PREVENTION OF HISTAMINE-INDUCED CARDIOVASCULAR REACTIONS DURING THE INDUCTION OF ANESTHESIA FOLLOWING PREMEDICATION WITH H1- + H2-ANTAGONISTS I. M.

In a prospective controlled double-blind study, 60 electivesurgical patients were randomly assigned to three premedicationgroups. Twenty patients received promethazine 0. 5 mg kg^–1i.m. 45 min before induction of anaesthesia; a further 20 patientsreceived an additional i. m. injection of cimetidine 400 mg120 min before induction. The third group (n = 20) served asthe control group. Following vecuronium 0.02 mg kg^–1,anaesthesia was induced with fentanyl, and etomidate. All patientsthen received suxamethonium 1.5 mg kg^–1 i. v. The combinedadministration of H₁- + H₂-antagonists as premedication ledto a significant reduction in the increase in heart rate whencompared with the effects in the other groups.     

INDUCTION DOSE-RESPONSE STUDIES WITH PROPOFOL AND THIOPENTONE

The relative potencies of propofol and thiopentone were assessedusing different indicators of induction of anaesthesia: abolitionof the response to verbal commands and eyelash stimulation.Log-probit dose-response curves for these end-points were determined30, 60 and 90 s after induction in 96 unpremedicated ASA groupI patients. For propofol, ED₅₀ values for abolition of the responseto verbal commands and eye/ash stimulation at different timeintervals were in the ranges 1.76–1.42 and 1.23–1.72mg kg^–1, respectively; corresponding ED₉₅ values were2.18–2.67 and 2.42–3.27 mg kg^–1, respectively.For thiopentone, the calculated ED₅₀ values for verbal commandsand eyelash stimulation at the same time intervals were 1.81–2.23and 3.55–3.40 mg kg^–1; corresponding ED₉₅ valueswere 5.11–6.29 and 6.41–6.70 mg kg^–1, respectively.The potency ratio of propofol to thiopentone observed in thisstudy varied from 1:1.27 to 1:2.88. It is concluded that a dose-responsecurve reflecting one end-point of anaesthesia cannot be usedto define another end-point of anaesthesia.     

METHOHEXITONE ANAESTHESIA FOR MICROLARYNGOSCOPY: CIRCULATORY MODULATION WITH METROPROLOL AND DIHYDRALAZINE

Anaesthesia for microlaryngoscopy was induced and maintainedwith fentanyl 3 µg kg^– and methohexitone (initialbolus of 1–1.5 mg-kg^–1 plus subsequent infusionof 4 mg kg^–1 h^–1). Suxamethonium was used to induceneuro-muscular blockade. Twenty minutes before induction ofanaesthesia, previously normotensive patients (n = 35), andpatients with hypertension well controlled by beta-receptorantagonists (n = 16) were pretreated with metoprolol (M) 0.2mg kg^–1i.v. and dihydralazine (DH) 0.2 mg kg^–1i.v.,dihydralazine 0.2 mg kg^–1 i.v. alone, or saline. Arterialpressure (AP) and heart rate (HR) were monitored: any arrhythmiaand ST₆₀T changes were noted. After the methohexitone infusionwas stopped, the times for emergence and full recovery wereshort (median 2 min 15s and 5 min later, respectively). Pretreatmentwith M+DH abolished increases in AP and HR during endoscopy.Arrhythmias were observed in fewer pretreated patients thanin controls (P < 0.05). ST₆₀-Tchanges in the ECG indicatingmyocardial ischaemia were found in two of 19 M+DH and in sixof 21 saline-pretreated patients. One of these six patientsdeveloped a myocardial infarction. Pretreatment with dihydralazinealone attenuated the pressor response to microlaryngoscopy,but was associated with consistently high HR and an incidenceof arrhythmias as well as ST₆₀T changes similar to that foundafter saline.     

DEXMEDETOMIDINE ATTENUATES SYMPATHOADRENAL RESPONSES TO TRACHEAL INTUBATION AND REDUCES THE NEED FOR THIOPENTONE AND PEROPERATIVE FENTANYL

The effects of the new, highly selective alpha₂-adrenergic agonist,dexmedetomidine, were studied in a randomized, placebo-controlled,double-blind trial in 24 ASA I patients. Dexmedetomidine 0.6µg kg^–1 or saline was given i.v. 10 min before inductionof anaesthesia. The required dose of thiopentone was significantly(P < 0.001) smaller in the dexmedetomidine group (mean 4.4(SD 0.9) mg kg^–1) than in the control group (6.9 (1.6)mg kg^–1), and the drug attenuated the cardiovascular responsesto laryngoscopy and tracheal intubation. The concentration ofnoradrenaline in mixed venous plasma was smaller in the dexmedetomidinegroup during all phases of induction (P < 0.01). During surgery,fentanyl was required in a dose of 0.5 (0.6) mg kg^–1 and2.8(2.6) mg kg^–1 in the dexmedetomidine and control groups,respectively (P < 0.001). During 2h postoperative follow-up,oxycodone 0.06 (0.06) mg kg^–1 and 0.16 (0.1) mg kg^–1(P < 0.05) was given to the two groups respectively.     

DOSE REQUIREMENTS OF PROPOFOL BY INFUSION DURING NITROUS OXIDE ANAESTHESIA IN MAN: I: Patients Premedicated with Morphine Sulphate

The study was performed to determine the ED₅₀ and ED₉₅ of acontinuous infusion of the emulsion formulation of propofolduring 67% nitrous oxide anaestheisa in 57 patients premed-icatedwith morphine sulphate 0.15 mg kg^–1. Anaesthesia was inducedwith propofol 2 mg kg^–1, and maintained before incisionwith a fixed-rate infusion of propofol to supplement nitrousoxide. The response to the first surgical incision, made atleast 30 min after induction of anaesthesia, was observed. TheED₅₀; was 53.5 µg kg^–1 min^–1 and the ED₉₅was 112.2 µg kg^–1 min^–1. At the time of thefirst surgical incision, the venous whole blood concentrationsof propofol at the ED₅₀ and ED₉₅ infusion rates (EC₅₀and EC₉₅were 1.66 µg ml^–1 and 3.39 fig ml^–1 respectively.The satisfactory maintenance of anaesthesia provided by nitrousoxide supplemented with propofol was associated with stabilityand rapid, uncomplicated recovery.     

EFFECTS OF FLUMAZENIL ON CEREBRAL BLOOD FLOW AND OXYGEN CONSUMPTION AFTER MIDAZOLAM ANAESTHESIA FOR CRANIOTOMY

Cerebral blood flow (CBF) and cerebral metabolic rate for oxygen(CMRO₂) were measured by a modification of the Kety-Schmidttechnique using i.v. xenon-133 in 20 patients undergoing craniotomyfor supratentorial cerebral tumours. Anaesthesia was inducedand maintained with midazolam, fentanyl and nitrous oxide. Pan-curoniumwas given for neuromuscular block. The lungs were ventilatedto normocapnia. The first flow measurements were performed approximately1 h after induction of anaesthesia. At the end of operationthe patients were allocated to two groups. Ten patients weregiven flu-mazenil 0.01 mg kg^–1and 5 min later the secondflow measurement was performed. In the other 10 patients thesecond flow measurement was performed before the administrationof flumaz-enil. Plasma concentrations of midazolam were measuredat the time of each measurement of CBF. There was no differencebetween the groups in plasma concentration of midazolam, CBFor CMRO₂. Flumazenil had noeffect on CBF and CMRO₂.     

EFFECT OF KETANSERIN ON GLOBAL CEREBRAL BLOOD FLOW AND CEREBRAL OXYGEN METABOLISM DURING MIDAZOLAM-FENTANYL OR ISOFLURANE ANAESTHESIA

We have studied the effect of ketanserin on cerebral blood flow(CBF), cerebral oxygen metabolism (CMRO₂) and cerebrovascularcarbon dioxide reactivity in 19 adult patients undergoing lumbardisc operation – 10 during midazolam-fentanyl anaesthesia(group A) and nine during isoflurane anaesthesia (group B).Measurements were made in each patient whilst awake, duringanaesthesia, during anaesthesia with ketanserin and during anaesthesiawith ketanserin and hyperventilation. CBF was measured by thei. v. xenon-133 technique. CMRO₂ was calculated as the productof CBF and the cerebral arterio-venous oxygen content difference.In the awake state, CBF was 52 and 51 ml/100g min_–1 andCMRo₂ 3.8 and 3.5 ml/100 g min_–1 in groups A and B, respectively.After induction of anaesthesia, CBF decreased 37% in group Aand 22% in group B (P < 0.05); CMRo₂ decreased 26% in groupA and 51% in group B (P < 0.05). Adding ketanserin did notchange CBF or CMRo₂ in either group. The carbon dioxide reactivityof the cerebral vessels during anaesthesia with ketanserin was15.4%kPa^–1 in group A and 24%kPa^–1 in group B. Weconcluded that ketanserin, in a clinically recommended dose,administered during midazolam-fentanyl or isoflurane anaesthesiahad no effect on global CBF, CMRo₂ or the relationship betweenthe two factors. Cerebrovascular carbon dioxide reactivity waspreserved.     

SYNERGISTIC INTERACTION BETWEEN MIDAZOLAM AND PROPOFOL

We gave either midazolam or propofol for induction of anaesthesiato 140 ASA I or II female patients (18–60 yr). ED₅₀, valueswere obtained by probit analysis for three clinical end-points:loss of response to command; loss of eyelash reflex; failureto respond to application of an anaesthetic face mask delivering1 % isoflurane. Propofol ED₅₀ values (95% confidence intervals)were 1.25 (0.99–1.48) mgkg^–1, 1.61 (1.29–1.94)mg kg^–1 and1.51 (1.20–1.82) mg kg^–1, respectively.ED₅₀ values for midazolam were 0.26 (0.20–0.37) mg kg^–1,0.29 (0.23–0.47) mgkg^–1 and 0.25 (0.20–0.32)mg kg^–1, respectively. An additional 92 similar patientsreceived one of nine dose combinations of midazolam and propofolfor induction of anaesthesia, propofol being administered 2min after midazolam. Success of induction was based on the clinicalend-point of loss of response to command. Administration of25% of the ED₅₀ of midazolam followed by 50% of the ED₅₀ ofpropofol resulted in loss of response to command in 50 % ofpatients, while 50 % of the ED₅₀ of midazolam, followed by 25%of the ED₅₀ of propofol had the same effect. A probit regressionmodel specifying a synergistic interaction between midazolamand propofol fitted the data significantly better than a modelspecifying no interaction. ^*Present address, for correspondence: Department of Anaesthetics,Royal Group of Hospitals, Grosvcnor Road, Belfast BT12 6BA,N. Ireland     

Effect of 1 or 2 MAC isoflurane with or without ketanserin on cerebral blood flow autoregulation in man

We have studied the effect of 1 or 2 MAC isoflurane with orwithout ketanserin on cerebral blood flow (CBF), cerebral oxygenmetabolism (CMRO₂) and CBF autoregulation in 20 adult patientsundergoing lumbar disc surgery. Ten patients received ketanserinand 10 isotonic saline. CBF measurements were started after1 h of infusion of saline or ketanserin. The patients were anaesthetizedwith thiopentone 5 mg kg^–1 followed by isoflurane. During1 MAC of isoflurane, baseline values were recorded and thenCBF autoregulation was examined (mean arterial pressure increasedby about 30% with angiotensin). The sequence was repeated with2 MAC of isoflurane. CBF was measured by the i.v. xenon-133technique. CMRo₂ was calculated as the product of CBF and thecerebral arterio-venous oxygen content difference. Ketanserinhad no effect on CBF, CMRo² or CBF autoregulation during isofluraneanaesthesia, therefore all patients were pooled for evaluationof the effect of isoflurane. Increasing isoflurane anaesthesiafrom 1 to 2 MAC increased mean CBF from 41 to 49 ml /100 g min^–1(P<: 0.01) and decreased mean CMRo₂ from 1.5 to 1.1 ml/100g min^–1 (P < 0.001) and thus abolished the couplingbetween flow and metabolism. The CBF autoregulation test indicatedthat autoregulation was disrupted at 2 MAC, but not during 1MAC isoflurane anaesthesia. (Br. J. Anaesth. 1994; 72: 66–71)     

THIOPENTONE-NITROUS OXIDE-HALOTHANE ANAESTHESIA AND SUXAMETHONIUM: PRETREATMENT WITH PANCURONIUM AND GALLAMINE

Eighty healthy adult patients randomly allocated to four groupsreceived pancuronium 0.01, 0.015, 0.02 mg kg^–1 or gallamine0.3 mg kg^–1 i.v. 3 min before induction. Just before inductionof anaesthesia, the patients were examined for signs and symptomsof neuromuscular blockade. After induction of anaesthesia withthiopentone, suxamethonium 1.5 mg kg^–1 was administeredi.v. Five minutes later the second dose was injected. No seriousarrhythmia was seen in any of the four groups following therepeated dose of suxamethonium. However, the highest dose ofpancuronium (0.02 mg kg^–1) caused an unacceptably highfrequency of partial neuromuscular blockade.     

Effect of prophylactic bronchodilator treatment with i.v. carperitide on airway resistance and lung compliance after tracheal intubation

Background. Lung resistance increases after induction of anaesthesia.We hypothesized that prophylactic bronchodilation with i.v.carperitide before tracheal intubation would decrease airwayresistance and increase lung compliance after placement of thetracheal tube in both smokers and nonsmokers. Methods. Ninety-seven adults aged between 24 and 59 yr wererandomized to receive i.v. normal saline (0.9% saline) (control)or carperitide, 0.2 µg kg^–1 min^–1 throughoutthe study. The 97 patients included smokers and nonsmokers.Thus the patients were allocated to one of the four groups:smokers who received normal saline (n=21), nonsmokers who receivednormal saline (n=27), smokers who received carperitide (n=19)or nonsmokers who received carperitide (n=30). Thirty minutesafter starting normal saline or carperitide infusion, we administeredthiamylal 5 mg kg^–1 and fentanyl 5 µg kg^–1to induce general anaesthesia and vecuronium 0.3 mg kg^–1for muscle relaxation. Continuous infusion of thiamylal 15 mgkg^–1 h^–1 followed anaesthetic induction. Mean airwayresistance (R_awm), expiratory airway resistance (R_awe) and dynamiclung compliance (C_dyn) were determined 4, 8, 12 and 16 min aftertracheal intubation and compared between the four groups. Results. At 4 min after intubation, R_awm and R_awe were higherand C_dyn lower in smokers than in nonsmokers in the controlgroup. R_awm and R_awe were lower and C_dyn higher in smokers inthe carperitide group than in smokers in the control group.R_awm and R_awe were lower in nonsmokers in the carperitide groupthan in nonsmokers in the control group. Conclusions. Marked bronchoconstriction occurred in the controlgroups (smokers and nonsmokers) 4 min after tracheal intubation.Prophylactic treatment with carperitide before induction ofanaesthesia and tracheal intubation was advantageous, particularlyin smokers.     

Oral clonidine vs midazolam in the prevention of sevoflurane-induced agitation in children. a prospective, randomized, controlled trial

Background: This randomized, double-blind study tested the hypothesis that,in comparison with midazolam, premedication with oral clonidinereduces the incidence of emergence agitation in preschool childrenanaesthetized with sevoflurane. Methods: Sixty-eight ASA I–II children undergoing circumcisionwere randomized into three groups to receive different oralpremedication given 30 min before anaesthesia: midazolam 0.5mg kg^–1, clonidine 2 µg kg^–1, and clonidine4 µg kg^–1. Sevoflurane anaesthesia was administeredvia a facemask (O₂/N₂O: 40/60). Analgesia was with penile block(bupivacaine 0.5% 0.3 ml kg^–1) and rectal paracetamol(30 mg kg^–1). During the first postoperative hour, childrenwere evaluated using a modified ‘objective pain scale’. Results: Only the 4 µg kg^–1 dose of clonidine was associatedwith a significant reduction in emergence agitation. Fewer childrenin the clonidine 4 µg kg^–1 group displayed agitation(25%) than in the midazolam group (60%) (P = 0.025). Incidenceof hypotension and bradycardia, time to first micturition andfirst drink did not differ among groups. Conclusions: In comparison with midazolam, clonidine 4 µg kg^–1reduced sevoflurane-induced emergence agitation without increasingpostoperative side-effects.     

ANOTHER LOOK AT ACUTE TOLERANCE TO THIOPENTONE

The phenomenon of "acute tolerance" to thiopentone was re-examinedin 82 subjects with induction doses of 2–15 mg kg^–1.There was a strong positive correlation between the venous plasmathiopentone concentrations on recovery from anaesthesia andthe induction dose, expressed as either mg kg^–1 or mgkg^–1. Recovery time was proportionately shorter with largerdoses, being directly related to log₁₀ of the plasma concentrationat awakening.     

Oral clonidine premedication attenuates the hypertensive response to ketamine

Clonidine diminishes sympathetic nervous system activity viaa central action. To test if the haemodynamic responses to ketamine,a centrally acting sympathomimetic drug, are attenuated by clonidine,we studied arterial pressure (AP) and heart rate (HR) changesafter ketamine 1 mg kg^–1 in 40 normotensive patients undergoinggeneral anaesthesia. They were allocated randomly to receiveclonidine 5 µg kg^–1 and famotidine 20 mg (n = 20)or to a control group (n = 20) which received only famotidine20 mg orally 90 mm before induction of anaesthesia. After administrationof ketamine 1 mg kg^–1 and vecuronium 0.2 mg kg^–1ventilation of the lungs was controlled with 67% nitrous oxidein oxygen to maintain end-tidal carbondioxide at 4–4.7kPa. AP and HR were measured non-invasively at 1-min intervalsfor 10 min after ketamine. After induction of anaesthesia, APwas increased significantly from resting values in the controlgroup, but remained unchanged in the clonidine group (P <0.05). Maximum changes in mean AP were also significantly greaterin the control group compared with the clonidine group (29.2(12.8) vs 19.5 (13.1) mm Hg, P = 0.02). However, no change inHR was noted throughout the 10-min study.     

NEUROMUSCULAR AND CARDIOVASCULAR EFFECTS OF MIVACURIUM CHLORIDE (BWB1090U) DURING NITROUS OXIDE-FENTANYL-THIOPENTONE AND NITROUS OXIDE-HALOTHANE ANAESTHESIA

Seventy-two adult surgical patients were studied to compareneuromuscular and cardiovascular effects of mivacurium chlorideduring nitrous oxide-fentanyl-thiopentone (BAL group) or nitrousoxide-halothane (HAL group) anaesthesia. Eighteen patients inthe BAL group received an initial bolus of mivacurium, eitherthe ED₂₅ (n = 9) or the ED50 (n = 9) (0.03 and 0.05 mg kg^–1).These doses were based on the assumption that the slope of thedose-response curve during nitrous oxide-opioid anaesthesiawould be approximately the same as the slope of the neuromuscularresponse from the first human studies with mivacurium. Twenty-sevenadditional patients were allocated to subgroups of nine patientsto receive mivacurium 0.04. 0.08 or 0.15 mg kg^–1. Twenty-sevenpatients in the HAL group were allocated also to subgroups ofnine patients to receive mivacurium 0.03, 0.04 or 0.15 mg kg^–1.During stable anaesthesia, mean endtidal halothane concentrationswere maintained at 0.49±0.01%. The estimated ED₅₀, ED₇₅and ED₉₅ for BAL and HAL groups were 0.039, 0.05 and 0.073 mgkg^–1 and 0.040, 0.053 and 0.081 mg kg^–1, respectively.Halothane did not potentiate maximum block or time to maximumblock. Halothane did affect spontaneous recovery. With the 0.15-mgkg^–1 dose, time to 95% recovery was prolonged significantlyin the HAL group (30.0 (SEM 1.4) min) compared with the BALgroup (24.1 (1.5) min). Recovery index from 25% to 75% recoverywas also prolonged significantly in the HAL group (7.0 (0.4)min) compared with the BAL group (5.4 (0.4) min). There wereno significant haemodynamic changes in groups given mivacuriumdoses up to and including 2 x ED₉₅ by bolus i.v. administration ^*Department of Anesthesia, University of Iowa Hospitals andClinics, Iowa City, Iowa 52242, U.S.A.     

EFFECTS OF ATRACURIUM ON INTRAOCULAR PRESSURE

The effects of attacurium on intraocular pressure (IOP) werecompared with those of pancuronium in 20 patients less than45 years-of-age requiring surgery for trauma of one eye. Aftera standard premedication and the application of topical analgesiato the upper airway, anaesthesia was induced with thiopentonei.v. and the trachea was intubated without the use of neuromuscularblockade. Following 20min of steady state anaesthesia duringwhich measurements of IOP, arterial pressure, heart rate, F_IO2,F_E'CO2 and CVP were recorded, one group of patients receivedatracurium 0.45 mg kg^–1 and the other pancuronium 0.1mg kg^–1. The observations were repeated for a further15 min before surgery commenced. Neither atracurium nor pancuroniumproduced any change in IOP. Atracurium was associated with greatercardiovascular stability than pancuronium.     

DOSE-RESPONSE RELATIONSHIPS FOR EDROPHONIUM AND NEOSTIGMINE ANTAGONISM OF MIVACURIUM-INDUCED NEUROMUSCULAR BLOCK

We have studied the dose-response relationships for neostigmineand edrophonium during antagonism of neuromuscular block inducedby mivacurium chloride. Sixty-four ASA group I or II adultswere given mivacurium 0.15 mg kg^–1 during fentanyl-thiopentone-nitrousoxide-iso flurane anaesthesia. Train-of-four stimulation (TOF)was applied to the ulnar nerve every 10 s, and the force ofcontraction of the adductor pollicis muscle was recorded. Whenspontaneous recovery of first twitch height reached 10% of itsinitial control value, edrophonium 0.1, 0.2, 0.4, or 1 mg kg^–1or neostigmine 0.005, 0.01, 0.02, or 0.05 mg kg^–1 wasadministered by random allocation. Neuromuscular function inanother 16 subjects was allowed to recover spontaneously. Spontaneousrecovery from 90% mivacurium block to 95% twitch height andTOF ratio 0.75 occurred within 15 min. This study demonstratedthat the dose-response curves for these two drugs for antagonismof neuromuscular block (first twitch and train-of-four ratio)were parallel. The doses of neostigmine required to achieve50% (ED₅₀) and 70% (ED₇₀) recovery of the first twitch after10 min were 2 (1.5– 2.5) µg kg^–1 and 4.7 (4.1–5.4)µg kg^–1 (mean (95% confidence intervals)), respectively.Corresponding ED₅₀ and ED₇₀ values for edrophonium were 2.8(0.75–10.2) pg kg^–1 and 9.2 (3.6–23.6) µgkg^–1, respectively. These values corresponded to neostigmine:edrophonium potency ratios of 1.4 (0.4–2.4) and 1.95(0.9–2.9) for first twitch ED₅₀ and ED₇₀ height, respectively.The calculated doses producing 50% (ED₅₀ recovery of the TOFratio at 10 min were neostigmine 2.57 (1.8–3.6) µgkg^–1 and edrophonium 26.9 (14.6–49.6) pg kg^–1.These values corresponded to a potency ratio of 10.4 (0.7–20).(Br. J. Anaesth. 1993; 71: 709–714)     

INFUSION OF PROPOFOL TO IDENTIFY SMALLEST EFFECTIVE DOSES FOR INDUCTION OF ANAESTHESIA IN YOUNG AND ELDERLY PATIENTS

We studied 110 patients older than 60 yr or aged 18–50yr as separate groups in two stages to identify the smallesteffective doses of propofol for induction of anaesthesia. Inthe elderly patients, in stage 1, at infusion rates of 25, 50or 100 mg min^–1 the mean (SD) doses administered werepropofol 0.82 (0.14) mg kg^–1, 1.22 (0.24) mg kg^–1and 1.65 (0.60) mg kg^–1 and the induction times 140.1(21.9) s, 103.2 (23.5) s and 69.4 (10.0) s, respectively. Instage 2, after induction with a fixed dose of 0.82 mg kg^–1as a bolus over 5 s or as an infusion at 25 mg min^–1,the times for induction were 38.5 (14.0) s and 144.5 (36.6)s, respectively. In the young patients, at induction rates of33.3, 50, 100 or 200 mg min^–1, the doses administeredwere propofol 1.36 (0.28) mg kg^–1, 1.46 (0.12) mg kg^–1,1.85 (0.43) mg kg^–1 and 2.39 (0.50) mg kg^–1 andthe induction times 145.0 (25.4) s, 120.0 (18.4) s, 80.2 (19.2)s and 54.5 (10.4) s, respectively. In stage 2, a fixed inductiondose of 1.46 mg kg^–1 resulted in induction times of 35.0(8.5) s and 134.0 (26.8) s, respectively. In stage 2 of eachage group, induction was achieved with smaller doses than thoserecommended previously and there was no difference in the numberof patients in whom induction of anaesthesia was successfulor in the measured cardiorespiratory variables between the twoinduction regimens. This suggests the latter effects are causedby the dose administered and not the rate of administration.     

I.V. PRACTOLOL DURING MICROLARYNGOSCOPY. EFFECT ON ARTERIAL PRESSURE, HEART RATE, BLOOD GLUCOSE AND LIPOLYSIS

Twenty-five patients undergoing microlaryngoscopy were anaesthetizedwith thiopentone and nitrous oxide with suxamethonium as a musclerelaxant. Thirteen received practolol 0.4 mg kg^–1 andatropine 1.5mg i.v. shortly before anaesthesia. During anaesthesiapractolol 0.2 mg kg^–1 was given. Twelve (control) receivedatropine 0.5 mg before anaesthesia. Practolol reduced the frequencyof tachycardia and arrhythmia. The treatment group had a greaterreduction in systolic arterial pressure during induction. Thehypertensive response to laryngoscopy was not significantlyattenuated by practolol. A weak hyperglycaemic response to microlaryngoscopywas not affected, nor was the plasma concentration of glycerol.     

CARDIAC EFFECTS OF ATROPINE AND GALLAMINE IN PATIENTS RECEIVING SUXAMETHONIUM

Eighty healthy patients were randomly allocated to four groups.Atropine 0.01 mg kg^–1 i.v. (group I), gallamine 0.3 mgkg^–1 i.v. (group II), atropine 0.01 mg kg^–1 i.m.and gallamine 0.3 mg kg^–1 i.v. (group III), or atropine0.01 mg kg^–1 i.v. and gallamine 0.3 mg Lrg^–1 i.v.(group IV) were given before operation. After induction of anaesthesiawith thiopentone, suxamethonium 1 mg kg^–1 was given i.v.The lungs were ventilated with halothane in nitrus oxide inoxygen. Five minutes later the same dose of suxamrthonium wasrepeated. E.c.g. was monitored continuously. No serious bradycardiawas observed following a second injection of suxamethonium inany group. The results suggest that thiopentone protects againstsuxamethonium-induced bradycardia during halothane anaesthesia.