The incidence of masseter muscle rigidity after succinylcholine in infants and children

To determine whether the incidence of masseter muscle rigidity is affected by the anaesthetic induction sequence, we prospectively studied for ten months the anaesthetic course in 5,641 infants and children who received muscle relaxation to facilitate tracheal intubation. The anaesthetic induction sequence consisted of intravenous sodium thiopentone (STP) 5 mg · kg^?1 alone, halothane induction alone 1–4%, or halothane followed by STP. Inhalational inductions with halothane included nitrous oxide and oxygen. Tracheal intubation was facilitated by either intravenous succinylcholine (Sch) at least 1.5 mg · kg^?1 or by a non-depolarizing muscle relaxant. The induction sequence and all episodes of MMR were recorded. Ninety percent of the patients received Sch and 10% received a non-depolarising agent. Of those who received Sch, 88% (5,064 patients) were anaesthetised with STP and 12% (607 patients) were anaesthetised with halothane alone or halothane followed by STP Masseter muscle rigidity was defined clinically by the transient inability to distract the mandible from the maxilla such that the mouth could not be opened or could only be opened with force. No children anaesthetised with STP followed by Sch developed MMR. One child (0.9%) developed MMR after halothane and Sch and two developed MMR after halothane, STP and Sch (0.4%). The incidence of MMR after Sch was less with STP than with halothane alone or with halothane and STP (P < 0.025). The peak CPK values in the three children who developed MMR were 17,580 IU · L^?1 after halothane and Sch, and 7,280 IU·^?1 and 3,273 IU ·^?1 after halothane, STP and Sch. There was no evidence of MH reactions in these patients. No child developed malignant ventricular arrhythmias or cardiac arrest after Sch or a non-depolarising neuromuscular relaxant. There were no episodes of succinylcholine apnoea. We conclude that MMR is less likely to occur following STP and Sch than after halothane and Sch.     

Propofol sequestration within the extracorporeal circuit

Various drugs administered during cardiac anaesthesia are sequestered in the extracorporeal circuit in vitro, but it is uncertain whether this sequestration phenomenon affects plasma drug concentration in vivo. The present study was undertaken to evaluate (1) in vitro sequestration of propofol in the extracorporeal circuit and (2) whether the change in plasma propofol concentration induced by initiation of cardiopulmonary bypass in vivo can be explained by haemodilution. For the in vitro evaluation, three separate experiments with a closed circuit (membrane oxygenator, reservoir, and tubings) were performed. The pH and PCO₂ of the circulating solution (a mixture of Ringer’s acetate and whole blood) were maintained within the normal physiological range, and the temperature of the solution was 28° C. The solution was circulated at a flow of 4 L · min^?1 and propofol was added to the solution to achieve a concentration of 2 μg · ml^?1. Serial samples were taken from the circulating solution for measurement of propofol concentration by high performance liquid chromatography. In the in vivo part of the study, 14 patients received a continuous infusion of propofol, and samples for the determination of plasma propofol concentration and blood haematocrit were taken before and five and ten minutes after initiation of cardiopulmonary bypass. In vitro, at 5 and 120 min after addition of propofol into the circulating solution, approximately 65% and 25%, respectively, of the predicted propofol level was measurable in the solution. In vivo, five minutes after initiation of the cardiopulmonary bypass plasma propofol concentration decreased (P < 0.001) more (from 2.8 ±0.7 (mean ± SD) to 1.5 ± 0.5 μg · ml^?1, a 45 ± 12% decrease) than would have been predicted on the basis of acute haemodilution (a decrease in haematocrit from 0.39 ± 0.04 to 0.28 ± 0.03 is a 29 ± 4% decrease). Ten minutes after initiation of cardiopulmonary bypass, plasma propofol concentration was 1.6 ± 0.5 μg · ml^?1 (a 37 ± 27% decrease from the pre-bypass level) and haematocrit was 0.27 ± 0.04 (a 30 ± 6% decrease): the decrease in plasma propofol concentration was not different from the decrease observed in the haematocrit. In conclusion, propofol is markedly sequestered within the extracorporeal circuit in vitro. This sequestration may, to some extent, affect plasma propofol concentration in vivo.     

Hypoxaemia and hypotension after intravenous codeine phosphate

This report describes a case of accidental intravenous administration of codeine phosphate (1 mg · kg^?1) to a previously healthy five-year-old boy, who was undergoing strabismus surgery. Hypoxaemia (SpO₂ 85% with FiO₂ of 1) and hypotension (systolic BP 65 mmHg) resulted, which responded to resuscitation with lactated Ringers (20 ml · kg^?1) and phenylephrine (2 μg · kg^?1). The degree of hypoxaemia observed in this case was severe, but was not associated with clinical evidence of bronchospasm. Possible mechanisms for this reaction might have included direct myocardial depression and histamine release. This case adds further support to the recommendation that codeine phosphate should never be administered intravenously.     

Adjuvant propofol enables better control of nausea and emesis secondary to chemotherapy for breast cancer

We investigated the prophylactic antiemetic effect of added lowdose infusion of propofol in patients exhibiting nausea and vomiting refractory to dexamethasone and serotonin antagonist during non-cisplatin chemotherapy for breast cancer. In a prospective open longitudinal study, 117 patients who had more than five episodes of nausea and vomiting in their first chemotherapy cycle during the first 24 hr completed the study. They received in addition to the usual prophylactic antiemetic regimen a continuous intravenous infusion of 1 mg · kg^?1 · hr^?1 propofol started four hours before chemotherapy and continued up to 24 hr for the two subsequent cycles. The number of vomiting / nausea episodes, level of sedation, patient activity, appetite and preference for future chemotherapy cycles were assessed. In the propofol supplemented cycles 90 and 80% of patients, during the 1st and 2nd propofol-assisted cycle respectively, were free of nausea and vomiting during the first 24 hr after chemotherapy. Patients were more frequently active and had more appetite during the propofol-assisted cycles. No propofol-associated side effects were observed. We conclude that the addition of a subhypnotic infusion of propofol enables better control of nausea and vomiting caused by non-cisplatin chemotherapy in the first 24 hr post-treatment.     

Hydromorphone patient-controlled analgesia (PCA) after coronary artery bypass surgery

We conducted a study to compare the effectiveness of patientcontrolled analgesia (PCA) technique to conventional analgesic therapy (CAT) after coronary artery bypass graft (CABG). The PCA group received hydromorphone 0.1 mg · hr^?1 basal infusion and bolus doses of 0.2 mg Q 5 min (maximum 1.2 mg · hr^?1) while the CAT group received morphine 2.5 mg iv Q 30 min prn until extubation followed by prn meperidine 1 mg · kg^?1 im Q4 hr or acetaminophen 325 mg with codeine 30 mg po (1 or 2 tablets) when oral intake was possible. The degree of pain was assessed using a Visual Analogue Scale (VAS) starting after extubation and every 6–8 hr for the next 60 hr. Holter monitoring was initiated one hour after patient arrival in the Intensive Care Unit (ICU) and continued for 72 hr. Other measured variables were pulmonary function, sedation, side effects and total opioid requirements. Results show that the day-to-day VAS pain score decreased in the PCA group (P < 0.001) while it remained unchanged in CAT patients. The PCA patients had lower VAS pain scores at extubation (P < 0.05). During the third postoperative day, the PCA group had a lower VAS pain score, a lower incidence of severe pain defined as a score > 5 on the VAS scale, and a reduced incidence of myocardial ischaemia (P < 0.01). However, there was no difference in the duration, severity, area under the curve (AUC), or heart rate during ischaemic events. Postoperative pulmonary function was abnormal in both groups (NS) with minimal recovery by the fourth day. Opioid requirements, incidence of side effects and the degree of sedation were similar. We conclude that the PCA technique for analgesia provided slightly better results. The finding of a reduced incidence of myocardial ischaemia in the PCA group warrants further clinical investigation.     

Reversal of doxacurium and pancuronium neuromuscular blockade with neostigmine in children

Recovery after doxacurium and pancuronium neuromuscular blockade and their acceleration by neostigmine have not been compared in children. Therefore, 60 paediatric surgical patients aged 2–10 yr (ASA 1–2) were studied. They were randomized to receive doxacurium 30 μg · kg^?1 or pancuronium 70 μg · kg^?1 iv during propofol, fentanyl, isoflurane and nitrous oxide anaesthesia. Electromyographic (EMG) responses of the adductor pollicis to train-of-four (TOF) stimulation of the ulnar nerve were recorded every ten seconds using a Datex NMT monitor. Six patients in each relaxant group received neostigmine (0, 5, 10, 20 or 40 μg · kg^?1) with atropine by random allocation when first twitch height (T_I) had recovered to 25% of control. Spontaneous recovery after ten minutes was similar following doxacurium (mean ± SEM values of 45.0 ± 3.9 vs 49.5 ± 10.0 % for T_I and 25.2 ± 3.8 vs 14.8 ± 3.6% for TOF ratios). Dose-responses to neostigmine were calculated from the log dose vs logit of T_I or TOF ratio after ten minutes. Neostigmine-assisted recovery was not different in the two groups, with ED₇₀ and ED₉₀ doses for T_I of 14.3 ± 1.8 and 25.7 ± 2.7 μg·kg^?1 for doxacurium and 12.5 ± 1.7 and 25.3 ± 2.3 μg· kg^?1 for pancuronium. Time to recovery of TOF ratio to 70% after neostigmine 40 ng · kg^?1 was 2.3 ± 1.0 and 4.2 ± 1.7 min (P = NS) following pancuronium and doxacurium, respectively. Adjusted recovery due to neostigmine alone (spontaneous recovery subtracted from the total) required two to three times higher doses of neostigmine. Thus, in children, the spontaneous recovery and reversal of neuromuscular blockade is similar with doxacurium and pancuronium. However, compared with previous adult studies, they recover twice as quickly from doxacurium neuromuscular blockade and neostigmine antagonism is achieved at 25–50% of the adult doses.     

Nicardipine and verapamil attenuate the pressor response to laryngoscopy and intubation

In a prospective, double-blind study, we compared the efficacy of iv nicardipine hydrochloride and verapamil hydrochloride in attenuating the cardiovascular responses to laryngoscopy and tracheal intubation, in 45 patients undergoing elective surgery with general anaesthesia. Patients were allocated randomly to one of three groups of 15 patients. Patients in Group I received saline while those in Groups II and III received nicardipine hydrochloride, 0.03 mg · kg^{? 1} or verapamil hydrochloride, 0.1 mg · kg^{? 1} iv three minutes before laryngoscopy and intubation. Patients in Group I showed the greatest increase in SBP 25.4 ± 2.2 mmHg and HR 35.7 ± 3.8 beats · min^{? 1} at one minute after intubation (P < 0.001), and these changes persisted throughout the study period albeit with decreasing magnitude. After drug administration, patients in Groups II and III demonstrated increases in HR of 26 ± 2.4 and 15.1 ± 2.2 beats · min^{? 1} and decreases in SBP of 24.8 ± 2.0 and 18.8 ± 2.4 mmHg respectively (P < 0.001). It is concluded that nicardipine and verapamil are effective in attenuating pressor responses to laryngoscopy and intubation but did not control the tachycardia.     

Propofol anaesthesia in paediatric ambulatory patients: a comparison with thiopentone and halothane

The purpose of this study was to evaluate the haemodynamic changes during induction, as well as the speed and quality of recovery when propofol (vs thiopentone and/or halothane) was used for induction and maintenance of anaesthesia in paediatric outpatients. One hundred unmedicated children, 3–12-yr-old, scheduled for ambulatory surgery were studied. The most common surgical procedures performed were eye muscle surgery (42%), plastic surgery (21%), dental restoration (15%), and urological procedures (15%). The children were randomized to an anaesthetic regimen for induction/maintenance as follows: propofol/propofol infusion; propofol/halothane; thiopentone/halothane; halothane for both induction and maintenance. Succinylcholine 1.5 mg · kg^?1 was used to facilitate tracheal intubation and N₂O/O₂ were used as the carrier gases in each case. All maintenance drugs were titrated according to the clinical response of the patient to prevent movement and/or maintain BP ± 20% of baseline. Two patients (4%) who received propofol expressed discomfort during injection. The mean propofol dose required to prevent movement was 267 ± 83 μg · kg^?1 · min^?1. The overall pattern of haemodynamic changes, as well as awakening (extubation) times were not different among the four groups. Children who received propofol recovered faster (22 vs 29–36 min) (P < 0.05), were discharged home sooner (101 vs 127–144 min) (P < 0.05), and had less postoperative vomiting (4 vs 24–48%) (P < 0.05) than all others. There were no serious complications or adverse postoperative sequelae in any of the patients in the study. It is concluded that induction and maintenance of anaesthesia with propofol is a well-tolerated anaesthetic technique in children, and is associated with faster recovery and discharged as well as less vomiting than when halothane is used.     

Isoflurane compared with nitrous oxide anaesthesia for intraoperative monitoring of somatosensory-evoked potentials

Intraoperative monitoring of somatosensoryevoked potentials is a routine procedure. To determine the depressant effect of nitrous oxide relative to isoflurane, the authors recorded the scalp, cervical and brachial plexusevoked responses to stimulation of the median nerve under different anaesthetic conditions. Eight subjects, age 35 ± 6 (SD) yr, weight 68 ± 12 kg, were studied. Following recording of awake control responses, anaesthesia was induced with thiopentone 5 mg· kg^{? 1} and fentanyl 3 μg· kg^{? 1} and was followed by succinylcholine 1 mg· kg^{? 1}. During normocapnia and normothermia, and with a maintenance infusion of fentanyl 3 μg · kg^{? 1}· hr^{? 1}, evoked potential recording was repeated under three different anaesthetic conditions; 0.6 MAC nitrous oxide, 0.6 MAC nitrous oxide ± 0.6 MAC isoflurane, and 0.6 MAC isoflurane. Among the anaesthetic conditions, the combination of nitrous oxide-isoflurane had the most depressant effect on the cortical amplitude (67 ± 4% reduction, P < 0.05). Nitrous oxide decreased the cortical amplitude more than an equipotent dose of isoflurane (60 ± 4% vs 48 ± 7%, P < 0.05). The latency was unchanged by nitrous oxide, but increased slightly by isoflurane and isofluranenitrous oxide anaesthesia (1.0 and 0.9 msec respectively, P < 0.05). We conclude that somatosensory-evoked potential monitoring is feasible both during nitrous oxide anaesthesia and isoflurane anaesthesia, but the cortical amplitude is better preserved during 0.6 MAC of isoflurane alone relative to 0.6 MAC of nitrous oxide alone. The depressant effect is maximal during nitrous oxideisoflurane anaesthesia but less than the predicted additive effect.     

Cigarette smoke increases bupivacaine metabolism in rats

This study was designed to document possible changes in bupivacaine kinetics in rats after exposure to cigarette smoke. Rats (n = 15) were exposed to cigarette smoke (Borgwaldt type Hamburg II) for ten minutes per day during four days (C) or eight days (B); controls (A) were used simultaneously without exposure to cigarette smoke. After bupivacaine 20 mg · kg^?1 ip at day 4 (C) or day 8 (B), blood was sampled (0.5 ml of blood collected by puncture at the retro-orbital sinus 0.25, 0.5, 1, 2, 4, 6 and 8 hours after administration) and bupivacaine and its main metabolite i.e., desbutylbupivacaine (PPX) were determined by gas liquid chromatography. The sensitivity of the method was 15 ng · ml^?1 and the reproductibility was <6%. Serum bupivacaine concentrations were plotted against time and the pharmacokinetic variables were determined assuming a two compartment open model: Cmax, Tmax were derived directly from individual data. The β phase elimination halflives (T_1/2β), the area under the serum concentration curve (AUC₀ ^∞), the total plasma clearance (Cl) and the total volume of distribution (Vd) were calculated. These variables were assessed according to non-linear fitting method. Cigarette smoking exposure did not change the pharmacokinetic variables of bupivacaine. However, the pharmacokinetic parameters of PPX, Cmax (0.175 ± 0.007 μg · ml^?1, 0.119 ± 0.014 μg · ml^?1 and 0.312 ± 0.023 μg · ml^?1, for groups A, B and C, respectively), AUC (0.170 ± 0.006 μg · ml^?1 · hr^?1, 0.104 ± 0.013 μg · ml^?1 · hr^?1 and 0.433 ± 0.017 μgv· ml^?1 · hr^?1 for groups A, B and C, respectively) and the ratio AUC PPX/ AUC bupivacaine (0.306 ± 0.042, 0.153 ± 0.021 and 0.660 ± 0.054 for groups A, B and C, respectively) were higher (P < 0.0001) for group C. These results indicate an enzymatic induction after only short exposure to cigarette smoking and justify further studies to document possible variations of the metabolism of bupivacaine induced by exposure to cigarette smoke in humans.     

Pain management for children following selective dorsal rhizotomy

Selective dorsal rhizotomy (SDR) is a neurosurgical procedure used for treating lower extremity spasticity in patients with cerebral palsy. The purpose of this paper is to present a review of our institution’s first three years’ experience with postoperative pain and spasticity management in patients who have undergone SDR. The medical records of the 55 patients who had an SDR during the study period were reviewed. The basis of postoperative analgesia was morphine, with the majority of patients receiving continuous morphine infusions (20–40 μg · kg^?1 · hr^?1(n = 49), 60 μg · kg^?1 · hr^?1 (n = 1)). Four patients used a patient-controlled delivery system. One patient had successful analgesia with epidural morphine. Ketorolac (1 mg · kg^?1iv loading dose followed by 0.5 mg · kg^?1 iv every six hr for 48 hr) was used as an adjunct to morphine in six patients. For management of postoperative muscle spasm, an intravenous benzodiazepine was used (diazepam 0.1 mg · kg^?1 (n = 2), or midazolam infusion 10–30 μg · kg^?1· hr^?1 (n = 51)). All patients were cared for on a ward where nurses were familiar with the use of continuous opioid and benzodiazepine infusions. All patients received continuous cardiorespiratory monitoring as well as frequent nursing assessment. There were no episodes of postoperative apnoea or excessive sedation. We have found the use of continuous infusions of morphine and midazolam, along with adjunct ketorolac, to be effective in treating postoperative pain and muscle spasms following SDR.     

Mechanisms of inhibition of endothelium-dependent relaxation by halothane,isoflurane, and sevoflurane

Volatile anaesthetics inhibit endothelium-dependent relaxation, but the underlying mechanism(s) have not been clarified. In an attempt to elucidate the mechanism(s), we determined the effects of halothane, isoflurane and sevoflurane on relaxation induced by acetylcholine and sodium nitro-prusside (SNP) and the cGMP formation elicited by exogenous nitric oxide (NO) and SNP in rat aortas. Acetylcholine (10^?7?10^?5M) - induced relaxation was attenuated by halothane (2%), isoflurane (2%) and sevoflurane (4%). SNP (10^?8 M) - induced relaxation was reduced by halothane (2%), but not by isoflurane (2%) or sevoflurane (4%). The cGMP level of NO-stimulated aorta was reduced by halothane (2%) and sevoflurane (4%), but not by isoflurane (2%). The cGMP level of SNP (10^?7 M) - stimulated aorta was reduced by halothane (2%), but not by isoflurane (2%) and sevoflurane (4%). We conclude that the mechanisms responsible for the inhibition of endothelium-dependent relaxation differ among anaesthetics. Isoflurane inhibits the relaxation mainly by inhibiting the formation of NO in the endothelium. In contrast, the effect of halothane on endotheliumdependent relaxation may be largely due to the inhibition of action of NO in the vascular smooth muscle and the effect of sevoflurane may be to inactivate NO or to inhibit the action of NO.     

Preliminary investigations of the clinical pharmacology of three short-acting non-depolarizing neuromuscular blocking agents,Org 9453, Org 9489 and Org 9487

Three muscle relaxants, Org 9453, Org 9489 and Org 9487, short-acting in animals, were investigated to establish their profiles in humans. Potency, time course of action, and pharmacokinetic behaviour were studied in 90 healthy patients during fentanyl/halothane/N₂O anaesthesia. Neuromuscular Junction was monitored mechanomyographically. Plasma and urine concentrations (three patients per compound) were measured by HPLC, and these data were analyzed by iterative linear least square regression analysis. The ED₉₀ values for Org 9453, Org 9489 and Org 9487 were 1.4, 0.45 and 1.15 mg · kg^?1 respectively. The onset times of Org 9453 (1.5 mg · kg^?1,1.1 × ED₉₀), Org 9489 (0.9 mg · kg^?1, 2 × ED₉₀) and Org 9487 (1.5 mg · kg^?1, 1.3 × ED₉₀) were 1.2, 1.6 and 1.5 min, and the durations until 25% twitch recovery were 8.6, 22.0 and 8.9 min, respectively. Clearances of these doses were 6.9, 5.8, and 11.1 ml · kg^?1 · min^?1, and mean residence times 26, 79, and 41 min, respectively. Mean renal excretion (parent compound and metabolites) within 24 hr amounted to 5, 11.3 and 12.2% respectively. No side effects other than a moderate short-lasting decrease of blood pressure and a concomittant increase in heart rate were noted. It is concluded that Org 9453 and Org 9487 are short-acting muscle relaxants in humans.     

Respiratory depression associated with meperidine spinal anaesthesia

Intrathecal meperidine administration can provide surgical anaesthesia and postoperative analgesia for about two to six hours. We have observed two cases of respiratory depression associated with meperidine spinal anaesthesia. An 81-yr-old woman received 50 mg intrathecal meperidine for inguinal hernia repair. Supplemental oxygen was administered at 3 L · min^?1 by nasal prongs. About 40 min later, the patient’s oxygen saturation decreased from 97% to 87% and she was asked to take big breaths. She responded immediately and oxygen saturation returned to 97%. Two more similar episodes followed in the next five minutes. Naloxone 0.1 mg iv was administered and the oxygen saturation remained at 96–97% until completion of surgery about 15 min later. She had an uneventful recovery. A 24-yr-old healthy woman presented for tubal ligation eight hours after vaginal delivery of an infant. The surgical procedure was performed under spinal anaesthesia produced by 50 mg meperidine. During surgery, midazolam 2 mg iv was given for anxiolysis. About five minutes after admission to the postanaesthesia care unit, the patient’s respiratory rate decreased to ten breaths per minute and oxygen saturation decreased to 89%. Supplemental oxygen at 3 L · min^?1 was administered by nasal prongs. The patient was encouraged to take big breaths and the arterial oxygen saturation rapidly increased to 98–99%. Forty minutes later, nasal oxygen was discontinued. The patient maintained her oxygen saturation while breathing room air. She was then discharged to the ward and had an uneventful recovery course. We recommend that a patient’s respiratory variables and oxygenation be closely monitored for at least one hour after intrathecal meperidine administration.     

Absence of antitrifluoroacetate antibody after halothane anaesthesia in patients exhibiting no or mild liver damage

It has been shown that the circulating antibodies, which bind to rat hepatic microsomal proteins obtained after in vivo exposure to halothane, are detectable by immunoblotting in patients with “halothane hepatitis (HH),” and that rabbit immunized anti-sera against trifluoroacetylated rabbit serum albumin (TFA-RSA) recognizes rat microsomal distorted polypeptides in almost the same way as do sera from patients with HH. In this paper, we report first the development of a novel method of synthesizing TFA-RSA using p-nitrophenyl TFA, and second the results of tests for circulating anti-TFA antibodies in the serum of 86 patients who had received halothane anaesthesia and developed no (67 patients) or mild (19 patients, the maximum activity of serum alanine aminotransaminase 519 IU · L^?1) liver damage. Serum was selected from stored sera of post-transfusion patients. The new method of synthesizing TFA-RSA was convenient and was able to be done at neutral pH. Rabbit sera obtained after immunization with the newly synthesized TFA-RSA recognized the same polypeptides (109 kDa, 92 kDa, 80 kDa, 76 kDa, 64 kDa and 59 kDa) as the established anti-sera against TFA-RSA, and these reactions were inhibited in the presence of TFA-lysine. Circulating antibodies were not detected in our patients who had developed no or mild liver damage. The present finding supports the hypothesis that the appearance of circulating antibodies against microsomal distorted proteins are specific to patients with HH. Furthermore, we have shown here that the halothane-induced mild increase in ALT activity is not associated with the appearance of those circulating antibodies, supporting the pathophysiological difference between HH and halothane-induced mild hepatic damage.     

Malignant hyperthermia and calcium-induced heat production

The abnormal increase in intracellular Ca⁺⁺ in malignant hyperthermia (MH) is well documented, but the link between the increased Ca⁺⁺ concentration and high temperature remains speculative. We investigated the possibility that the Ca⁺⁺-induced change in the state of cell membranes may contribute to the temperature elevation. Calcium ion transforms phosopholipid membranes from the fluid to solid state. This is analogous to the freezing of water, and liberates latent heat. Differential titration calorimetry (DTC) measures heat production or absorption during ligand binding to macromolecules. When CaCl₂ solution was added to anionic dimyristoylphosphatidic acid (DMPA) and dimyristoylphosphatidylglycerol (DMPG) vesicle membranes in incremental doses, DTC showed that the heat production suddenly increased when the Ca⁺⁺ concentration exceeded about 120/μM. At this Ca⁺⁺ concentration range, these lipid membranes underwent phase transition. The latent heat of transition was measured by differential scanning calorimetry (DSC). The values were 7.1 ± 0.7 (SD, n = 4) kcal · mol^?1 of DMPA and 6.8 ± 0.7 (SD, n = 4) kcal · mol^?1 of DMPG. The study shows that Ca⁺⁺ produces heal when bound to lipid membranes. We are not proposing, however, that this is the sole source of heat. We contend that the lipid phase transition is one of the heat sources and it may trigger a hypermetabolic state by elevating the temperature of cell membranes. Because Ca⁺⁺ is implicated as the second messenger in signal transduction, multiple systems may be involved. More studies are needed to clarify how Ca⁺⁺ increases body temperature.     

Is hypoxic pulmonary vasoconstriction important during single lung ventilation in the lateral decubitus position?

Hypoxic pulmonary vasoconstriction (HPV) has not been demonstrated in human single lung anaesthesia in the lateral decubitus position (LDP). The purpose of this study was to determine whether (1) HPV occurs in the non-dependent, nonventilated lung, and (2) if the infusion of sodium nitroprusside (SNP) inhibits HPV During intravenous anaesthesia the tracheas of seven patients were intubated with double lumen endotracheal tubes. Standard monitors plus radial and pulmonary arterial catheters were placed. Patients were positioned in the LDP and haemodynamic and gas exchange data were recorded for each of three stages; I: two-lung ventilation, II: single, dependent lung ventilation (1LV) and III: 1LV with infusion of SNP. In stage II the PaO₂ decreased from 531 ± 42 mmHg to 285 ± 42 mmHg (P < 0.05) and Qs/Qt increased from 12.3 ± 2.7 to 29.0 ± 6.3% (P < 0.05). With SNP infusion there was a 30% increase in cardiac index (CI) (P < 0.05). The SNP infusion was not associated with changes in Qs/ Qt or PaO₂. This model demonstrates changes in Qs/ Qt and PaO₂ associated with single-lung ventilation in ASA I and II patients in the LDP but we were unable to demonstrate inhibition of HPV by SNP.     

Cutaneous ionto-phoretic application of condensed lidocaine

The purpose of this study was to determine whether iontophoretic application of high concentrations of lidocaine, with the same current, would produce cutaneous local anaesthesia rapidly enough for clinical practice. Twenty healthy volunteers, 17 male and three female, were selected for study. After fiveminute or ten-minute iontophoresis using lidocaine 4, 10, 20, 30, 50%, we assessed the response to pin prick with a 27-gauge sterile needle inserted to the depth of 2 mm at five random locations in the iontophoretically-stimulated area. Also, plasma lidocaine concentrations were measured in the venous blood samples which had been taken from three male subjects, at 3, 10, and 30 min after iontophoresis with lidocaine 50%. The pain score after five-minute iontophoresis was higher than that after ten-minute iontophoresis, using each concentration of lidocaine (P< 0.001), whereas the pain scores had no correlation with lidocaine concentration within five-minute and ten-minute iontophoresis groups, respectively (P: NS). On the other hand, plasma lidocaine concentration was <1.0 μg · ml^?1 in all samples. No side effects other than erythema were observed after iontophoresis using high concentrations of lidocaine up to 50%. These results showed that by increasing the lidocaine concentration of the applied solution up to 50%, the application time of iontophoresis cannot be reduced from ten to five minutes without losing analgesic effect, although iontophoresis itself can be performed with safety.     

Anaesthesia for Caesarean delivery of a malignant hyperthermia susceptible parturient

The anaesthetic management for Caesarean delivery of a parturient with a strong family history of malignant hyperthermia (MH) is presented. Before surgery an anaesthetic machine that was in regular use was prepared by replacing all rubber or disposable components and flushing with O₂ at 10 L · min^?1 for one hour. Dantrolene prophylaxis was not used, and the patient received a bupivacaine and fentanyl spinal anaestheslic. Hypotension was treated with ephedrine. Current management of the MH patient no longer mandates a dedicated vapourfree machine, dantrolene is not indicated as pre-treatment, and amide local anaesthetics are considered safe. The role of vasopressors and ergot preparations is less clear.     

The microcirculation during enflurane and isoflurane anaesthesia in dogs

The effects of enflurane and isoflurane of 0.75 and 1.5 MAC on capillary blood flow were studied by the microsphere (9 ± 1 μm in diameter) method in two groups of seven dogs. Simultaneously, changes in the arteriolo-venular shunt were studied by collection of venous blood at a rate of 4.8 ml · min^?1 for two minutes. Enflurane anaesthesia at 0.75 MAC decreased capillary blood flow in the thyroid glands (35% of control), left and right ventricular wall (59% and 50%), adrenal gland (59%), liver (63%), spleen (56%), pancreas (35%), omentum (20%), and small intestine (60%) and at 1.5 MAC it decreased further in the thyroid glands (15%), left and right ventricular wall (31% and 32%), adrenal gland (42%), liver (47%), spleen (31%), pancreas (23%), omentum (20%), stomach (45%), and small intestine (54%). No marked changes were noted in the brain, kidney, large intestine or skeletal muscle. The arteriolo-venular shunt was decreased in the kidney from an initial rate of 12.1 to 3.8% at 0.75 MAC and to 2.5% at 1.5 MAC enflurane. In contrast, during isoflurane anaesthesia, capillary blood flow remained unchanged, except for a decrease to the thyroid glands (43%) and right ventricular wall (74%) during 1.5 MAC anaesthesia. However, the arteriolo-venular shunt was increased in the brain from 12.0 to 29.7% and 33.0% during 0.75 and 1.5 MAC isoflurane anaesthesia, respectively. It also increased from 25.0 to 41.0% and 46.3% in the skeletal muscle, and from 8.9 to 19.9% and 17.4% in the whole systemic circulation. These data indicate that capillary blood flow is better preserved during isoflurane than during enflurane anaesthesia, but is associated with increased arteriolo-venular shunting.