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Background and objective: The aim was to train artificial neural nets to predict the recovery of a neuromuscular block during general anaesthesia. It was assumed that the initial/early neuromuscular recovery data with the simultaneously measured physical variables as inputs into a well-trained back-propagation neural net would enable the net to predict a rough estimate of the remaining recovery time. Methods: Spontaneous recovery from neuromuscular block (electrically evoked electromyographic train-of-four responses) were recorded with the following variables known to affect the block: multiple minimum alveolar concentration, end-tidal CO[sub 2] concentration, and peripheral and central temperature. Results: The mean prediction errors, mean absolute prediction errors, root-mean-squared prediction errors and correlation coefficients of all the nets were significantly better than those of average-based predictions used in the study. The root-mean-squared prediction error of the net — employing minimum alveolar concentrations from the whole recovery period (the recovery time from E2/E1 : 0.30 to E4/EI -0.75; E1 = first response of train-of-four, E2 = second response of train-of-four, etc.) — were significantly smaller than those of other nets, or the same net employing minimum alveolar concentrations only from the initial recovery period (from E2/E1 = 0.30 to E4/E1 = 0.25). Conclusions: Neural nets could predict individual, recovery times from the neuromuscular block significantly better than the average-based method, used here, which was supposed to be more accurate than guesses by any clinician. The minimum alveolar concentration was the only monitored variable that influenced the recovery rate, but it did not aid neural net prediction. [ABSTRACT FROM AUTHOR]

Reports on the efficacy and pharmacokinetics of local anesthetics in uremic patients have been controversial. Our study involved 29 uremic and 28 nonuremic patients. We performed axillary block with ropivacaine 300 mg (50 mL). Venous blood samples were drawn for 24 h for assay of total and unbound plasma ropivacaine, 3-hydroxyropivacaine, pipecoloxylidide (PPX), and serum alpha(1)-acid glycoprotein (AAG). Block quality was similar in both groups. No toxicity occurred. Plasma clearance of ropivacaine was smaller and the area under the concentration-time curve of ropivacaine, 3-hydroxyropivacaine, and PPX larger in the uremic patients. The plasma concentration of PPX increased until 24 h in uremic patients whose AAG concentrations were also larger throughout the study. The free fraction of ropivacaine in plasma was smaller in the uremic group when measured 60 min and 12 h after the block, but the unbound concentration of ropivacaine was larger in the uremic group at 12 h. Enhanced absorption of ropivacaine into circulation, increased binding to AAG, and probably reduced urinary excretion of the metabolites lead to larger total plasma concentrations of ropivacaine and its main metabolites in uremic patients.

The purpose of this study was to compare the perioperative effects of the intramuscular (i.m.) alpha 2 agonist, dexmedetomidine (DEX), and midazolam (MID) premedication. The study comprised 192 women (64 per group) scheduled for abdominal hysterectomy. The doses of the study drugs were chosen to obtain equal sedative effects. The three groups were: 1) i.m. DEX (2.5 micrograms/kg) and intravenous (i.v.) placebo (DexPla group), 2) i.m. DEX and i.v. fentanyl (FENT) (1.5 micrograms/kg) (DexFent group), and 3) i.m. MID (0.08 mg/kg) and i.v. FENT (MidFent group). I.m. drugs were administered 45-90 min before induction of anesthesia. Preoperative sedation and anxiolysis after DEX was comparable to that after MID. The maximum arterial blood pressure response to endotracheal intubation was blunted in the DexFent group, while in the two other groups blood pressure increased 30-34 mm Hg after endotracheal intubation. The mean isoflurane concentration during surgery was 0.14% in the DexFent group, 0.24% in the DexPla group, and 0.34% in the MidFent group (P < 0.001). During surgery, bradycardia (heart rate < 40 bpm) was observed in 6.2% of DEX patients, and no MID patients, whereas postoperatively 14.1% of DEX patients and 1.6% of MID patients had bradycardia. Fewer patients suffered from postoperative shivering after DEX (10%) than after MID (52%). We conclude that DEX has many desirable effects, but side effects such as bradycardia may limit its routine use in ASA physical status I-II patients.

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.

The present investigation was designed to study the interaction of temperature, lidocaine, and ischemia during intravenous regional anesthesia (IVRA) of the arm. Five volunteers were studied during exposure of one of their arms to four different experimental conditions: hypothermia and ischemia; hypothermia, ischemia, and lidocaine; normothermia and ischemia; normothermia, ischemia, and lidocaine. Each subject was tested on four different occasions with only one test condition imposed per occasion and with 3 or more days between experiments. Somatosensory evoked responses (SERs) and muscle responses to ulnar nerve stimulation were measured, and sensory testing was done to determine whether the neural effects of the particular treatments differed. Anesthesia developed sooner and was more extensive when local anesthetic was injected. A 5-10 degrees C decrease in tissue temperature did not accentuate the anesthetic effects of lidocaine as determined by time to loss of pinprick and touch sensation. With ischemia alone, anesthesia of the finger tips with preservation of sensation on the arm was observed in all subjects 20 min after tourniquet inflation. Anesthesia at all cutaneous test sites was achieved in 7 of 10 lidocaine experiments; no systematic order of sensory loss, such as progression from distal to proximal sites, was observed. Decrease in limb temperature slowed the development of lidocaine effects on evoked responses and recovery from the effect. Under conditions of ischemia, deterioration of sensation generally began earlier under cold rather than warm conditions. Primary differences between changes in the SERs and muscle responses under condition of ischemia versus ischemia and lidocaine were the rate and magnitude of change of potential latency and amplitude.(ABSTRACT TRUNCATED AT 250 WORDS)