Comparison of ropivacaine 2 mg ml(-1) and prilocaine 5 mg ml(-1) for i.v. regional anaesthesia in outpatient surgery

Background. Ropivacaine 2 mg ml^–1 (0.2%) provides longer-lastinganalgesia after deflation of the tourniquet cuff, with fewerside-effects, than lidocaine 5 mg ml^–1 (0.5%) after i.v.regional anaesthesia (IVRA). Whether ropivacaine 2 mg ml^–1also exerts this advantage over prilocaine 5 mg ml^–1,the local anaesthetic of choice in IVRA in most European countrieswas investigated in this study. Methods. Sixty outpatients scheduled for forearm or hand surgeryreceived IVRA with 40 ml of ropivacaine 2 mg ml^–1 (Ropi)or prilocaine 5 mg ml^–1 (Prilo) in a randomized, double-blindedfashion. The development and recovery of pin-prick analgesiaand motor power of the hand, as well as ropivacaine and prilocaineplasma concentrations (n=30), were assessed during and afteroperation. Results. Anaesthesia for surgery was adequate in both groups.Pin-prick analgesia was achieved at a similar rate, except inthe radial nerve distribution area where at 10 min 60% of Ropiand 90% of Prilo patients had analgesia (P=0.017). At 10 min100 and 97% had motor block of the hand in the Ropi and Prilogroups, respectively. Recovery of the sensory block in all innervationareas was already observed 2 min after the tourniquet cuff release.At 10 min after releasing the tourniquet cuff 31% of the Ropipatients and none of the Prilo patients still had analgesiain the median nerve distribution (P=0.004). At 12 min, 42% inthe Ropi group and none in the Prilo group had decreased gripstrength. After the release of the tourniquet, mean plasma concentrationsof ropivacaine were higher than those of prilocaine. The highestindividual concentration of ropivacaine was 1.65 µg ml^–1and that of prilocaine 0.6 µg ml^–1. None of theRopi patients experienced any symptoms of local anaesthetictoxicity. Conclusions. Compared with prilocaine 5 mg ml^–1, analgesiain IVRA with ropivacaine 2 mg ml^–1 developed slightlymore slowly, while motor block developed at a similar rate.After the release of the tourniquet, sensation recovered quicklyand at a similar rate in the two groups, except for a slightlyslower recovery after ropivacaine in the innervation area ofthe median nerve, but no surgically useful extended analgesiaafter the cuff deflation was observed. Despite a 60% lower milligram-dose,ropivacaine plasma concentrations were markedly higher thanthose of prilocaine.     

Effects of intramuscular administration of lidocaine or bupivacaine on induction and maintenance doses of propofol evaluated by bispectral index

Background. Interest in combining local and general anaesthesiahas lead to studies investigating possible interactions. Ina prospective, randomized, double-blind study, we tested whetherlocal anaesthetics administered i.m. potentiate the hypnoticeffect of propofol. Methods. Sixty patients (three groups, n=20) undergoing lowerabdominal surgery with total i.v. propofol anaesthesia wereinvestigated. Patients in Group B received i.m. bupivacaine(5 mg ml^–1) 1 mg kg^–1, patients in Group Lreceived i.m. lidocaine (100 mg ml^–1) 2 mg kg^–1and patients in Group C received i.m. saline 5 ml beforeoperation. Hypnosis was measured with bispectral index (BIS). Results. The induction (BIS <45), and the maintenance dosesof propofol (BIS between 40 and 50) were significantly lessin Group B and Group L compared with the control group. Inductiondoses were 1.58 (SD 0.39), 1.56 (0.24) and 2.03 (0.33) mg kg^–1respectively; P<0.0001. Maintenance doses were 6.33 (2.06),7.08 (1.23) and 9.95 (2.02) mg kg^–1 respectively in thefirst hour; P<0.0001. Groups B and L were associated withan attenuated haemodynamic response to both induction and intubation. Conclusion. I.M. administered local anaesthetics are associatedwith a decrease in both the induction and maintenance dosesof propofol during total i.v. anaesthesia and a reduction inhaemodynamic responses. Br J Anaesth 2002; 89: 849–52     

FUNCTIONAL AND METABOLIC EFFECTS OF BUPIVACAINE AND LIGNOCAINE IN THE RAT HEART-LUNG PREPARATION

We have examined the effects of bupivacaine and lignocaine onmyocardial metabolism in the rat isolated heart-lung preparation.Bupivacaine 1, 5 or 25 µg ml^–1 or lignocaine 4,20 or 100 µg ml^–1 was administered 5 min after thestart of perfusion. Both bupivacaine 25 µg ml^–1and lignocaine 100 µg ml^–1 reduced heart rate significantly.Bupivacaine 25 µg ml^–1 was associated with a higherincidence of arrhythmias than the other groups. Three heartsin the bupivacaine 25 µg ml^–1 group (n = 8) andtwo hearts in the lignocaine 100 µg ml^–1 group (n= 8) failed (zero cardiac output) at the end of the experiment.Although there were no significant differences in myocardiallactate and glycogen concentrations between groups, ATP contentin the bupivacaine 25 µg ml^–1 and lignocaine 100µg ml^–1 groups was significantly less than thatin the control group. The results suggest that myocardial depressionand subsequent metabolic deterioration occurred with both thehigh doses of local anaesthetics; these findings do not accountfor the apparent increased cardiotoxicity of bupivacaine.     

EFFECT OF ADRENALINE ON PLASMA CONCENTRATIONS OF BUPIVACAINE FOLLOWING INTRA-ARTICULAR INJECTION OF BUPIVACAINE FOR KNEE ARTHROSCOPY

We administered 0.5% bupivacaine 30 ml either with or withoutadrenaline 5 ug ml^–1 randomly to 16 healthy outpatients,to determine the efficacy of local and intra-articular localanaesthesia for knee arthroscopy and whether or not adrenalineshould be added to intra-articular bupivacaine. Bupivacaineconcentrations were measured in plasma obtained 15, 30, 45 and60 min after intra-articular injection. Patients receiving bupivacainewith adrenaline had significantly smaller plasma concentrationsof bupivacaine at all times than did patients receiving plainbupivacaine. The maximal concentrations of bupivacaine in theplain group (median 515 ng ml^–1, range 46–875 ngml^–1) were greater than those in the adrenaline group(median 33 ng ml^–1, range 7–125 ng ml^–1) (P= 0.001). All patients found the anaesthetic satisfactory. Weconclude that intra-articular/local anaesthesia is satisfactoryfor outpatient arthroscopic surgery, and that adrenaline shouldprobably be added to bupivacaine before intra-articular injection.     

I.V. FLUNITRAZEPAM AND I.V. DIAZEPAM IN CONSERVATIVE DENTISTRY A cross-over trial

In a randomized cross-over trial in 82 outpatients aged 15–45yr undergoing conservative dentistry, a solution of flunitrazepam0.25 mg ml^–1 i.v. (average dose 0.014 mg kg^–1) wascompared with a solution of diazepam 5 mg ml^–1 i.v. (0.29mg kg^–1). Cardiovascular changes, operating conditionsand side-effects were similar. Forty minutes after the startof injection, about 85% of all patients could not remember thelocal anaesthetic injection. Thirty minutes after the end oftreatment, only 25% of all patients had recovered. One weeklater, most patients receiving each drug had only vague memoriesof their treatment; they had felt more relaxed immediately afterthe i.v. injection than before. Drowsiness was equally commonafter flunitrazepam and diazepam. Atazia was more prolongedwith flunitrazepam but arm pain and venous thrombophlebitiswere less frequent. ^* Present address: Department of Anaesthesia Nottingham UniversityMedical School, University Boulevard, Nottingham NG7 2UH.     

Density of spinal anaesthetic solutions of bupivacaine, levobupivacaine, and ropivacaine with and without dextrose

Background. Spread of intrathecal local anaesthetics is determinedprincipally by baricity and position of the patient. Hypobaricsolutions of bupivacaine are characterized by an unpredictablespread of sensory block whereas addition of dextrose 80 mg ml^–1provides a predictable spread but to high thoracic levels. Incontrast, dextrose concentrations between 8 and 30 mg ml^–1have shown reliable and consistent spread for surgery. Hence,the aim of this study was to determine the density of bupivacaine,levobupivacaine, and ropivacaine with and without dextrose atboth 23 and 37°C before embarking on clinical studies. Methods. Density (mg ml^–1) was measured using the methodof mechanical oscillation resonance, accurate to five decimalplaces on 1250 samples. 500 density measurements were performedin a randomized, blind fashion at 23 and 37°C on 10 plainsolutions of bupivacaine (2.5, 5, and 7.5 mg ml^–1) levobupivacaine(2.5, 5, and 7.5 mg ml^–1) and ropivacaine (2, 5, 7.5,and 10 mg ml^–1). Following this, 750 density measurementswere taken at 23 and 37°C on the 5 mg ml^–1 solutionsof bupivacaine, levobupivacaine, and ropivacaine with addeddextrose (10, 20, 30, 50, and 80 mg ml^–1). Results. There was a linear relationship between density anddextrose concentration for all three local anaesthetics (R²=0.99)at 23 and 37°C. The mean density of levobupivacaine 5 mgml^–1 was significantly greater than the densities of bupivacaine5 mg ml^–1 and ropivacaine 5 mg ml^–1 after adjustingfor dextrose concentration using analysis of covariance. Thisdifference existed both at 23 and 37°C. The mean (SD) densityof levobupivacaine 7.5 mg ml^–1 was 1.00056 (0.00003) mgml^–1, the lower 0.5% percentile (1.00047 mg ml^–1)lying above the upper limit of hypobaricity for all patientgroups. Conclusions. The density of local anaesthetics decreases withincreasing temperature and increases in a linear fashion withthe addition of dextrose. Levobupivacaine 5 mg ml^–1 hasa significantly higher density compared with bupivacaine 5 mgml^–1 and ropivacaine 5 mg ml^–1 at 23 and 37°Cboth with and without dextrose. Levobupivacaine 7.5 mg ml^–1is an isobaric solution within all patient groups at 37°C. Br J Anaesth 2004; 92: 547–51     

Effects of levobupivacaine and ropivacaine on rat sciatic nerve blood flow

Background. Ischaemia is one of the causative mechanisms ofperipheral nerve injury, a documented complication of regionalanaesthesia. Local anaesthetics per se and/or vasopressor adjuvantsmay account for changes in peripheral nerve blood flow. Theaim of this study was to test the effects of levobupivacaineand ropivacaine in a rat sciatic nerve model with respect tolocal blood flow and histopathological changes. Methods. Forty-eight female Sprague–Dawley rats were anaesthetizedfor left sciatic nerve exposure. After baseline nerve bloodflow measurement with a laser Doppler flowmeter, 0.2 ml of oneof the following solutions was applied topically to the nervein a random fashion: saline 0.9%; lidocaine 10 mg ml^–1;levobupivacaine 2.5 mg ml^–1; levobupivacaine 5 mg ml^–1;levobupivacaine 7.5 mg ml^–1; ropivacaine 2 mg ml^–1;ropivacaine 7.5 mg ml^–1; and ropivacaine 7.5 mg ml^–1plus epinephrine 5 µg ml^–1; all in saline 0.9%.Nerve blood flow was evaluated at 5-min intervals up to 30 minafter local application of anaesthetic solution. Three animalsper group were killed for histological evaluation 48 h later.Multiple one-way analyses of variance followed by Scheffé'spost hoc test was used for statistical analysis. P<0.05 wasconsidered significant. Results. Local anaesthetics at all concentrations tested causedsignificant reduction in nerve blood flow. The combination ofropivacaine 7.5 mg ml^–1 plus epinephrine did not reducenerve blood flow to a greater extent than ropivacaine 7.5 mgml^–1 alone. Low concentrations of levobupivacaine (2.5and 5 mg ml^–1) reduced nerve blood flow to the same extentas lidocaine 10 mg ml^–1. No significant histological changeswere observed at 48 h. Conclusion. Despite acute reductions in peripheral nerve bloodflow, significant histopathological changes were not observedin this rat sciatic nerve model after topical application oflevobupivacaine and ropivacaine at concentrations relevant toclinical practice.     

RATE OF FORMATION OF NORPETHIDINE FROM PETHIDINE

The concentrations of norpethidine in blood were determinedin patients recovering from abdominal surgery following bothmultiple i.m. injections (i.m. group) and the i.v. infusion(i.v. group) of pethidine. The rate of administration of pethidineaveraged 25mg h^–1 in both groups. Concentrations of norpethidinewere generally small compared with those of pethidine althoughthe ratio of norpethidine to pethidine concentrations increasedsteadily over the 2 days studied. The rate of increase of bloodconcentration of norpethidine was 0.013 µg ml^–1h^–1 in both groups of patients. No significant toxic effectswere observed.     

Spinal anaesthesia with ropivacaine 5 mg ml(-1) in glucose 10 mg ml(-1) or 50 mg ml(-1)

Forty patients undergoing spinal anaesthesia for a variety ofsurgical procedures were randomly allocated to receive 3 mlof ropivacaine 5 mg ml^–1 in glucose 10 mg ml^–1 or50 mg ml^–1. Onset of sensory block to T10 was significantlyfaster (P=0.03) with the glucose 50 mg ml^–1 solution (median5 min, range 2–20 min) than with the 10 mg ml^–1solution (median 10 min, range 2–25 min). Maximum extentof cephalad spread was virtually the same in both groups (10mg ml^–1 median T6/7, range T3–T10; 50 mg ml^–1median T6, range T3–T10) with similar times to regressionbeyond S2 (10 mg ml^–1 median 210 min, range 150–330min; 50 mg ml^–1 median 210 min, range 150–330 min).Complete motor block was produced in the majority of patients(10 mg ml^–1 90%; 50 mg ml^–1 85%) and the time tocomplete regression was the same in both groups (median 120min, range 90–210 min). A block adequate for the projectedsurgery was achieved in all patients. Br J Anaesth 2001; 86: 241–4     

DIAZEPAM IN RECTAL SOLUTION AS PREMEDICATION IN CHILDREN, WITH SPECIAL REFERENCE TO SERUM CONCENTRATIONS

The absorption of rectal diazepam solution was studied in 22children aged 1–9 yr by measuring serum concentrations.The mean dose was 0.27±0.09mg kg^–1. The mean serumconcentration was 98.5±53.5 ng ml^–1 4min afteradministration and 206.7±105.8ng ml^–1 at 11 min.The correlation between dose and scrum concentration was statisticallysignificant at both times. With a dose of 0.4–0.5 mg kg^–1an adequate serum concentration was achieved within 5–6min. No side-effects were observed. A rectal solution providesa faster, more effective and reliable alternative to tabletsand suppositories, and to the uncertain i.m. injection of diazepam.Meticulous nursing is important.     

EFFECTS OF I.A. LIGNOCAINE ON ADRENALINE-INDUCED VASOCONSTRICTION

The effects of i.a. administered lignocaine on the in vivo responseof the vascular bed supplied by the lingual, external maxillaryand posterior auricular branches of the common carotid arterywere studied in the rat. Infusions of lignocaine in concentrationsof 10–1000 µg ml^–1 administered at the rateof 0.05 ml min^–1 for 10 min did not affect vascular resistanceor arterial pressure in the common carotid artery. However,following such infusions, the increase of vascular resistancecaused by bolus doses of adrenaline (20–120 ng in 0.1ml) was inhibited, indicating lignocaine-adrenaline antagonism.Responses to adrenaline remained significantly depressed 60min after the termination of a 100-µg ml^–1 or higherlignocaine infusion. ^* Present address: Turner Dental School, University of Manchester,Bridgeford Street, Manchester M15.     

KETAMINE FAILS TO PROTECT AGAINST ISCHAEMIC NEURONAL NECROSIS IN THE RAT

Ketamine is a dissociative anaesthetic known to be an NmethylD aspartate receptor blocker. Since the NMDA excitatory receptoron neurones is implicated in ischaemic neuronal necrosis, ketaminemight be expected to have a beneficial effect in cerebral hypoxia-ischaemia.Ketamine was tested in a rat model of forebrain ischaemia allowing7 days recovery. Ketamine 6mg kg^–1 i.v. was administered5–10 min before ischaemia in one group of rats, and ketamine60mg kg^–1 day^–1 i.m. for 3 days and 7 continuousdays after ischaemia in two other groups. An additional groupreceived ketamine 24 mg kg^–1 i.v. before ischaemia and120 mg kg^–1 day^–1 i.m. after ischaemia for 7 dayscontinuously. Control rats received ischaemia but no treatment.The results were compared with untreated controls by neuropathologicalexamination of the entire brain, sectioned subserially. Therewas no significant difference in necrosis between treated anduntreated groups after any of the ketamine regimens. The findingsdemonstrate that systemically administered ketamine fails toprotect the brain against hypoxic-ischaemic injury in the rat.     

The effects of i.v. fentanyl administration on the minimum alveolar concentration of isoflurane in horses

Background. Fentanyl decreases the minimum alveolar concentration(MAC) of inhaled anaesthetics and has been used clinically toreduce the requirements of other anaesthetic drugs in humansand small animals. We hypothesized that i.v. fentanyl woulddecrease the MAC of isoflurane in horses in a dose-dependentmanner. Methods. Following determination of baseline MAC of isoflurane,fentanyl was administered i.v. to target plasma concentrationsof 1, 8 and 16 ng ml^–1. Each horse was randomly assignedtwo of three target concentrations administered in ascendingorder. Loading and infusion doses for each horse were determinedfrom previously derived individual pharmacokinetic values. IsofluraneMAC determination began 45 min after fentanyl administrationat each target fentanyl concentration. Venous blood was collectedat fixed intervals during the infusion for measurement of plasmafentanyl concentrations. Results. Mean actual fentanyl plasma concentrations were 0 (baseline),and 0.72 (SD 0.26), 8.43 (3.22), and 13.31 (6.66) ng ml^–1for the target concentrations of 1, 8 and 16 ng ml^–1,respectively. The corresponding isoflurane MAC values were abaseline of 1.57 (0.23), and 1.51 (0.24), 1.41 (0.23) and 1.37(0.09)%, respectively. The fentanyl concentrations of 0.72 and8.43 ng ml^–1 did not significantly alter the MAC of isoflurane,but an 18 (7)% ISO-MAC reduction was observed at the 13.31 ngml^–1 concentration. Conclusions. These results cautiously encourage further studyof fentanyl as an opioid anaesthetic adjunct to inhalant anaesthesiain horses.     

MODIFICATION OF CENTRAL NERVOUS SYSTEM EFFECTS OF LAUDANOSINE BY INHALATION ANAESTHETICS

To determine the effect of inhalation anaesthetics on the plasmaconcentration of laudanosine necessary to produce CNS excitation,we administered laudanosine 0.5 mg kg^–1 min^–1 i.v.to 40 rabbits under eight study conditions: 1.0 or 0.7% halothane,1.6% isoflurane, 2.0% enflurane, during normocapnia and hypocapnia;70% nitrous oxide, alone and with 1.0% halothane, and room air(control). At the onset of purposeless, unco-ordinated movementsof the entire body, blood samples were obtained to determinethe CNS excitation-threshold plasma concentration (ETPC) oflaudanosine. During normocapnia, 1.0% halothane, 1.6% isofluraneand 2.0% enflurane increased ETPC (mean (SD) 11.8 (2.5), 11.3(2.8) and 9.1 (1.4) µg ml^–1, respectively) fromcontrol (5.0 (0.9) µg ml^–1). ETPC during enfluraneanaesthesia did not change significantly with hypocapnia. Nitrousoxide, alone or in combination with halothane, did not changeETPC. The combination of nitrous oxide with 1.0% halothane significantlydecreased ETPC to less than that for halothane alone (6.7 (1.2)v. 11.8 (2.5) µg ml^–1, respectively). ^*Present address: Department of Anesthesia, Peking Medical College,Beijing, People's Republic of China.     

VARIATION IN THE DISPOSITION OF MORPHINE AFTER I.M. ADMINISTRATION IN SURGICAL PATIENTS

The disposition of morphine when administered by i.m. injectionwas studied in 36 patients receiving morphine as part of premedicationbefore general anaesthesia, and in five patients who receivedmorphine as a postoperative analgesic after median sternotomyfor coronary artery surgery (PCA group). Maximum plasma concentrationof morphine (Cp_max) was 75.3 ± 6.0 (mean±standarderror (SEM)) ng ml^–1 (range 30–160 ng ml(^–1),mean elimination rate constant (k) 4.85 x 10^–3 min^–1and half-life (T₁₂) = 143 min for the preanaesthetic group.The corresponding values for PCA group were Cp_max = 58.0 ±18.0 ng ml^–1 (range 30–130 ng ml^–1), k = 5.63x 10^–3 min^–1 and T₁₂ = 123 min. Analysis of varianceshowed no differences between the groups. Within the preanaestheticgroup, there was a significant difference in k between males(k = 4.01 x 10^–3 min^–1) and females (6.30 x 10^–3min^–1, P<0.01). The corresponding T₁₂ for males was173 min; and 110 min for females. The variation in the dispositionof morphine is thought to be the result of variations in restingmuscle blood flow and inadvertent injection into adipose tissue.There were no significant differences between males and femalesin the preanaesthetic group with respect to age, CP_max timefrom injection to Cp_max.     

EFFECTS OF I.V. LIGNOCAINE ON AIRWAY REFLEXES ELICITED BY IRRITATION OF THE TRACHEAL MUCOSA IN HUMANS ANAESTHETIZED WITH ENFLURANE

We have investigated the effects of bolus administration oflignocaine 1.5 mg kg^–1 i.v. on respiratory responses toairway irritation induced by instillation of distilled waterinto the trachea in 10 patients anaesthetized with enflurane(1.5% end-tidal). Before administration of lignocaine, airwayirritation elicited not only the cough reflex, but also otherrespiratory reflexes such as expiration, apnoea and spasmodicpanting. Immediately after administration of i.v. lignocaine,when plasma concentrations of lignocaine exceeded 4.7 µgml^–1, tracheal irritation elicited only brief apnoea.Other reflex responses were suppressed completely; they recoveredgradually with progressive decrease in plasma concentrationof lignocaine. The apnoeic reflex was not eliminated at plasmalignocaine concentrations greater than 7.0 ug ml^–1, whereasthe expiration reflex, cough reflex and spasmodic panting wereeliminated effectively by plasma concentrations of lignocainegreater than 3.5, 2.8 and 2.2 ug ml^–1, respectively.     

CONTINUOUS I.V. INFUSION OF LABETALOL FOR POSTOPERATIVE HYPERTENSION: Haemodynamic Effects and Plasma Kinetics

Labetalol is a combined -and ß-adrenoreceptor blockingagent. A loading dose may be used to antagonize sympatheticoveractivity rapidly after surgery and be followed by a continuousinfusion to achieve a stable effect. The haemodynamic effectsand pharmacokinetics of this method of labetalol administrationwere studied in six rewarmed, extubated and sedated patients15±2 h after aortobifemoral bypass surgery. Patientswere monitored with radial and thermistor-tipped pulmonary arterycatheters. Labetalol 1.5 mg kg^–1 was injected i.v. over5 min and a maintenance infusion of 0.2 mg kg ^–1 h^–1was started 30 min later and continued for 5.5 h. Within 5 minof the loading dose, i.v. labetalol induced significant (P <0.05) decreases in mean arterial pressure (–32 ±11%),in heart rate (–20±11%) and in cardiac index (–26± 15%) that lasted throughout the infusion. Changes insystemic vascular resistance were not uniform, but an increasewas not observed in any patient. Mean stroke volume index andventricular filling pressures were not significantly affectedby labetalol administration. The mean measured steady stateplasma concentration (C^ss) (264 ±46 ng ml^–1) washigher than predicted (170 ng ml^–1) because the clearance(13.1 ±2.4 ml kg^–1 min^–1) was lower thanthat used to calculate the infusion rate. We conclude that labetalolis an effective antihypertensive agent in the postoperativeperiod. A C^ss can be achieved rapidly by such i.v. administrationand this offers the advantage of inducing rapid and stable haemodynamiceffects. However, calculation of the infusion rate must be basedon a clearance of 13 ml kg^–1 min^–1.     

EFFECT OF I.V. LIGNOCAINE ON PAIN AND THE ENDOCRINE METABOLIC RESPONSES AFTER SURGERY

Pain intensity, and blood glucose and plasma cortisol concentrationswere measured following abdominal hysterectomy in 18 patientsallocated randomly to receive either i.v. lignocaine 1.5 mgkg^–1 plus 2 mg kg^–1 h^–1, or saline. The administrationof lignocaine resulted in plasma conentrations between 1.5 and2.0 µg ml^–1 during the 2-h study period. However,the administration of lignocaine i.v. had no effect on the intensityof pain after surgery, or on the adrenocortical and hyperglycaemicresponses to surgery.     

OESOPHAGEAL CONTRACTILITY DURING TOTAL I.V. ANAESTHESIA WITH AND WITHOUT GLYCOPYRRONIUM

Somatic movement and spontaneous and provoked oesophageal contractionswere noted at time of incision in 51 patients receiving totali.v. anaesthesia with alfentanil and propofol. Probit analysisof the dose of propofol required to prevent spontaneous movementrevealed an ED₅₀ (95% confidence limits) of 2.5 (1.8-2.9) mgkg^–1 h^–1 and ED₉₅ of 4.7 (4.0-7.5) mg kg^–1h^–1. Corresponding venous blood concentrations gave anEC₅₀ of 1.2 (0.4-1.6) µg ml^–1 and an EC₉₅ of 4.0(2.8-18.5) µg ml^minus;1. ED₅₀ of propofol for preventingspontaneous oesophageal contraction was 3.0 (1.9-3.6) mg kg^–1h^–1. ED₉₅ was 6.9 (5.0-27.3) mg kg^–1 h^–1;EC₅₀ for oesophageal contractions was 1.7 (0.7-2.3) µgml^–1 and EC₉₅ was 5.9 (3.7-70.6) µg ml^–1.Another group of 10 patients were given glycopyrronium 5 µgkg^–1 at induction; oesophageal contractility was significantlyreduced in this group. Preliminary results of this research were presented to the AnaestheticResearch Society, Nottingham, July 1990. ^*Department of Anaesthesia, Derriford Hospital, Plymouth, DevonPL6 8DH. Department of Anaesthesia, Darlington Memorial Hospital, Darlington,Durham DL3 6HX.     

PREMEDICATION DETERMINES THE CIRCULATORY RESPONSES TO RAPID SEQUENCE INDUCTION WITH SUFENTANIL FOR CARDIAC SURGERY

Thirty-three patients undergoing elective aortocoronary bypasswere allocated randomly to receive morphine 0.1 mg kg^–1i.m. and either lorazepam 50 µg kg^–1 by mouth orhyoscine 6 µg kg^–1 i.m. before rapid sequence inductionof anaesthesia with sufentanil 5 µg kg^–1 i.v. andsuxamethonium 1 mg kg^–1 i.v. Following induction and trachealintubation, patients premedicated with hyoscine had a significantlyhigher mean heart rate, mean arterial pressure, cardiac indexand left ventricular stroke-work index than patients premedicatedwith lorazepam. The incidence of new myocardial ischaemia waslow in both groups.