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Several studies have shown that surgical patients cannot consciously recall or recognize events to which they had been exposed during general anesthesia. Might evidence of memory for intraoperative events be revealed through the performance of a postoperative test that does not require remembering to be deliberate or intentional? Results of the present study, involving the recognition and spelling of semantically biased homophones, suggest a negative answer to this question and imply that intraoperative events cannot be remembered postoperatively, either with or without awareness.

The neuromuscular sensitivity of 71 patients (A.S.A. class I or II) was tested by scoring on a scale from 1 to 6 the ability to lift the upper eyelid 2 minutes after pretreatment with 1 mg of pancuronium. Subsequently, each patient also received an additional "intubation dose" pancuronium (in milligrams) equal to the eye-opening test score (group I), or either 1 mg (group II) or 2 mg (group III) in excess. The resultant depression of the neurally evoked muscle response of the little finger was quantified by another score (the response score) which allowed for assessment of neuromuscular block beyond the limit of 100% depression of the twitch. The criteria for the response score, in the response score, in the order of increasing magnitude of block, were: (1) visible twitch responses to all 4 of the train-of-four stimulation remained; (2) part of the train-of-four twitches was eliminated; (3) all twitches were eliminated; (4) tetanus was eliminated; (5) post-tetanic twitch following a 5-second 50 Hz tetanus was also eliminated; and (6) not even the post-tetanic twitch became elicitable again in 30 minutes. It was found that 1 mg of pancuronium depressed the eye-opening score to 4.0 +/- 0.2, from 5.1 +/- 0.1 (mean +/- SEM, p < 0.01). Following the additional "intubation dose" of pancuronium, patients in group I had an average response score of 2.2 +/- 0.3, those in group II a score of 3.4 +/- 0.2, and those in group III, a score of 4.8 +/- 0.6. Each additional 1 mg of pancuronium (increasing from group I to III) linearly increased the average response score. In terms of frequency response, patients in group I had more than a 50% change of being scored 1, while those in group II had a greater than 50% chance of being scored 3, 4, or 5, and those in group III had more than a 50% chance of being scored 6. It is concluded that sensitivity to pancuronium can be quantified by the ptotic response to a 1-mg test dose of pancuronium, and that a sensitivity-adjusted additional "intubation dose" of pancuronium can be predetermined in individual patients.

To study neuromuscular transmission, observation of the evoked compound electromyogram (EMG) has important advantages over observation of the evoked mechanical muscle contraction. Technically, however, recording of the evoked compound EMG, especially in continuous study of several hours duration, has been difficult. Investigators have employed various complicated systems, including tape recording, photorecording, and photographing for such purposes. The authors have applied modern computer technology to construction of an EMG analyzer which enables handling the evoked EMG even more easily than the evoked mechanical contraction. The principle involves digital dissection, storage with memory, readout with time expansion, and analog reconstruction of the compound EMG. The signal can be recorded with ease by use of any suitable hot-stylus or ink-writing oscillographic recorder. Both the waveform and the amplitutde of the EMG can be on-line recorded. The cost compares favorably with comparable devices for similar studies.

A double-blind study comparing four narcotic analgesics of different potencies, meperidine, morphine, fentanyl, and sufentanil, was performed on consenting patients undergoing general or orthopedic surgery under balanced anesthesia. Blood pressure, measured through an indwelling arterial catheter, was recorded continuously, as were ECG and heart rates. The narcotics, made up in equipotent concentrations, were given as indicated by hemodynamic and clinical signs. Arterial blood samples were taken before and after induction, after intubation, before and after incision, at intervals during the operation, and postoperatively. Hemodynamic values and plasma levels of catecholamines during and after induction, intubation, incision, and throughout the operation were least in patients given sufentanil and greatest in those who received morphine or meperidine. Heart rates increased significantly after induction with meperidine and were significantly higher after intubation in morphine-treated and meperidine-treated patients than they were in patients receiving sufentanil. Intraoperatively, mean arterial blood pressure, rate-pressure product, and plasma norepinephrine levels were lowest in patients receiving sufentanil. Intraoperative plasma epinephrine levels were lowest in patients receiving sufentanil and meperidine. Because of increases in blood pressure, heart rate, or both to greater than 15% above control values, supplementation with a potent inhalational agent was necessary in 38%, 30%, and 29% of the patients given meperidine, morphine, and fentanyl, respectively. No sufentanil patient required supplementation. Side effects, including histamine release accompanied by tachycardia and hypotension, were most frequent and most severe in patients who received meperidine. After extubation, marked increases in heart rate, blood pressure, and plasma norepinephrine and epinephrine occurred in some patients in each group. The incidence of postoperative respiratory depression was greatest in patients given morphine (mean dose of naloxone 8.6 micrograms/kg) and least with sufentanil (mean dose of naloxone 1.8 micrograms/kg) and fentanyl (3.2 micrograms/kg naloxone).

The effects of adenosine triphosphate (ATP) on cardiovascular responses to epinephrine were evaluated in dogs anesthetized with halothane. The dose of epinephrine required to induce arrhythmias averaged 1.05 +/- 0.52 microgram/kg/min. The dose of ATP required to abolish these arrhythmias averaged 1.64 +/- 0.67 mg/kg/min. ATP had not only an antiarrhythmic effect but also antagonized epinephrine-induced increases in heart rate, systemic vascular resistance, mean arterial blood pressure, and further increased cardiac index. ATP had, however, no significant effect on epinephrine-induced increases in myocardial contractility.

The neuromuscular effects of atracurium were studied in 25 A.S.A. class I or II patients anesthetized by a N2O-O2 narcotic technique. In five patients incremental doses of 0.05 to 0.1 mg/kg of atracurium were given intravenously every 3 minutes until approximately 95% depression of the evoked electromyographic (EMG) response of the adductor policus muscle was produced. This required 0.25 to 0.35 mg/kg of atracurium. The duration of block (return to 95% of control) was 25 to 50 minutes. In addition, four groups of five patients each received 0.15, 0.25, 0.375, or 0.6mg/kg of atracurium. The block produced by 0.15 mg/kg was 10% to 92% and lasted 8 to 55 minutes. The block produced by 0.25, 0.375, and 0.6 mg/kg was 95% or greater with a duration of action of 30 to 68 minutes, 52 to 70 minutes, and 65 to 95 minutes, respectively. Tracheal intubation was easily carried out in all patients in whom there was a block of 90% or greater. The block could be antagonized by the common clinical combination of atropine and neostigmine. Changes in heart rate and blood pressure following atracurium were less than 5%.

RO 21-3981, a new water soluble benzodiazepine, was studied in 24 patients both as an intravenous premedicant and to induce anesthesia. The premedicant dose of 5 mg produced lack of recall and marked sedation within 1 to 2 minutes after injection and persisted for at least 32 minutes. Subsequent induction of anesthesia required an additional 5 to 25 mg of RO 21-3981. However, anesthesia was not induced in 1 patient with 25 mg and was accomplished only with inhalation anesthesia. Loss of lid reflex was unreliable as a sign of induction for patients in whom tracheal intubation was planned. Although decreases in blood pressure of 10 to 30 mm Hg were noted after administration of RO 21-3981, systolic pressure was not recorded below 90 mm Hg. RO 21-3981, because of its amnesic, sedative, and anxiolytic properties, appears to be an excellent premedicant although the 5 mg dose studied was probably larger than necessary. For induction of anesthesia, RO 21-3981 may be an effective alternative to thiopental.

The neuromuscular effects of atracurium were studied in 20 patients anesthetized with 0.8% end-tidal halothane. Neuromuscular blockade was monitored by recording the electromyographic activity of the adductor pollicis muscle resulting from stimulation of the ulnar nerve. Four groups of five patients received single atracurium doses of 0.1, 0.15, 0.2, or 0.4 mg/kg, respectively. The block produced by 0.1 mg/kg was 25-72% and lasted 6-21 min. The block produced by 0.15 mg/kg was 69-93% and lasted 16-32 min. The blocks produced by 0.2 and 0.4 mg/kg were 95% or greater and lasted 42-84 min and 55-104 min, respectively. When indicated, intubation was easily performed in all patients receiving 0.2 and 0.4 mg/kg. The block could be readily antagonized by neostigmine and atropine. Changes in heart rate and blood pressure following atracurium administration averaged less than 5%.

Intravenous diazepam was administered to 4 groups of 35 patients as a surgical premedicant, double blind and according to a randomized sequence. Four dosages were used: 2.5, 5, 10, and 20 mg. Amnesia, relief of anxiety, sedation, and patient acceptance were primarily evaluated. While a significant linear dose effect was found for sedation, anxiety releief, and patient acceptance, this was not true for anmesia, which was clinically present only with doses of 10 and 20 mg. No significant adverse effects were noted at any dosage, and vital signs remained stable in all patients studied.

Trains of neurally evoked compound electromyographic responses of the thenar muscles were studied in 20 patients anesthetized with enflurane and N2O and paralyzed with d-tubocurarine. Fade was correlated with stimulus frequency (0.1 to 50 Hz) and degree of neuromuscular block. The lowest response in a train occurred on the 4th and the 6th-to-8th responses when the train was elicited at 2 Hz and 50 Hz, respectively. Fade was more observable with deeper block and could best be demonstrated by 5 Hz stimuli. With 50 Hz stimuli, a concomitant facilitation, observable from the beginning of the train, partially compensated for the fade.

A recent study suggested that cimetidine prolongs the duration of action of succinylcholine (SCh). We examined this reported interaction, and investigated whether it is the result of inhibition of plasma cholinesterase (PChE). We also studied the effect of ranitidine on the duration of action of succinylcholine. Thirty patients were randomly assigned to three groups to receive oral cimetidine 300 mg or ranitidine 150 mg or no H2-antagonist the night before surgery and again 1-2 hours prior to induction of anesthesia. Succinylcholine (1.5 mg/kg i.v.) was given to facilitate tracheal intubation after induction of anesthesia; neuromuscular function was monitored by evoked compound electromyogram. Pretreatment blood samples were analyzed for PChE activity. PChE activity and levels of appropriate H2-antagonists were measured in preinduction blood samples. No significant effect of either cimetidine or ranitidine on the duration of action of SCh or PChE activity was demonstrated. We conclude that H2-antagonists administered preoperatively do not prolong the duration of action of succinylcholine or alter PChE activity.

Diazepam in a dose of 0.05 mg/kg was studied to determine its effect on a subsequently administered dose of 1 mg/kg of succinylcholine. This dose of diazepam prior to succinylcholine (1) significantly diminished the incidence of postoperative muscle pain; (2) decreased the usual increase in serum potassium; (3) did not prevent the rise in creatine phosphokinase; (4) reduced the incidence of muscle fasciculation; and (5) did not affect the magnitude or duration of the succinylcholine neuromuscular block. It was concluded that diazepam had several advantages over d-tubocurarine in the prevention of succinylcholine-induced muscle pain.

Halothane (H), kanamycin (KM), streptomycin (SM), and chloramphenicol (CM) had direct negative inotropic effects on isometric contractions of isolated rat-heart muscles. Potassium penicillin-G did not show any significant changes in isometric contractions. The depression produced by these antibiotics was characterized by an abrupt onset, rapid progression, and rapid complete recovery, which suggests direct physicochemical rather than metabolic effects. On the other hand, the depression produced by H progressed slowly. When KM, SM, or CM were combined with H, there was a greater depression in isometric contractions than seen in the absence of H, suggesting that the innate characteristics of the antibiotics are augmented when any of them is administered together with halothane.

The clinical effectiveness and safety of compounded mixtures of lidocaine + bupivacaine and chloroprocaine + bupivacaine for either epidural or brachial-plexus block was studied in 48 adult patients. Of the several alternatives, chloroprocaine + bupivacaine with epinephrine was found the best choice for patients with typical plasma cholinesterase.

Two hundred seventy patients received morphine 5 mg or 10 mg alone or with promethazine 6.25 mg, 12.5 mg, or 25 mg. Promethazine 25 mg alone also was studied. All drugs were given intravenously. Anxiety relief, sedation, patient acceptance, lack of recall, and side effects were the variables examined. Promethazine improved relief of anxiety, sedation, and patient acceptance when added to morphine. Doses of promethazine larger than 12.5 mg intravenously failed to improve these effects. Memory remained unaffected by any of the drugs.

Although pain and subsequent thrombophlebitis are complications in patients receiving intravenous (IV) diazepam, the mechanism and accompanying histology are unknown. To further elucidate the pathogenesis for this and determine whether it can be minimized, adult female rats received IV diazepam, diazepam vehicle, lidocaine, a combination of lidocaine and diazepam, or N saline solution, and underwent subsequent tissue light microscopy. Vascular tissue from animals receiving IV diazepam alone revealed marked inflammation with inflammatory edema and intramural polymorphonuclear-cell infiltration. Intravascular thrombosis and complete vein-wall destruction were also present in some animals as early as 48 hours after IV diazepam. Diazepam vehicle and diluted diazepam produced similar morphologic alterations. Lidocaine or saline IV resulted in no histologic alterations, while lidocaine added to diazepam did not reduce the inflammatory response. These results represent the first systematic morphologic evaluation of vein response to intravascular diazepam and suggest that it produces rapid and detrimental morphologic alterations. The dilution of diazepam or combination with lidocaine does not appear to alter these findings, and diazepam vehicle appears to assume a role in the production of the vascular injury.

A new stimulator is described with characteristics designed to take advantage of recent knowledge of the pharmacology of neuromuscular relaxants and events involved in normal neuromuscular transmission. The stimulator has proven as useful in performance of peripheral nerve blocks as in monitoring neuromuscular blockade.

During an exploratory laparotomy for a pheochromocytoma under isoflurane anesthesia, the blood pressure of the patient rose to 250/115 torr, without ventricular arrhythmias. The authors consider isoflurane worthy of further study for pheochromocytoma-surgery anesthesia, in comparison with other presently used agents.