Effect of two anaesthetic regimens on airway nitric oxide production in horses

There is evidence that halothane inhibits nitric oxide synthasein vitro, but the effect of intravenous anaesthetic agents isless clear. This study was undertaken to compare the rate ofexhaled nitric oxide production (V_NO) in spontaneously breathinghorses anaesthetized with halothane or an intravenous regimen.Seven adult horses were studied twice in random order. Afterpremedication with romifidine 100 µg kg^–1,anaesthesia was induced with ketamine 2.2 mg kg^–1and maintained with halothane in oxygen (HA) or by an intravenousinfusion of ketamine, guaiphenesin and romifidine (IV). Inhaledand exhaled nitric oxide (NO) concentrations, respiratory minuteventilation (V_E), pulmonary artery pressure (P_PA), fractionalinspired oxygen concentration (FI_O2), end-tidal carbon dioxideconcentration (E'_CO2), cardiac output (Q) and partial pressuresof oxygen and carbon dioxide in arterial blood (Pa_O2, Pa_CO2)were measured. Exhaled nitric oxide production rate was significantlylower (40 min, P<0.01; 60 min, P<0.02) duringHA [40 min, 1.4 (SD 1.4) pmol l^–1 kg^–1 min^–1;60 min, 0.7 (0.7) pmol l^–1 kg^–1 min^–1]than during IV [40 min, 9.3 (9.9) pmol l^–1 kg^–1min^–1; 60 min, 12.5 (13.3) pmol l^–1 kg^–1min^–1). Mean pulmonary artery pressure was significantlyhigher (40 min, P<0.01; 60 min, P<0.001) during HA[40 min, 5.9 (1.1) kPa; 60 min, 5.9 (0.9) kPa] comparedwith IV (40 min, 4.4 (0.4) kPa; 60 min, 4.4 (0.5) kPa].NO is reduced in the exhalate of horses anaesthetized with halothanecompared with an intravenous regimen. It is suggested that increasedmean pulmonary artery pressure during halothane anaesthesiamay be linked to the differences in NO production. Br J Anaesth 2001; 86: 127–30     

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.     

Spasmolytic effects of prostaglandin E1 on serotonin-induced bronchoconstriction and pulmonary hypertension in dogs

In this study, we simultaneously evaluated the spasmolytic effectsof prostaglandin E₁ (PGE₁) on serotonin-induced bronchoconstrictionand pulmonary hypertension. Eleven mongrel dogs (8–12kg) anaesthetized with pentobarbital were assigned to two groups:saline (n=4) and PGE₁ (n=7). Bronchoconstriction and pulmonaryhypertension were elicited with serotonin 10 µg kg^–1+ 1 mg kg^–1 h^–1 and assessed as the percentage changein bronchial cross-sectional area (BCA) measured by bronchoscopyand pulmonary vascular resistance (PVR), respectively. Thirtyminutes after starting the serotonin infusion, saline or PGE₁0 (saline), 0.01, 0.1, 1.0 or 10 µg kg^–1 i.v. wasgiven. %BCA and %PVR (basal=100%) were assessed before and 30min after serotonin, and 30 and 60 min after saline (salinegroup) or 5 min after each dose of PGE₁ (PGE₁ group). In thesaline group, pulmonary hypertension and bronchoconstrictionwere stable. In the PGE₁ group, PGE₁ at     

Effects of xenon anaesthesia on the circulatory response to hypoventilation

Background. Circulatory response to hypoventilation is aimedat eliminating carbon dioxide and maintaining oxygen delivery(DO₂) by increasing cardiac output (CO). The hypothesis thatthis increase is more pronounced with xenon than with isofluraneanaesthesia was tested in pigs. Methods. Twenty pigs received anaesthesia with xenon 0.55 MAC/remifentanil0.5 µg kg^–1 min^–1 (group X, n=10) or isoflurane0.55 MAC/remifentanil 0.5 µg kg^–1min^–1 (groupI, n=10). CO, heart rate (HR), mean arterial pressure (MAP)and left ventricular fractional area change (FAC) were measuredat baseline, after 5 and 15 min of hypoventilation and after5, 15 and 30 min of restored ventilation. Results. CO increased by 10–20% with both anaesthetics,with an equivalent rise in HR, maintaining DO₂ in spite of a20% reduction in arterial oxygen content. Decreased left ventricular(LV) afterload during hypoventilation increased FAC, and thiswas more marked with xenon (0.60–0.66, P<0.05 comparedwith baseline and isoflurane). This difference is attributedto negative inotropic effects of isoflurane. Increased pulmonaryvascular resistance during hypoventilation was found with bothanaesthetics. Conclusion. The cardiovascular effects observed in this modelof moderate hypoventilation were sufficient to maintain DO₂.Although the haemodynamic response appeared more pronouncedwith xenon, differences were not clinically relevant. An increasein FAC with xenon is attributed to its lack of negative inotropiceffects.     

Cerebral pressure autoregulation and carbon dioxide reactivity during propofol-induced EEG suppression

We studied cerebral pressure autoregulation and carbon dioxidereactivity during propofol-induced electrical silence of theelectroencephalogram (EEG) in 10 patients. Anaesthesia was inducedwith propofol 2.5 mg kg^–1, fentanyl 3 µg kg^–1and vecuronium 0.1 mg kg^–1, and a propofol infusion of250–300 µg kg^–1 min^–1 was used to induceEEG silence. Cerebral pressure autoregulation was tested byincreasing mean arterial pressure (MAP) by 24 (SEM 5) mm Hgfrom baseline with an infusion of phenylephrine and simultaneouslyrecording middle cerebral artery blood flow velocity (vmca)using transcranial Doppler. Carbon dioxide reactivity was testedby varying Pa_co2 between 4.0 and 7.0 kPa and recording vmcasimultaneously. Although absolute carbon dioxide reactivitywas reduced, relative carbon dioxide reactivity was within normallimits for all patients studied (mean 8.5 (SEM 0.8) cm s^–1kPa^–1 and 22 (2)% kPa^–1, respectively). No significantchange in vmca (34 (2) and 35 (2) cm s^–1) was observedwith the increase in MAP (77 (4) to 101 (4) mm Hg) during autoregulationtesting. We conclude that cerebral carbon dioxide reactivityand pressure autoregulation remain intact during propofol-inducedisoelectric EEG.     

Effects of thoracic epidural anaesthesia on microvascular gastric mucosal oxygenation in physiological and compromised circulatory conditions in dogs

Background. The effects of thoracic epidural anaesthesia (TEA)on gastric mucosal microvascular haemoglobin oxygenation (µHbO₂)are unclear. At the splanchnic level, reduction of sympathetictone may promote vasodilation and increase µHbO₂. However,these splanchnic effects are counteracted by systemic effectsof TEA (e.g., decreased cardiac output (CO) and mean arterialpressure (MAP)), thus making the net effect on µHbO₂ difficultto predict. In this respect, effects of TEA on µHbO₂ maydiffer between physiological and compromised circulatory conditions,and additionally may depend on adequate fluid resuscitation.Furthermore, TEA may alter the relationship between regionalµHbO₂ and systemic oxygen-transport (DO₂). Methods. Chronically instrumented dogs (flow probes for CO measurement)were anaesthetized, their lungs ventilated and randomly receivedTEA with lidocaine (n=6) or epidural saline (controls, n=6).Animals were studied under physiological and compromised circulatoryconditions (PEEP 10 cm H₂O), both with and without fluid resuscitation.We measured gastric mucosal µHbO₂ by reflectance spectrophotometry,systemic DO₂, and systemic haemodynamics (CO, MAP). Results. Under physiological conditions, TEA preserved µHbO₂(47 (3)% and 49 (5)%, mean (SEM)) despite significantly decreasingDO₂ (11.3 (0.8) to 10.0 (0.7) ml kg^–1 min^–1) andMAP (66 (2) to 59 (3) mm Hg). However, during compromised circulatoryconditions, TEA aggravated the reduction in µHbO₂ (to32 (1)%), DO₂ (to 6.7 (0.8) ml kg^–1 min^–1) and MAP(to 52 (4) mm Hg), compared with controls. During TEA, fluidresuscitation completely restored these variables. TEA preservedthe correlation between µHbO₂ and DO₂, compared with controls. Conclusions. TEA maintains µHbO₂ under physiological conditions,but aggravates the reduction of µHbO₂ induced by cardiocirculatorydepression, thereby preserving the relationship between gastricmucosal and systemic oxygenation. Presented in part at the German Anaesthesia Congress 2003 (April9–12, Munich, Germany) and the European Society of IntensiveCare Congress 2003 (October 5–8, Amsterdam, The Netherlands).     

Comparison of propofol/remifentanil and sevoflurane/remifentanil for maintenance of anaesthesia for elective intracranial surgery

Background. Propofol and sevoflurane are suitable agents formaintenance of anaesthesia during neurosurgical procedures.We have prospectively compared these agents in combination withthe short-acting opioid, remifentanil. Methods. Fifty unpremedicated patients undergoing elective craniotomyreceived remifentanil 1 µg kg^–1 followed by an infusioncommencing at 0.5 µg kg^–1 min^–1 reducing to0.25 µg kg^–1 min^–1 after craniotomy. Anaesthesiawas induced with propofol, and maintained with either a target-controlledinfusion of propofol, minimum target 2 µg ml^–1 orsevoflurane, initial concentration 2%_ET. Episodes of mean arterialpressure (MAP) more than 100 mm Hg or less than 60 mm Hg formore than 1 min were defined as hypertensive or hypotensiveevents, respectively. A surgical assessment of operating conditionsand times to spontaneous respiration, extubation, obey commandsand eye opening were recorded. Drug acquisition costs were calculated. Results. Twenty-four and twenty-six patients were assigned topropofol (Group P) and sevoflurane anaesthesia (Group S), respectively.The number of hypertensive events was comparable, whilst morehypotensive events were observed in Group S than in Group P(P=0.053, chi-squared test). As rescue therapy, more labetolol[45 (33) vs 76 (58) mg, P=0.073] and ephedrine [4.80 (2.21)vs 9.78 (5.59) mg, P=0.020] were used in Group S. Between groupdifferences in recovery times were small and clinically unimportant.The combined hourly acquisition costs of hypnotic, analgesic,and vasoactive drugs appeared to be lower in patients maintainedwith sevoflurane than with propofol. Conclusion. Propofol/remifentanil and sevoflurane/remifentanilboth provided satisfactory anaesthesia for intracranial surgery.     

Xenon increases total body oxygen consumption during isoflurane anaesthesia in dogs

Background. This study was designed to examine whether the couplingbetween oxygen consumption (V^·O₂) and cardiac output(CO) is maintained during xenon anaesthesia. Methods. We studied the relationship between V^·O₂ (indirectcalorimetry) and CO (ultrasound flowmetry) by adding xenon toisoflurane anaesthesia in five chronically instrumented dogs.Different mixtures of xenon (70% and 50%) and isoflurane (0–1.4%)were compared with isoflurane alone (1.4% and 2.8%). In addition,the autonomic nervous system was blocked (using hexamethonium)to study its influence on V^·_O2 and CO during xenon anaesthesia. Results. Mean (SEM) V^·O₂ increased from 3.4 (0.1) ml kg^–1 min^–1during 1.4% isoflurane to 3.7 (0.2) and 4.0 (0.1) ml kg^–1 min^–1after addition of 70% and 50% xenon, respectively (P<0.05),whereas CO and arterial pressure remained essentially unchanged.In contrast, 2.8% isoflurane reduced both, V^·O₂ [from3.4 (0.1) to 3.1 (0.1) ml kg^–1 min^–1]and CO [from 96 (5) to 70 (3) ml kg^–1 min^–1](P<0.05). V^·O₂ and CO correlated closely during isofluraneanaesthesia alone and also in the presence of xenon (r²=0.94and 0.97, respectively), but the regression lines relating COto V^·_O2 differed significantly between conditions, withthe line in the presence of xenon showing a 0.3–0.6 ml kg^–1 min^–1greater V^·O₂ for any given CO. Following ganglionic blockade,50% and 70% xenon elicited a similar increase in V^·O₂,while CO and blood pressure were unchanged. Conclusions. Metabolic regulation of blood flow is maintainedduring xenon anaesthesia, but cardiovascular stability is accompaniedby increased V^·O₂. The increase in V^·_O2 is independentof the autonomic nervous system and is probably caused by directstimulation of the cellular metabolic rate. Br J Anaesth 2002; 88: 546–54     

HYPOXIC VENTILATORY DRIVE IN THE DOG UNDER ALTHESIN ANAESTHESIA

Althesin was administered i.v. to eight dogs, using two differentrates of infusion (6.55 +mn; 2.13 µl kg^–1 min and12.80 +mn; 2.00 µl kg^–1 min). Ventilation (T_I, T_E,RR, T_I/T_tot, V_T, V_E, V_T/T_I) and arterial blood-gas tensionswere measured in air and during a 10-min period of 100% oxygenbreathing. For both rates of Althesin infusion the ventilatoryresponse to oxygen was identical: there was significant depressionof ventilation (decrease in V_E and of the ventilatory drive,V_T/T_I) from the 1st min of inhalation lasting up to the 10thmin. This decrease in ventilation was more marked and persistentthan the decrease noticed in the unanaesthetized dog. We concludethat the hypoxic ventilatory drive persists in the dog underAlthesin anaesthesia.     

Low-dose remifentanil to suppress haemodynamic responses to noxious stimuli in cardiac surgery: a dose-finding study

Background: High-dose remifentanil (1–5 µg kg^–1 min^–1),commonly used for cardiac surgery, has been associated withmuscle rigidity, hypotension, bradycardia, and reduced cardiacoutput. The aim of this study was to determine an optimal lowerremifentanil dose, which should be accompanied by fewer adverseevents, that still effectively suppresses haemodynamic responsesto typical stressful stimuli (i.e. intubation, skin incision,and sternotomy). Methods: Total i.v. anaesthesia consisted of a target-controlled propofol(2 µg ml^–1) and a remifentanil infusion. Forty patientswere allocated to receive either a constant infusion of remifentanilat 0.1 µg kg^–1 min^–1 or up-titrations to 0.2,0.3, or 0.4 µg kg^–1 min^–1, respectively, 5min before each stimulus. Subsequently, changes in heart rateand mean arterial blood pressure were recorded for 8 min. Increasesexceeding 20% of baseline were considered to be of clinicalrelevance. Patients who exhibited these alterations were termedresponders. Results: The number of responders was less with the two higher remifentanildosages (P < 0.05) while propofol target doses could eitherbe kept at the same level or even be reduced without affectingthe plane of anaesthesia. Although single phenylephrine bolushad to be applied more frequently in these two groups (P <0.05), no severe haemodynamic depression was observed. Conclusions: Remifentanil at 0.3 and 0.4 µg kg^–1 min^–1in combination with a target-controlled propofol infusion inthe pre-bypass period is well tolerated. It appears to mitigatepotentially hazardous haemodynamic responses from stressfulstimuli equally well as higher doses when compared with datafrom the literature.     

RENAL TISSUE OXYGENATION FOLLOWING INDUCED HYPOTENSION IN DOGS

Renal oxygenation was studied during indnrrd hypotension inmongrel dogs, anaesthetized with 1–1.5% halothane in oxygen.Hypotension was induced with an infusion i.v. of sodium nitroprusside(SNP) 70±l7 µg kg-1^–1min^–1 (mean±SEM)or trimetaphan (TMP) 36±16 µg kg^–1min^–1,or by controlled arterial haemorrhage (45±6 ml/kg ofbody weight). Mean arterial pressure (MAP), cortical (Pct₂)and medullary (Pmt_O2) tissue oxygen tensions, arterial (Pa_O2),renal venous (Prv_O2), and urine Pu_O2) oxygen tensions were measuredduring the 40-min control, hypotension, and recovery periods.MAP was decreased to approximately 60% of the control value,Pct_O2 decreased significantly (P<0.05) in all three groupswhile Pmt_O2 decreased significantly only in the haemorrhagegroup. Upon restoration of MAP to normal values, renal tissueoxygen tensions recovered in all groups, somewhat more rapidlyin the SNP group. There were no significant differences in Pa_O2,Prv_O2 and PuO₂ during control, hypotension and recovery periodsin the three groups. Tissue oxygen tension values followed thechanges in MAP; but were not hypoxic, leading us to believethat both SNP and TMP are hypotensive agents safe for the kidney     

Propofol-alfentanil vs propofol-remifentanil for posterior spinal fusion including wake-up test

Background. Wake-up test can be used during posterior spinalfusion (PSF) to ensure that spinal function remains intact.This study aims at assessing the characteristics of the wake-uptest during propofol–alfentanil (PA) vs propofol–remifentanil(PR) infusions for PSF surgery. Methods. Sixty patients with scoliosis and candidates for PSFsurgery were randomly allocated in either alfentanil (PA) orremifentanil (PR) group. After an i.v. bolus of alfentanil 30µg kg^–1 in the PA group or remifentanil 1 µgkg^–1 in the PR group, anaesthesia was induced with thiopentaland atracurium. During maintenance, opioid infusion consistedof alfentanil 1 µg kg^–1 min^–1 or remifentanil0.2 µg kg^–1 min^–1, in the PA group and thePR group, respectively. All patients received propofol 50 µgkg^–1 min^–1. Atracurium was given to maintain therequired surgical relaxation. At the surgeon's request, allinfusions were discontinued. Patients were asked to move theirhands and feet. Time from anaesthetic discontinuation to spontaneousventilation (T₁), and from then until movement of the handsand feet (T₂), and its quality were recorded. Results. The average T₁ and T₂ were significantly shorter inthe PR group [3.6 (2.5) and 4.1 (2) min] than the PA group [6.1(4) and 7.5 (4.5) min]. Quality of wake-up test, however, didnot show significant difference between the two groups studied. Conclusion. Wake-up test can be conducted faster with remifentanilcompared with alfentanil infusion during PSF surgery.     

DEPRESSION OF HYPOXIC PULMONARY VASOCONSTRICTION IN THE DOG BY DOPAMINE AND ISOPRENALINE

The effects of dopamine and isoprenaline on the pulmonary vasoconstrictorresponse to alveolar hypoxia were assessed by measuring theredistribution of blood flow between the lungs in response tounilateral hypoxia. Dose rates of dopamine 25 µg kg^–1min^–1 and isoprenaline 0.25 µg kg^–1 min^–1(which produced equal increments in the contractile force ofthe heart in dogs) produced a similar degree of depression ofthe hypoxic vasoconstrictor response, whereas dopamine 2.5 µgkg ^–1 min^–1 had little effect on the response. Pa_O2during unilateral hypoxia was inversely related to the bloodflow through the hypoxic lung.     

CARDIOVASCULAR AND RENAL HEMODYNAMIC EFFECTS OF DOPEXAMINE: COMPARISON WITH DOPAMINE

We have studied the effects of dopexamine and dopamine on systemicand renal haemodynamics in 20 male patients undergoing electivecoronary artery bypass surgery. Patients were allocated randomlyto two groups (n = 10) who were treated with incremental dosesof either dopexamine 1, 2 and 4 µg kg^–1 min^–1,or dopamine 2.5 and 5 µg kg^–1 min^–1, eachdose being maintained for 15 min. Measurements were performedbefore administration of the drug and at the end of the infusionperiod at each dose. Fentanyl and midazolam were used as anaestheticagents. Renal blood flow was measured with the argon washintechnique. Dopexamine 4 µg kg^–1 min^–1 producedan increase in cardiac index of 117% caused by a 65% reductionin afterload and an increase in heart rate by 61%. Dopamine5 µg kg^–1 min^–1 caused a 40% increase in cardiacindex as a result of an increase in stroke volume. Renal vascularresistance decreased more than systemic vascular resistancewith dopamine. With dopexamine, the increase in renal bloodflow (66%) was less than the increase in cardiac index, whilerenal vascular resistance and systemic vascular resistance declinedto almost the same extent. The results show that dopexamineexerts systemic and renal effects mainly via stimulation ofß₂-receptors. An action of dopexamine at renal DA₁-receptorscould not be demonstrated in this study.     

Haemodynamic effects of haemorrhage during xenon anaesthesia in pigs

Background. It was hypothesized that xenon would stabilize meanarterial pressure (MAP) in haemorrhagic shock, recovery, andvolume resuscitation, because a higher MAP has been observedwith xenon, when compared with isoflurane anaesthesia. The responsesto haemorrhage and subsequent volume replacement were thereforecompared between xenon and isoflurane anaesthesia, in pigs. Methods. Pigs were randomized to anaesthesia with xenon 0.55MAC (group Xe, n=9) or isoflurane 0.55 MAC (group Iso, n=9),each with remifentanil 0.5 µg kg^–1 min^–1.MAP, heart rate, cardiac output (CO), and left ventricular fractionalarea change (FAC) were collected at control (1), after haemorrhage(20 ml kg^–1) (2), after 10 min of recovery (3), aftervolume replacement (4), and 30 min later (5). Data were analysedby two-way repeated measures ANOVA. Results. Blood loss decreased MAP (Xe: 103 [21] to 53 [24] mmHg; Iso: 92 [18] to 55 [14] mm Hg) and CO (Xe: 4.1 [0.8] to2.6 [0.5] litre min^–1; Iso: 5.1 [1.1] to 3.8 [1.2] litremin^–1), in spite of significant tachycardia. MAP and COrecovered to about 75% of control, and subsequent volume replacementcompletely reversed symptoms in both groups, but increased FAConly with xenon. Conclusion. Haemodynamic response to acute haemorrhage appearedfaster with xenon/remifentanil than with isoflurane/remifentanilanaesthesia. In particular MAP decrease and short-term recoverywere more marked with xenon (P<0.02). In the xenon group,volume replacement increased FAC compared with control and isoflurane(P<0.02).     

Does the optimization of cardiac output by fluid loading increase splanchnic blood flow?

We studied the effects of increasing cardiac output by fluidloading on splanchnic blood flow in patients with haemodynamicallystabilized septic shock. Eight patients (five female, 39–86yr) were assessed using a transpulmonary thermo-dye-dilutiontechnique for the measurement of cardiac index (CI) intrathoracicblood volume (ITBV) as a marker of cardiac preload and totalblood volume (TBV). Splanchnic blood flow was measured by thesteady state indocyanine-green technique using a hepatic venouscatheter. Gastric mucosal blood flow was estimated by regionalcarbon dioxide tension (PR_CO2). Hydroxyethyl starch was infusedto increase cardiac output while mean arterial pressure waskept constant. In parallel, mean norepinephrine dosage couldbe reduced from 0.59 to 0.33 µg kg^–1 min^–1.Mean (SD) TBV index increased from 2549 (365) to 3125 (447)ml m^–2, as did ITBV index from 888 (167) to 1075 (266)ml m^–2 and CI from 3.6 (1.0) to 4.6 (1.0) litre min^–1m^–2. Despite marked individual differences, splanchnicblood flow did not change significantly neither absolutely (from1.09 (0.96) to 1.19 (0.91) litre min^–1 m^–2) norfractionally as part of CI (from 28.4 (19.5) to 24.9 (16.3)%).Gastric mucosal PR_CO2 increased from 7.7 (2.6) to 8.3 (3.1)kPa. The PCO₂-gap, the difference between regional and end-tidalPCO₂, increased slightly from 3.2 (2.7) to 3.4 (3.1) kPa. Thus,an increase in cardiac output as a result of fluid loading isnot necessarily associated with an increase in splanchnic bloodflow in patients with stabilized septic shock. Br J Anaesth 2001; 86: 657–62     

DOSE REQUIREMENTS OF PROPOFOL BY INFUSION DURING NITROUS OXIDE ANAESTHESIA IN MAN: II: Patients Premedicated with Lorazepam

The infusion rate of propofol required to supplement 67% nitrousoxide in oxygen to maintain surgical anaesthesia was determinedin 72 patients premedicated with lorazepam. Following an inductiondose of propofol 2 mg kg^–1, groups of eight patients receivedan infusion of propofol varying from 60 to 200 µg kg^–1.Probit analysis was used to determine the ED₅₀ (130 µgkg^minus;1 min^–1; 95% confidence limits: 106–167µg kg^–1 min^–1) and ED₉₅ (348 µg kg^–1min^–1; 95% confidence limits: 233–1296 µgkg^–1 min^–1;) for propofol infusion. Whole bloodpropofol concentrations at the time of surgical incision correlatedstrongly with the infusion rate, giving an EC₅₀ value of 2.5µg ml ^–1, and an EC₉₅ value of 5.92 µg ml^–1.There was no significant correlation between the rate of infusionof propofol, or the total propofol dose, and the times to responseto command, or to recall of birthdate.     

CONTINUOUS INFUSION OF MIVACURIUM IN CHILDREN

Mivacurium is a new short-acting competitive neuromuscular blockingagent. Infusion requirements for the maintenance of a stable90–99% muscle twitch depression were determined in 28children anaesthetized with nitrous oxide and 1% halothane (inspired)in oxygen or nitrous oxide in oxygen and opioid. Neuromuscularblock was assessed by monitoring the force of contraction ofthe adductor of the thumb during train-of-four (TOF) stimulationat 0.1 Hz. Infusion rate and twitch depression were analysedfrom 15 to 75 min and from 75 to 135 min after the start ofthe infusion. In the first period of evaluation, the mean infusionrequirement was 10.4 (SEM 0.92) µg kg^–1 min^–1during the halothane anaesthesia and 13 (1.4) µg kg^–1min^–1 during the opioid anaesthesia (P < 0.05). Thisdifference was present also during the second 60-min period.There was no significant correlation between infusion ratesrequired to maintain > 90% depression of the first twitch(T1) of the TOF and plasma cholinesterase concentrations. Regardlessof the anaesthetic regimen, children recovered rapidly afterdiscontinuing the infusion. The recovery index (25–75% recovery of T1) for all patients was 5.4 (0.57) min with nosignificant differences between the groups.     

EFFECT OF VERAPAMIL ON CANINE LEFT VENTRICULAR FUNCTION IN THE PRESENCE OF FENTANYL WHEN APICAL BLOOD FLOW IS CRITICALLY LIMITED

Instruments were inserted to seven dogs under halothane anaesthesia,to measure global and regional left ventricular function. Anaesthesiawas continued with fentanyl (100 µg kg^–1 bolus,then 1.5 µg kg^–1 min^–1). Critical constrictionwas applied to the left anterior descending coronary artery.Control recordings were made, followed by bolus administrationof verapamil 0.08, 0.16 and 0.32 mg kg^–1, with recordings10 min after each bolus. At the highest dose, verapamil decreasedsystemic arterial pressure, left ventricular dP/dt, stroke volumeand systemic vascular resistance, and increased heart rate significantly.Coronary perfusion pressure decreased and, in the presence ofcritical constriction, coronary flow per beat decreased significantly.In the region with constriction, systolic shortening of myocardiumdecreased and post-systolic shortening increased significantlywith addition of verapamil. The addition of a high dose of verapamilto fentanyl anaesthesia caused reduction in systolic functionand development of early diastolic dysfunction in myocardiumwith critically limited blood supply.     

Early recovery after remifentanil-pronounced compared with propofol-pronounced total intravenous anaesthesia for short painful procedures

Background. We compared recovery from high-dose propofol/low-doseremifentanil (‘propofol-pronounced’) compared withhigh-dose remifentanil/low-dose propofol (‘remifentanil-pronounced’)anaesthesia. Methods. Adult patients having panendoscopy, microlaryngoscopy,or tonsillectomy were randomly assigned to receive either propofol-pronounced(propofol 100 µg kg^–1 min^–1; remifentanil0.15 µg kg^–1 min^–1) or remifentanil-pronounced(propofol 50 µg kg^–1 min^–1; remifentanil 0.45µg kg^–1 min^–1) anaesthesia. In both groups,the procedure was started with remifentanil 0.4 µg kg^–1,propofol 2 mg kg^–1, and mivacurium 0.2 mg kg^–1.Cardiovascular measurements and EEG bispectral index (BIS) wererecorded. To maintain comparable anaesthetic depth, additionalpropofol (0.5 mg kg^–1) was given if BIS values were greaterthan 55 and remifentanil (0.4 µg kg^–1) if heartrate or arterial pressure was greater than 110% of pre-anaestheticvalues. Results. Patient and surgical characteristics, cardiovascularmeasurements, and BIS values were similar in both groups. Therewere no differences in recovery times between the groups (timeto extubation: 12.7 (4.5) vs 12.0 (3.6) min, readiness for transferto the recovery ward: 14.4 (4.4) vs. 13.7 (3.6) min, mean (SD)). Conclusions. In patients having short painful surgery, lesspropofol does not give faster recovery as long as the same anaestheticlevel (as indicated by BIS and clinical signs) is maintainedby more remifentanil. However, recovery times were less variablefollowing remifentanil-pronounced anaesthesia suggesting a morepredictable recovery. Br J Anaesth 2003; 91: 580–2