Comparison of eltanolone and propofol in anesthesia for termination of pregnancy

A randomized study was designed to compare eltanolone (pregnanolone) and propofol anesthesia in 60 unpremedicated women undergoing outpatient termination of pregnancy. The initial doses for induction of anesthesia were 0.8 mg/kg for eltanolone and 2 mg/kg for propofol followed by an additional 25% increment if necessary. The doses required for successful induction were 0.82 +/- 0.06 and 2.1 +/- 0.3 (mean +/- SD) mg/kg for eltanolone and propofol, respectively. Discomfort or pain on injection occurred in none of the patients given eltanolone and in 20% of those receiving propofol (P < 0.05). To maintain satisfactory anesthesia, 29% of the patients given eltanolone and 70% of the patients given propofol needed extra bolus doses of the study drug (P < 0.01). Excitation (twitching of extremities or slight hypertonus) occurred in 29% of the patients in the eltanolone group compared to none in the propofol group (P < 0.05). Both clinical (opening eyes, orientation, walking, tolerating oral fluids, voiding) and psychomotor recovery (Maddox Wing test and Digit Symbol Substitution test) returned to baseline more slowly after eltanolone than after propofol. Overall home readiness was achieved later in the eltanolone group [median 57 min (range 41-190 min)] compared to the propofol [37 (32-100 min)] group. We conclude that recovery from anesthesia is more rapid from propofol as compared to eltanolone anesthesia.     

Use of Diprivan in radiology

For radiological examinations, propofol is administered, depending on the indications, at following doses: for anxiolysis: i.v. bolus of 10-20 mg, repeated as required; for sedation with maintenance of spontaneous ventilation: i.v. bolus of 0.5 mg.kg-1 or continuous infusion of 3 mg.kg.h-1. for general anaesthesia: i.v. bolus of 2 mg.kg-1 and maintenance with a continuous infusion of 6-10 mg.kg-1.h-1. These doses are modified according to the patient's reactions and painful episodes. In neuroradiology, indications for anaesthesia include vascular explorations, MRI, computerized axial tomography, as well as biopsies of organs and tumors, with the exception of explorations in patients with tight stenoses of the carotid artery. The use of propofol for cardiological explorations is questioned in adults and mainly in children with a congenital cardiopathy. For some authors this agent is contra-indicated, as during induction it decreases, sometimes excessively, the mean arterial pressure.     

Comparative effects of propofol, pentobarbital, and isoflurane on cerebral blood flow and blood volume

While intravenous and volatile anesthetics have widely differing effects on cerebral blood flow (CBF), clinical studies suggest that the relative differences in their effects on intracranial pressure (ICP) may be smaller. Because acute changes in ICP are determined primarily by changes in cerebral blood volume (CBV), we compared the impact of propofol, pentobarbital, and isoflurane on CBF and CBV in rats. Equipotent doses of the three agents were determined by tail-clamp studies. Animals were then anesthetized with propofol (20 mg/kg load, 38 mg.kg-1.h-1 infusion), pentobarbital (30 mg/kg load, 20 mg.kg-1.h-1 infusion), or isoflurane 1.6-1.8%. Two hours later, CBF and CBV were measured using 3H-nicotine as a CBF tracer, and 14C-dextran and 99mTc-labeled red cells as markers for cerebral plasma and red blood cell volumes (CPV and CRBCV), respectively. Total CBV was the sum of CPV and CRBCV. CBF was 2.0-2.6 times greater with isoflurane than with propofol or pentobarbital (137 vs. 67 and 52 ml.100 g-1.min-1, respectively). By contrast, while CBV was greater in the isoflurane group than in either the propofol or pentobarbital groups, the magnitude of the intergroup differences were much smaller (propofol = 2.49 +/- 0.28 ml/100 g; pentobarbital = 2.27 +/- 0.15 ml/100 g; isoflurane = 2.77 +/- 0.24 ml/100 g, mean +/- SD). These results suggest that the simple measurement of CBF may not adequately describe the cerebrovascular effects of an anesthetic, at least with respect to predicting the magnitude of the agents likely effects on ICP.     

Cardiopulmonary and anesthetic effects of propofol in wild turkeys

OBJECTIVE: To determine safety, anesthetic variables, and cardiopulmonary effects of i.v. infusion of propofol for induction and maintenance of anesthesia in wild turkeys. ANIMALS: 10 healthy, adult wild turkeys. PROCEDURE: Anesthesia was induced by i.v. administration of propofol (5 mg/kg of body weight) over 20 seconds and was maintained for 30 minutes by constant i.v. infusion of propofol at a rate of 0.5 mg/kg/min. Heart and respiratory rates, arterial blood pressures, and arterial blood gas tensions were obtained prior to propofol administration (baseline values) and again at 1, 2, 3, 4, 5, 10, 15, 20, 25, and 30 minutes after induction of anesthesia. All birds were intubated immediately after induction of anesthesia, and end-tidal CO2 concentration was determined at the same time intervals. Supplemental oxygen was not provided. RESULTS: Apnea was observed for 10 to 30 seconds after propofol administration, which induced a decrease in heart rate; however, the changes were not significant. Compared with baseline values, respiratory rate was significantly decreased at 4 minutes after administration of propofol and thereafter. Systolic, mean, and diastolic pressures decreased over the infusion period, but the changes were not significant. Mean arterial blood pressure decreased by 30% after 15 minutes of anesthesia; end-tidal CO2 concentration increased from baseline values after 30 minutes; PO2 was significantly decreased at 5 minutes after induction and thereafter; PCO2 was significantly (P < 0.05) increased after 15 minutes of anesthesia; and arterial oxygen saturation was significantly (P < 0.05) decreased at the end of anesthesia. Two male turkeys developed severe transient hypoxemia, 1 at 5 and the other at 15 minutes after induction. Time to standing after discontinuation of propofol infusion was 11 +/- 6 minutes. Recovery was smooth and unremarkable. CONCLUSION: Propofol is an effective agent for i.v. induction and maintenance of anesthesia in wild turkeys, and is useful for short procedures or where the use of inhalational agents is contraindicated.     

Is patient-controlled sedation good for elderly patients?

The purpose of this study was to evaluate the safety and advantage of intra-operative patient-controlled sedation (PCS) in elderly patients. Propofol PCS was compared with anesthesiologist-controlled sedation (ACS) during knee arthroplasty under epidural anesthesia. Eleven elderly patients scheduled for unilateral knee total or partial arthroplasty were divided randomly into PCS group (n = 6) and ACS group (n = 5). Epidural anesthesia was performed to produce an appropriate level of sensory block (T 10 through S). Firstly a mixture of pentazocine 0.2 mg.kg-1 and 2% mepivacaine 6-9 ml was injected to the epidural space, and anaesthesia was maintained using 2% mepivacaine afterward. Patients in both groups received propofol 0.3 mg.kg-1 i.v. as a loading dose and 0.6 mg.kg-1.h-1 continuous infusion. Furthermore patients in PCS group received propofol PCS (bolus: 0.2 mg.kg-1, lockout time: 3 min). Patients in ACS group were administered propofol continuously and infusion rates were regulated to maintain a sedation score 3 (Wilson et al) by anesthesiologist. Respiratory rate, blood pressure, heart rate, SpO2, arterial blood gas analysis and plasma levels of propofol were measured 4 times during and after the surgery. Satisfaction of patients and surgeons was questioned. Patients in PCS group received a mean propofol dose of 1.9 +/- 0.1 mg.kg-1 during procedures with a mean duration of 147 min. On the other hand patients in ACS group received propofol 2.9 +/- 0.3 mg.kg-1 with 142 min of procedures. Satisfaction of patients and surgeons, the incidence of complication were similar between the groups. For elderly patients who undergo epidural anesthesia, PCS is a safe and effective technique providing similar good sedation as with ACS.     

Pharmacokinetics and pharmacodynamics of cisatracurium after a short infusion in patients under propofol anesthesia

Fourteen patients, ASA physical status I or II, were recruited to assess the pharmacokinetic-pharmacodynamic relationship of cisatracurium under nitrous oxide/sufentanil/propofol anesthesia. The electromyographic response of the abductor digiti minimi muscle was recorded on train-of-four stimulation of the ulnar nerve. A 0.1-mg/kg dose of cisatracurium was given as an infusion over 5 min. Arterial plasma concentrations of cisatracurium and its major metabolites were measured by using high-performance liquid chromatography. A nontraditional two-compartment pharmacokinetic model with elimination from central and peripheral compartments was used. The elimination rate constant from the peripheral compartment was fixed to the in vitro rate of degradation of cisatracurium in human plasma (0.0237 min(-1)). The mean terminal half-life of cisatracurium was 23.9+/-3.3 min, and its total clearance averaged 3.7+/-0.8 mL x min(-1) x kg(-1). Using this model, the volume of distribution at steady state was significantly increased compared with that obtained when central elimination only was assumed (0.118+/-0.027 vs 0.089+/-0.017 L/kg). The effect-plasma equilibration rate constant was 0.054+/-0.013 min(-1). The 50% effective concentration (153+/-33 ng/mL) was 56% higher than that reported in patients anesthetized with volatile anesthetics, which suggests that, compared with inhaled anesthetics, a cisatracurium neuromuscular block is less enhanced by propofol. IMPLICATIONS: The drug concentration-effect relationship of the muscle relaxant cisatracurium has been characterized under balanced and isoflurane anesthesia. Because propofol is now widely used as an IV anesthetic, it is important to characterize the biological fate and the concentration-effect relationship of cisatracurium under propofol anesthesia as well.     

Hemodynamic response to induction and intubation. Propofol/fentanyl interaction

BACKGROUND: When given as an intravenous bolus for induction of anesthesia, propofol can decrease postintubation hypertension but can also create moderate to severe postinduction, preintubation hypotension. The addition of fentanyl usually decreases the postintubation hypertension but can increase the propofol-induced preintubation hypotension. The goal of the study was to determine the relation between propofol and fentanyl doses and the hemodynamic changes post-induction, preintubation and postintubation. METHODS: Twelve groups of 10 patients, ASA physical status 1 or 2, first received fentanyl 0, 2, or 4 micrograms.kg-1 and then 5 min later received propofol 2.0, 2.5, 3.0, or 3.5 mg.kg-1 as an intravenous bolus for induction of anesthesia. Arterial blood pressure was continuously monitored. The trachea was intubated 4 min after propofol administration. RESULTS: The mean decrease in systolic blood pressure after propofol was 28 mmHg when no fentanyl was given, 53 mmHg after 2 microgram.kg-1 of fentanyl (P < 0.05 vs. no fentanyl), and 50 mmHg after 4 micrograms.kg-1 (P < 0.05 vs. no fentanyl; no statistically significant difference 4 vs. 2 micrograms.kg-1). There was no statistically significant difference in hemodynamic response to intubation relative to propofol dose. Hemodynamic response to intubation was decreased by the administration of fentanyl; the mean increase of systolic blood pressure after intubation was 65 mmHg from preintubation value without fentanyl, 50 mmHg after 2 micrograms.kg-1, and 37 mmHg after 4 micrograms.kg-1 (P < 0.05 for 2 and 4 micrograms.kg-1 vs. no fentanyl and for 4 vs. 2 micrograms.kg-1). Hemodynamic changes postintubation were not statistically different with increasing doses of propofol. CONCLUSIONS: Hemodynamic changes after induction with propofol or propofol/fentanyl, pre- or postintubation, are not modified when the propofol dose is increased from 2 to 3.5 mg.kg-1. Maximal hypotension preintubation occurs with a fentanyl dose of 2 micrograms.kg-1, whereas the magnitude of postintubation hypertension is significantly decreased with an increase in the fentanyl dose to 4 micrograms.kg-1.     

Should interstitial thermometry be used for deep hyperthermia?

This study was performed to determine whether premedication with midazolam and fentanyl prevents reliable detection of an i.v. lidocaine test dose. Thirty ASA physical status I or II patients received either 3 mL of saline or 1.5 mg of midazolam (1.5 mL) plus 75 microg of fentanyl (1.5 mL) i.v. in a randomized, double-blind fashion. Five minutes later, lidocaine 1 mg/kg was injected i.v. At 1.5 min before and every minute after lidocaine administration, each subject was questioned regarding the presence of four symptoms of systemic lidocaine toxicity. Any new tinnitus, perioral numbness, metallic taste, or light-headedness within 5 min after lidocaine administration was considered a positive response. All 15 patients in the saline group (100% sensitivity) had a positive response to i.v. lidocaine, but only 9 of 15 patients in the sedation group had a positive response (60% sensitivity; P = 0.017). We conclude that midazolam and fentanyl premedication decreases the reliability of subjective detection of i.v. lidocaine. Implications: Anesthesiologists often rely on subjective symptoms to prevent local anesthetic toxicity while performing regional anesthesia. Sedatives are often administered during the administration of regional anesthesia. This study demonstrates that typical sedation decreases the reliability of detection of local anesthetic toxicity by subjective symptoms.     

Is there reliable experimental evidence for a chromosomal "fingerprint" of exposure to densely ionizing radiation?

BACKGROUND: As an inhibitor of the reuptake of serotonin and norepinephrine in the spinal cord, the mechanism of action of tramadol resembles that of nefopam, which has been used in the treatment of postanesthetic shivering. METHODS: In a randomized, placebo-controlled, double-blind study, we assessed the effects of tramadol (0.5 mg.kg-1, 1 mg.kg-1 and 2 mg.kg-1 i.v.) or normal saline on shivering after a standardized general anesthesia in 40 adult patients, ASA physical status I or II (group 1), and in 64 adult patients regardless of the foregoing general anesthesia and ASA physical status (group 2). RESULTS: Tramadol 1 mg.kg-1 or more abolished shivering completely 5 min after treatment in all patients of groups 1 and 2. In group 1, the three dosages of tramadol were not statistically different in lowering the severity and prevalence of postanesthetic shivering. Tramadol 0.5 mg.kg-1 was significantly slower than tramadol 1 or 2 mg.kg-1 in tempering the severity as well as lowering the prevalence of postanesthetic shivering in group 2. CONCLUSION: Tramadol's distinct features in the treatment of shivering reside in its high safety profile and weak sedative properties, particularly in patients with poor cardiorespiratory reserve, in outpatients and on recurrence of shivering.     

Anesthetic management of a patient with hypertrophic cardiomyopathy using propofol, fentanyl and ketamine

A 59-year-old male with hypertrophic cardiomyopathy was scheduled for resection of a maxillary cyst. Metoprolol was discontinued the day before surgery. Thirty min before anesthesia, meperidine 35 mg was administered intramuscularly. After intravenous administration of midazolam 3 mg, a pulmonary catheter was inserted for monitoring hemodynamic parameters. Anesthesia was induced with propofol 75 mg, fentanyl 0.15 mg and ketamine 75 mg. Anesthesia was maintained with continuous infusion of propofol 5 mg.kg-1.h-1 and ketamine 1 mg.kg-1.h-1. Moreover, fentanyl was added as necessary during surgery. Blood pressure (BP), pulmonary arterial pressure (PA), systemic vascular resistance index (SVRI) and pulmonary vascular resistance index (PVRI) were measured using a pulmonary catheter during anesthesia. Since BP decreased after intubation, dopamine 3 micrograms.kg-1.min-1 was administered for 20 min. The hemodynamic state was stable during surgery. However, BP, PA, SVRI and PVRI increased temporally at extubation. His postoperative course was uneventful. In conclusion, total intravenous anesthesia with propofol, fentanyl and ketamine may be useful for anesthetic management of a patient with hypertrophic cardiomyopathy.     

Single vital capacity inhalational anaesthetic induction in adults--isoflurane vs sevoflurane

PURPOSE: To evaluate whether isoflurane is as suitable as sevoflurane for the single vital capacity breath (VCB) method of inhalational induction in patients premedicated with midazolam. METHODS: A randomised, controlled, double-blind study involving 67 ASA I-II patients aged between 18-50 yr undergoing elective surgery under general anaesthesia. All participants received premedication with 0.03 mg.kg-1 midazolam i.v. Using a primed circle absorber circuit, inhalational induction of anaesthesia was performed with the single VCB method using either isoflurane 3.5% or sevoflurane 7.5% in nitrous oxide 67% in oxygen, representing approximately equivalent MAC-multiples of 3.6 MAC. Isoflurane was compared with sevoflurane in terms of rapidity, efficacy, safety and acceptability of induction. RESULTS: With the single VCB method, sevoflurane produced a faster (45 +/- 21 vs 71 +/- 22 sec, P < 0.01), more successful (100% vs 75.8%, P < 0.01) induction of anaesthesia, with fewer induction-related complications (11.8% vs 84.8%, P < 0.01) than did isoflurane. There was also greater patient acceptability of induction with sevoflurane (76.4% vs 42.4%, P < 0.05). CONCLUSION: In adults given midazolam premedication, isoflurane is not as suitable as sevoflurane for single VCB inhalational anaesthetic induction technique as it is associated with slower, more complicated induction and less patient acceptability.     

Circulatory changes at the time of anesthetic induction and endotracheal intubation--comparison of thiamylal induction group and propofol induction group

We examined the circulatory changes after intravenous thiamylal with additional injection of thiamylal 1 minute before intubation and after propofol at the time of anesthetic induction and endotracheal intubation. Sixty ASA I or II patients were studied after the institutional and informed consents. We compared the following three groups. Group I (n = 20): Anesthesia was induced with thiamylal 5 mg.kg-1 and intubation with the aid of vecuronium 0.1 mg.kg-1. Group II (n = 20): Anesthesia was induced with thiamylal 3 mg.kg-1 and vecuronium 0.1 mg.kg-1. One minute before the intubation, the patients received additional thiamylal 4 mg.kg-1. Group III (n = 20): Anesthesia was induced with propofol 2.5 mg.kg-1 and intubation was performed with the aid of vecuronium 0.1 mg.kg-1. We examined the systolic, diastolic and mean blood pressures, heart rate, and rate pressure product (RPP) in the three groups. The examinations were performed before and after induction, soon after intubation, and every one minute after intubation for 5 minutes. After the endotracheal intubation, the systolic blood pressure and heart rate increased in Group I. But the systolic and diastolic pressures were significantly more stable in Group II and Group III. The change of the RPP was slight and most stable in Group II compared with the other two groups. We conclude that additional injection of thiamylal 4 mg.kg-1 following induction of anesthesia with thyamylal 3 mg.kg-1 1 minute before endotracheal intubation is an effective method for minimizing the increase in blood pressure and circulatory changes at the time of rapid induction of anesthesia and endotracheal intubation.     

Antiemetic activity of propofol after sevoflurane and desflurane anesthesia for outpatient laparoscopic cholecystectomy

BACKGROUND: Controversy exists regarding the effectiveness of propofol to prevent postoperative nausea and vomiting. This prospective, randomized, single-blinded study was designed to evaluate the antiemetic effectiveness of 0.5 mg/kg propofol when administered intravenously after sevoflurane- compared with desflurane-based anesthesia. METHODS: Two hundred fifty female outpatients undergoing laparoscopic cholecystectomy were assigned randomly to one of four treatment groups. All patients were induced with intravenous doses of 2 mg midazolam, 2 microg/kg fentanyl, and 2 mg/kg propofol and maintained with either 1-4% sevoflurane (groups 1 and 2) or 2-8% desflurane (groups 3 and 4) in combination with 65% nitrous oxide in oxygen. At skin closure, patients in groups 1 and 3 were administered 5 ml intravenous saline, and patients in groups 2 and 4 were administered 0.5 mg/kg propofol intravenously. Recovery times were recorded from discontinuation of anesthesia to awakening, orientation, and readiness to be released home. Postoperative nausea and vomiting and requests for antiemetic rescue medication were evaluated during the first 24 h after surgery. RESULTS: Propofol, in an intravenous dose of 0.5 mg/kg, administered at the end of a sevoflurane-nitrous oxide or desflurane-nitrous oxide anesthetic prolonged the times to awakening and orientation by 40-80% and 25-30%, respectively. In group 2 (compared with groups 1, 3, and 4), the incidences of emesis (22% compared with 47%, 53%, and 47%) and requests for antiemetic rescue medication (19% compared with 42%, 50%, and 47%) within the first 6 h after surgery were significantly lower, and the time to home-readiness was significantly shorter in duration (216 +/- 50 min vs. 249 +/- 49 min, 260 +/- 88 min, and 254 +/- 72 min, respectively). CONCLUSIONS: A subhypnotic intravenous dose of propofol (0.5 mg/kg) administered at the end of outpatient laparoscopic cholecystectomy procedures was more effective in preventing postoperative nausea and vomiting after a sevoflurane-based (compared with a desflurane-based) anesthetic.     

The effects of sevoflurane, isoflurane, halothane, and enflurane on hemodynamic responses during an inhaled induction of anesthesia via a mask in humans

A rapid increase in isoflurane or desflurane concentration induces tachycardia and hypertension and increases-plasma catecholamine concentration. Little information is available as to whether sevoflurane, halothane, and enflurane induce similar responses during anesthesia induction via mask. Fifty ASA physical status I patients, aged 20-40 yr, and scheduled for elective minor surgery, received one of four volatile anesthetics: sevoflurane, isoflurane, halothane, or enflurane. Anesthesia was induced with thiamylal, followed by inhalation of 0.9 minimum alveolar anesthetic concentration (MAC) of the anesthetic in 100% oxygen via mask. The inspired concentration of anesthetic was increased by 0.9 MAC every 5 min to a maximum of 2.7 MAC. Heart rate (HR) and systolic blood pressure (SBP) were measured before and every minute for 15 min during anesthetic inhalation. In the sevoflurane and isoflurane groups, venous blood samples were drawn to determine the concentrations of plasma epinephrine and norepinephrine 3 min after each increase in anesthetic concentration. Sustained increments in HR were observed after increases in inspired isoflurane concentration to 1.8 MAC and 2.7 MAC (peak changes of 15 +/- 3 and 17 +/- 3 bpm, respectively). Isoflurane also increased SBP transiently after the inspired concentration was increased to 2.7 MAC (peak change of 10 +/- 4 mm Hg). Enflurane increased HR after the inspired concentration was increased to 2.7 MAC (peak change of 9 +/- 2 bpm). In contrast, changes in sevoflurane and halothane concentrations did not induce hyperdynamic responses. Plasma norepinephrine concentration in the isoflurane group was significantly higher than that in the sevoflurane group during 2.7 MAC (P = 0.022). We propose that there is a direct relationship between airway irritation of the anesthetic and immediate cardiovascular change during an inhaled induction of anesthesia.     

Diltiazem-lidocaine combination for the attenuation of cardiovascular responses to tracheal intubation in hypertensive patients

PURPOSE: Hypertensive patients are prone to haemodynamic changes after laryngoscopy and tracheal intubation. This study was undertaken to compare the efficacy of a combination of diltiazem and lidocaine with that of each drug alone for suppressing the cardiovascular responses to tracheal intubation. METHODS: Sixty hypertensive patients (ASA II), defined as systolic blood pressure > 160 mmHg and/or diastolic blood pressure > 95 mmHg (World Health Organization), undergoing elective surgery received, in a randomized, double-blind manner, 0.3 mg.kg-1 diltiazem, 1.5 mg.kg-1 lidocaine, or 0.3 mg.kg-1 diltiazem plus 1.5 mg.kg-1 lidocaine i.v. (n = 20 of each) before the initiation of laryngoscopy. Anaesthesia was induced with 5 mg.kg-1 thiopentone i.v., and tracheal intubation was facilitated with 2 mg.kg-1 succinylcholine i.v. after precurarization with 0.02 mg.kg-1 vecuronium i.v. Changes in heart rate (HR), mean arterial pressure (MAP) and rate-pressure product (RPP) were measured before and at immediate, 1, 2, 3, 5 and 10 min after tracheal intubation. RESULTS: The inhibitory effects of diltiazem-lidocaine combination on cardiovascular responses to tracheal intubation was greater than those of diltiazem or lidocaine as a sole medicine (RPP; 10,602 +/- 1448 (combination) vs 11,787 +/- 1345 (diltiazem), 15,428 +/- 1756 (lidocaine), mean +/- SD, P < 0.05). CONCLUSION: Prophylactic therapy with diltiazem-lidocaine combination is more effective than diltiazem or lidocaine alone for attenuating the cardiovascular changes associated with tracheal intubation in hypertensive patients.     

Neuromuscular blockade with vecuronium and its reversal with edrophonium during total intravenous anesthesia, neuroleptanalgesia and sevoflurane anesthesia

The neuromuscular blocking effect of vecuronium and its reversibility ith edrophonium were studied under total intravenous anesthesia (TIVA) and compared with those under NLA or sevoflurane anesthesia (SA) in 30 surgical patients. The degree of neuromuscular blockade was evaluated by acceleration of thumb adduction in response to supramaximal stimulation of the ulnar nerve using Accelograph (Biometer). TIVA was induced with droperidol 0.25 mg.kg-1, fentanyl 2-4 micrograms.kg-1 and ketamine 2 mg.kg-1, and maintained with continuous infusion of ketamine 2 mg.kg-1.h-1 with 30-35% O2 in air. NLA was induced with droperidol 0.25 mg.kg-1 and fentanyl 5-10 micrograms.kg-1 and maintained with 66% nitrous oxide in oxygen. SA was induced with thiamylal 5 mg.kg-1 i.v. and maintained with 66% nitrous oxide in oxygen supplemented with sevoflurane (1 MAC). A single bolus intravenous injection of vecuronium 0.1 mg.kg-1 was used for paralysis and reversed with edrophonium 0.75 mg.kg-1 followed by atropine 0.015 mg.kg-1 when the TOF ratio returned to 25%. The times required from administration of vecuronium to completion of maximal block with TIVA, NLA and SA were 196.5 +/- 52.2 sec, 182.5 +/- 47.6 sec and 166.0 +/- 69.0 sec, respectively. There was no significant difference among them. The times from completion of maximal block to 25% recovery of the twitch height in TIVA and NLA were 39.5 +/- 11.0 min and 37.4 +/- 5.8 min without significant difference. Those values, however, were significantly shorter than 64.5 +/- 35.2 min of SA.(ABSTRACT TRUNCATED AT 250 WORDS)     

Paraneoplastic and oncologic profiles of patients seropositive for type 1 antineuronal nuclear autoantibodies

The association of propofol with excitatory motor activity, such as myoclonic jerking and opisthotonus, in humans and in animals suggests that it may aggravate clinical seizure activity in some circumstances, although evidence suggests that under other circumstances, propofol inhibits seizure activity. In the current study, we assessed the effect of sedating doses of propofol on lidocaine-induced seizure activity in spontaneously breathing rats receiving no other anesthetics. Adult Sprague-Dawley male rats, 300-400 g, were divided into a control group and three experimental groups representing three graded levels of propofol sedation. The control rats then received a lidocaine infusion at the rate of 150 mg x kg(-1) x h(-1), resulting in a slow, progressive increase in systemic lidocaine concentrations. At the onset of electroencephalographic (EEG) seizure activity, arterial lidocaine concentrations were obtained. The treated rats received propofol according to three different dose schedules: Dose 1 = 10 mg x kg(-1) x h(-1) after a 2.5-mg/kg bolus; Dose 2 = 20 mg x kg(-1) x h(-1) after a 5-mg/kg bolus; Dose 3 = 40 mg x kg(-1) x h(-1) after a 10-mg/kg bolus. After 30 min, a steady level of sedation, dependent on the dose of propofol, was achieved. The lidocaine infusion was then started, and systemic lidocaine levels were obtained at the onset of EEG seizure activity. The lidocaine was continued until the onset of death by cardiac arrest. Plasma lidocaine was measured by gas chromatography. Analysis of variance and Dunnett's t-test were used for comparisons with the control values. Continuous propofol sedation increased the seizure dose of lidocaine from 37.7 +/- 3.5 mg/kg (mean +/- SEM) to 52.5 +/- 2.6 mg/kg (Dose 1, P < 0.05) and 67.9 +/- 8.6 mg/kg (Dose 2, P < 0.05), and completely abolished lidocaine seizures at Dose 3. The lethal dose of lidocaine, 89.4 +/- 10.5 mg/kg control versus 108.7 +/- 10.3 mg/kg (Dose 1), 98.3 +/- 10.1 mg/kg (Dose 2), and 93.5 +/- 10.4 mg/kg (Dose 3) did not differ among groups. The lidocaine levels at seizure threshold were increased in the propofol-treated rats: 16.9 +/- 0.5 microg/mL control versus 19.2 +/- 0.7 microg/mL (Dose 1, P = not significant) and 23.7 +/- 1.8 microg/mL (Dose 2, P < 0.05). Continuous propofol sedation in spontaneously breathing rats receiving no other anesthetics exerts a protective effect against lidocaine-induced seizures in a monotonic, dose-dependent fashion. The cardiac arrest dose of lidocaine is unaffected by propofol under these conditions. IMPLICATIONS: The i.v. anesthetic drug propofol, given to rats to produce sedation, was found to suppress seizure activity caused by overdosage of the local anesthetic lidocaine.     

Rate of cerebrospinal fluid formation, resistance to reabsorption of cerebrospinal fluid, brain tissue water content, and electroencephalogram during desflurane anesthesia in dogs

Propofol decreases intraocular pressure (IOP) and the IOP response to laryngoscopy and intubation, but the mechanisms responsible for this effect have not been reported. The present study examined the effect of propofol on IOP, intraocular fluid formation and outflow facility, and intraocular compliance. Twenty-two white New Zealand rabbits were anesthetized with halothane (0.8%-1.0% inspired concentration) in nitrous oxide (2 L/min) and oxygen (1 L/min). Muscle paralysis was established with pancuronium, and the lungs were mechanically ventilated through a tracheal tube. Twelve rabbits examined under these conditions served as controls. In the treatment group (n = 10), 6 mg/kg propofol followed by 18 mg.kg-1 x h-1 propofol intravenously was added to halothane/nitrous oxide/oxygen anesthesia. In both groups, a series of intraocular infusions was made via a 30-gauge needle in the anterior chamber, and IOP, the rate of aqueous humor formation (Fa), and trabecular outflow facility (Ctr) were determined using conventional analysis. These same measures, as well as intraocular compliance, were determined using a new method of analysis adapted from the manometric technique for determining cerebrospinal fluid dynamics. IOP was 11.3 +/- 1.8 mm Hg (mean +/- SD) in halothane-anesthetized controls and decreased to 9.4 +/- 2.2 mm Hg when propofol was added to halothane anesthesia (P < 0.05). By conventional analysis, Fa was 2.82 +/- 0.94 microL/min and Ctr was 0.121 +/- 0.044 microL.min-1 x mm Hg-1 in controls. After addition of propofol, Fa decreased by 24% to 2.15 +/- 0.62 microL/min (P < 0.05) and Ctr decreased by 18% to 0.099 +/- 0.034 microL.min-1 x mm Hg-1 (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Release, oxidation, and reesterification of fatty acids from infused triglycerides: effect of heparin

We have investigated the effects of heparin on rates of fatty acid (FA) release, oxidation, and reesterification from intravenously (IV) infused triglycerides (TGs) during euglycemic (4.7 mmol.L-1) hyperinsulinemia (approximately 450 pmol.L-1). Four healthy men (aged 31 +/- 3 years; body mass index, 26.1 +/- 0.9 kg/m2) received i.v. TGs (1.02 mmol TG.kg-1.4 h-1), four other men (aged 24.3 +/- 2.8 years: body mass index, 24.7 +/- 1.7 kg/m2) received TGs plus heparin (200-U bolus followed by 0.4 U.kg-1.min-1), and nine men and one woman (aged 28.8 +/- 2.3 years; body mass index, 23.1 +/- 0.9 kg/m2) received saline (controls). Heparin increased lipolysis from infused TGs (to 1.0 +/- 0.1 from 0.3 +/- 0.1 mmol.kg-1.4 h-1, P < .01), increased plasma free fatty acids ([FFA] to 737 +/- 32 from 597 +/- 136 mumol.L-1, P < .05). and increased FA reesterification (to 0.84 +/- 0>14 from 0.18 +/- 0.12 mmol.kg-1.4 h-1, P < .02), but had no effect o n FA oxidation (0.13 +/- 0.02 v 0.12 +/- 0.04 mmol.kg-4 h-1) or net energy gain (167 +/- 42 v 243 +/- 79 kJ.4 h-1). In summary, addition of heparin (1) increased lipolysis (to approximately 98% from approximately 29%) and reesterification (to approximately 82% from approximately 17%) of infused TG, but had no significant effects on fat oxidation (approximately 12%) and net energy gain. We conclude that heparin accelerated removal of infused lipid from the blood and its deposition into endogenous fat depots. Since the doses of heparin and insulin used in this study were higher than those generally used in total parenteral nutrition protocols, our results may not be strictly applicable to the usual clinical situation.     

Comparison of propofol and pentazocine combined with thiamylal for laryngeal mask insertion

We evaluated the combination of pentazocine and thiamylal as induction agents for laryngeal mask airway (LMA) insertion and compared this with propofol. Ninety-four patients, ASA grade 1 or 2, were randomly assigned to one of four induction groups as follows; group P: propofol 2.5 mg.kg-1, group p 0.3: pentazocine 0.3 mg.kg-1 followed by thiamylal 5 mg.kg-1, group p 0.6: pentazocine 0.6 mg.kg-1 followed by thiamylal 5 mg.kg-1, and group T: thiamylal 5 mg.kg-1. In group T (n = 5), insertion of LMA was impossible due to inadequate anesthesia. In contrast, good and acceptable conditions for LMA insertion were obtained in 85.2%, 86.7%, and 96.9% of group P, p 0.3, and p 0.6, respectively. Apneic interval, endtidal CO2 and arterial CO2 were significantly greater in pentazocine groups than in propofol group (group P < p 0.3 < p 0.6). Systolic pressure decreased after induction in all groups. Decreases in systolic and diastolic pressure were significantly greater in group P. Heart rate did not show any significant change. We conclude that the induction with the combination of pentazocine and thiamylal provides suitable conditions for LMA insertion with more stable hemodynamics compared with propofol. Doses of 0.3 mg.kg-1 seem to be desirable for LMA insertion.