into the culture media. The toxicity induced by brief exposure to GLU (10(-4) M) or to NMDA (10(-4) M) was significantly reduced by propofol, whereas that elicited by KA, AMPA (10(-4) M), or long GLU exposure was unaffected. In conclusion, high concentrations of propofol significantly attenuate NMDA receptor-mediated glutamate neurotoxicity in vitro. Further studies are needed to confirm this beneficial effect in vivo and to evaluate propofol as a neuroprotective anesthetic agent in pathologies involving glutamate release and NMDA-mediated toxicity.

Animals↗
PubMed1994

[Malformative and degenerative diseases of the cervical spine: preoperative evaluation].

Malformative or degenerative abnormalities of the cranio-cervical joint which are the most frequently encountered in neurosurgery concern the occipital bone, the atlantoaxial joint and the surrounding nervous or vascular structures. These pathologies may have an acquired or congenital origin. In the last eventuality, they are frequently associated with other malformative disorders involving the vertebral column, the thorax, the kidneys or the heart. The clinical picture is various and many systems can be affected. Therefore, preoperative assessment of patients implies a multifactorial evaluation. The anesthesiologist should refer to the following check list: examination of the neck and cervical spine, neurological status, evaluation of associated diseases, pulmonary and cardiac function tests, airways permeability and conditions of endotracheal intubation.

Arnold-Chiari Malformation↗
PubMed1994

[Sedation of patients with head injuries].

In severe head-injured patients, intravenous sedation is an integrant part of therapy. Its main objectives consist in facilitation of ventilation and other therapeutic procedures but also more specifically in the control of intracranial pressure and epileptic seizures. The ideal sedative drug must fulfil a number of criteria regarding pharmacokinetics, cerebral metabolism and hemodynamics. Opioids, midazolam and propofol are the most commonly used sedative drugs. The therapeutic response and the neurological status of the patients are the guidelines for the choice, the duration and the assessment of sedation.

Craniocerebral Trauma↗