Pre-emptive lidocaine inhibits arterial vasoconstriction but not vasopressin release induced by a carbon dioxide pneumoperitoneum in pigs

Background. We assessed the preventive effects of i.v. or i.p.lidocaine administration on increases in vascular resistanceproduced by carbon dioxide pneumoperitoneum and related thisto vasopressin release. Methods. Carbon dioxide pneumoperitoneum (14 mm Hg intra-abdominalpressure) was performed in 32 anaesthetized young pigs and monitoredusing a pulmonary artery catheter. Animals received lidocaine0.5% (0.5 mg kg^–1) i.v. (n=9) or 2 ml kg^–1 i.p.(n=9) or saline (n=5) 15 min before the pneumoperitoneum andwere compared with a control group (n=9). Results. I.V. and i.p. lidocaine inhibited increases in meansystemic vascular resistance induced by the pneumoperitoneum[2109 (SD 935) and 2282 (895), respectively, vs 3013 (1067)dyne s^–1 cm^–5 in the control group]. Cardiac outputwas increased. Plasma lidocaine concentrations were threefoldhigher after i.p. administration than after i.v. administration.After pneumoperitoneum insufflation, plasma lysine-vasopressinconcentrations increased in all groups (control 74%, saline65%, i.p. lidocaine 57%, i.v. lidocaine 74%). Conclusions. I.V. and i.p. lidocaine blunted systemic vascularresponses to carbon dioxide pneumoperitoneum in pigs, but withoutinfluencing vasopressin release. Br J Anaesth 2003; 90: 343–8     

Comparison of ocular microtremor and bispectral index during sevoflurane anaesthesia

Background. A practical and reliable monitor of depth of anaesthesiawould be a major advance on current clinical practice. Noneof the present monitors is both simple to use and accurate.Ocular microtremor (OMT) is a physiological tremor that is suppressedby propofol in a dose-dependent manner. We studied OMT duringpropofol induction and nitrous oxide– oxygen–sevofluranemaintenance of anaesthesia in 30 patients, and compared OMTwith the bispectral index (BIS) as a predictor of response toverbal command. Methods. OMT was measured using the closed-eye piezoelectricstrain-gauge technique. OMT and BIS were measured at specifictimes during the anaesthetic, including at loss of consciousness,at end-tidal sevoflurane 1 and 2%, and at emergence. Results. OMT decreased significantly after induction, did notdecrease as end-tidal sevoflurane was increased from 1 to 2%,and increased at emergence in all patients. By logistic regression,OMT was more sensitive and specific than BIS in distinguishingthe awake from the anaesthetized state (OMT, 84.9 and 93.1%respectively; BIS, 75.7 and 69.0%). Conclusions. OMT is suppressed by sevoflurane and accuratelypredicts response to verbal command. OMT may be a useful monitorof depth of hypnosis. Br J Anaesth 2002; 89; 551–5     

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.     

Effects of sevoflurane on sympathetic neurotransmission in human omental arteries and veins

Background. Sevoflurane reduces blood pressure, the regulationof which requires an intact sympathetic neurotransmission. Thisstudy was designed to evaluate the effect of sevoflurane onthe coupling between peripheral sympathetic neurones and vascularsmooth muscle in isolated human omental vessels. Methods. Segments of arteries and veins were exposed to sevoflurane1%, 2% and 4% (corresponding to approximately 0.5, 1 and 2 MACin humans, respectively). The vessels were studied in vitroto determine the effects on (i) isometric contraction duringelectrical field stimulation (EFS) or in the presence of exogenousnorepinephrine (NE); (ii) electrical field stimulated releaseof [³H]-NE from vessel segments previously incubated with [³H]-NE;(iii) uptake of [³H]-NE. Results. In artery segments, sevoflurane 4% attenuated the contractioninduced by both EFS and exogenous NE. In vein segments, sevoflurane4% attenuated only the EFS-induced contractions. Sevoflurane1% and 2% had no effect. The release of [³H]-NE was inhibitedby sevoflurane 2% and 4% in arteries and by sevoflurane 1%,2% and 4% in veins. Sevoflurane had no effect on the uptakeof [³H]-NE in either vessel. Conclusions. Sevoflurane depresses sympathetic neuromusculartransmission in human omental vessels by reducing neuronal NErelease and NE sensitivity in arteries and by reducing NE releasein veins. This could contribute to the hypotension seen duringsevoflurane anaesthesia, at least at concentrations above 1MAC. Br J Anaesth 2003; 90: 766–73     

Comparison of desflurane with sevoflurane for the incidence of oculocardiac reflex in children undergoing strabismus surgery

Background: The oculocardiac reflex (OCR) is frequently observed duringstrabismus surgery. This study was designed to evaluate andcompare the effect of sevoflurane and desflurane on the incidenceof OCR. Methods: After obtaining Institutional Review Board approval and informedconsent from parents, we enrolled 237 paediatric patients, aged2–10 yr, undergoing strabismus surgery. No premedicationwas given. Anaesthesia was induced with thiopental and rocuronium.Patients were randomly allocated to one of the two anaestheticregimens. Group S (n = 123) received sevoflurane and Group D(n = 114) received desflurane, both with 60% N₂O/O₂ for maintenanceof anaesthesia. The OCR was defined as a 20% decrease in heartrate (HR) from baseline values obtained immediately before musclemanipulation. If the HR did not increase after release of muscletension, atropine 0.01 mg kg^–1 was administered. Results: There were no significant differences between the two groupsin age, sex, body weight, and the number of muscles operatedupon. The mean values of baseline HR were 123 (16) min^–1in Group S and 121 (18) in Group D (NS). The minimum HR was106 (22) min^–1 in Group S and 103 (21) in Group D (NS).There was no difference in the incidence of OCR between sevoflurane(26.0%) and desflurane (28.0%) anaesthesia. Conclusions: Both agents can be used safely during strabismus surgery inpaediatric patients.     

Comparison of 1% and 2% lidocaine epidural anaesthesia combined with sevoflurane general anaesthesia utilizing a constant bispectral index

Background. The authors compared the effects of epidural anaesthesiawith lidocaine 1% and lidocaine 2% on haemodynamic variables,sevoflurane requirements, and stress hormone responses duringsurgery under combined epidural/general anaesthesia with bispectralindex score (BIS) kept within the range 40–50. Methods. Thirty-three patients undergoing lower abdominal surgerywere randomly divided into two groups to receive lidocaine 1%or 2% by epidural with sevoflurane general anaesthesia. Sevofluranewas adjusted to achieve a target BIS of 40–50 during maintenanceof anaesthesia with nitrous oxide 60% in oxygen. Measurementsincluded the inspired (FI_SEVO) and the end-tidal sevofluraneconcentrations (E'_SEVO), blood pressure (BP), and heart rate(HR) before surgery and every 5 min during surgery for2 h. Plasma samples were taken immediately before and duringsurgery for measurements of catecholamines, cortisol, and lidocaine. Results. During surgery, both groups were similar for HR, BPand BIS, but FI_SEVO and E'_SEVO were significantly higher andmore variable with lidocaine 1% than with 2%. Intraoperativeplasma concentrations of epinephrine and cortisol were foundto be higher with lidocaine 1% as compared with 2%. Conclusions. To maintain BIS of 40–50 during combinedepidural/general anaesthesia for lower abdominal surgery, sevofluraneconcentrations were lower and less variable with lidocaine 2%than with 1%. In addition, the larger concentration of lidocainesuppressed the stress hormone responses better. Br J Anaesth 2003; 91: 825–9     

Effects of propofol vs sevoflurane on arterial oxygenation during one-lung ventilation

Background: The inhibitory effect of anaesthetic agents on hypoxic pulmonaryvasoconstriction may depend upon their dose, especially whenusing a volatile agent. The aim of this randomized open studywas to compare the effects of sevoflurane and propofol, as primaryanaesthetic agents, on oxygenation during one-lung ventilation(OLV), with their administration being adjusted to maintainbispectral index (BIS) values between 40 and 60. Methods: Eighty patients scheduled for a lobectomy, receiving an epiduralmixture of ropivacaine and sufentanil, were randomly assignedto Group S (maintenance with sevoflurane) or Group P (maintenancewith propofol). After placement of a double-lumen tube, thelungs were ventilated at an inspiratory fraction of oxygen of1.0, a tidal volume of 6 ml kg^–1, and 12 bpm. Arterialblood gas samples were taken as follows: during two-lung ventilationbefore OLV, and during the first 40 min of OLV. Results: Fifteen patients were excluded (incorrect placement of the tubeor BIS outside the desired range). The two groups were comparablein terms of demographic variables, haemodynamic, and BIS levelsduring the operation. Four patients in each group had a Sp_O2<90%.Mean of the lowest Pa_O2 was 16.3 (7.5) kPa in Group S and 17.7(9.3) kPa in Group P (ns). Conclusions: Sevoflurane and propofol had similar effect on Pa_O2 during OLVwhen their administration is titrated to maintain BIS between40 and 60.     

The effect of clonidine on sevoflurane requirements for anaesthesia and hypnosis

We evaluated the effects of clonidine given orally on sevoflurane requirements for anaesthesia and hypnosis. Patients received either clonidine (5 μg.kg⁻¹) by mouth ( n  =21) 90 min before surgery or no premedication ( n  =21) by random allocation. MAC was calculated using repeated tetanic nerve stimulation with end-tidal sevoflurane concentration increased or decreased by 0.3 vol.% depending on the previous response. MAC awake was calculated according to the response to verbal command. The mean (SD) MAC in the clonidine-treated patients was 1.53 (0.20)% compared with 1.83 (0.15)% in the control group (p <0.001). Similarly, MAC awake was reduced in the clonidine group (0.50 (0.08)% compared with 0.60 (0.07)% in the control group) (p <0.001). We conclude that clonidine 5 μg.kg⁻¹ orally administered pre-operatively reduces sevoflurane requirements for anaesthesia and hypnosis.     

Entropy indices vs the bispectral index for estimating nociception during sevoflurane anaesthesia

Background. It is now possible to acquire and process raw EEGand frontal EMG signals to produce two spectral-entropy-basedindices (response entropy and state entropy) reflective of analgesicand hypnotic levels during general anaesthesia (with the Datex-OhmedaS/5 Entropy Module, Datex-Ohmeda, Helsinki, Finland). However,there are no data available on the accuracy of the Entropy Modulein estimating nociception during sevoflurane anaesthesia. Methods. Forty female patients were enrolled in the presentstudy. Each patient was allocated randomly to one of four end-tidalsevoflurane concentration (ET_sev) groups (1.3, 1.7, 2.1 or 2.5%).A BIS Sensor^TM (Aspect Medical Systems, Newton, MA) and an EntropySensor^TM (Datex-Ohmeda) were applied side-by-side to the forehead.The bispectral index (A-2000 BIS Monitor, version 3.4, AspectMedical Systems), response entropy, state entropy and patientmovement were observed after electrical stimulation (20, 40,60 and 80 mA, 100 Hz, 5 s) and after skin incision during sevofluraneanaesthesia (1.3, 1.7, 2.1 or 2.5%). Accuracy of the EEG variablesin differentiating the intensity of electrical stimulation wasestimated by the prediction probability (P_K) values. Results. Response entropy and state entropy [median, (range)]before skin incision were significantly lower in patients whodid not move [29 (15–41) and 24 (14–41)] than inthose that did [38 (24–53) and 37 (24–52)], butthere was no significant difference in BIS. All EEG variablesincreased significantly (P<0.0001 for all) with increasesin the intensity of electrical stimulation. The difference betweenresponse entropy and state entropy increased with increasesin the electrical stimulation (P<0.0001). However, no EEGvariables could differentiate the intensity of the electricalstimulations accurately because of low P_K-values (P_K<0.8). Conclusion. Noxious stimulation increased the difference betweenresponse entropy and state entropy. However, an increase inthe difference does not always indicate inadequate analgesiaand should be interpreted carefully during anaesthesia.     

Differential electroencephalographic response to tracheal intubation between young and elderly during isoflurane and sevoflurane nitrous oxide anaesthesia

BACKGROUND: Age-associated differences in the electroencephalographic (EEG) response to noxious stimuli with the presence of nitrous oxide (N(2)O) are unknown. We compared the EEG response with tracheal intubation between young and elderly. METHODS: Sixty young (<40 yr) and elderly (>70 yr) patients were randomly allocated to one of the four groups. Anaesthesia was induced with 66% N(2)O and isoflurane in oxygen (Young-isoflurane and Elderly-isoflurane groups) or 66% N(2)O and sevoflurane in oxygen (Young-sevoflurane and Elderly-sevoflurane groups). Inhaled isoflurane and sevoflurane concentrations were gradually increased and the end-tidal concentrations were maintained at 1.1% and 1.7%, respectively. Tracheal intubation was performed 12 min after induction of anaesthesia. RESULTS: There were significant differences in the overall changes in bispectral index (BIS) and 95% spectral edge frequency (SEF95) between young and elderly (P<0.001 for both), but not between patients receiving isoflurane and sevoflurane (P=0.4 and 0.3, respectively). Both BIS and SEF95 were significantly decreased after tracheal intubation in Young-isoflurane and Young-sevoflurane groups (P<0.05 for all). In sharp contrast, BIS and SEF95 remained unchanged in Elderly-isoflurane and Elderly-sevoflurane groups (P>0.7 for all). These results suggest that both BIS and SEF95 significantly decreased, despite the presence of increased sympathetic activity after tracheal intubation in young patients. CONCLUSIONS: A significant difference was detected in EEG response to tracheal intubation between young and elderly. BIS does not reflect the depth of anaesthesia after tracheal intubation during anaesthesia with isoflurane or sevoflurane with 66% of N(2)O in young patients.     

Loss of volition and pain response during induction of anaesthesia with propofol or sevoflurane

We compared the time to reach two anaesthetic end-points duringinduction of anaesthesia with a potent inhalation agent (sevoflurane)and an i.v. agent (propofol). We used a method to ensure steadybreathing during inhalation induction, and measured loss oftone in the outstretched arm and loss of response to a painfulstimulus. Thirty-eight female patients (age 39 (9) yr, weight65 (11) kg, and height 165 (8) cm) (mean (SD)) were randomlyallocated to receive either propofol or sevoflurane. The predictedinduction dose of propofol, estimated from age and weight foreach patient, was given at a rate of 1% of the induction doseper second, to a possible maximum of 2.5 times the predictedinduction dose. Sevoflurane was given with an inhaled concentrationof 8%, which was anticipated to cause loss of arm tone within90–120 s. After loss of consciousness, we applied a painfulelectrical stimulus to a finger at 15-s intervals and measuredthe time to loss of motor response. The median times and interquartilevalues for loss of arm tone were 105 (88–121) s for sevofluraneand 65 (58–80) s for propofol. This was equivalent to0.65 of the ED₅₀ of propofol. The time to loss of response topain was 226 (169–300) s for sevoflurane. The variancesof these three measurements were not significantly different,indicating that these dose–response relationships weresimilar. In contrast, only 11 of the patients given propofollost the response to pain after 2.5xED₅₀ had been given. Theseresults support previous evidence of substantial differencesbetween anaesthetic end-points, and show that this evidencecan be obtained using a simple and rapid method. Br J Anaesth 2001; 87: 283–6     

Blood/gas partition coefficients of halothane,isoflurane and sevoflurane in horse blood

Background. Blood/gas partition coefficients (_b/g) for volatileagents in horse blood are reported for halothane but not forisoflurane and sevoflurane. We measured the _b/g of halothane,isoflurane and sevoflurane in the blood of fasted horses. Thecorrelation with age, weight and some haematological and biochemicalvariables was studied. The temperature correction factor forisoflurane solubility was calculated. Methods. Twenty-four horses were randomly allocated to halothane(n=8), isoflurane (n=8) or sevoflurane (n=8). Blood sampleswere taken after 10 h’ fasting. Calculation of _b/g wasbased on the measurement of anaesthetic partial pressures inblood at 37 °C, which was achieved with tonometer equilibrationand headspace gas chromatography. Results. Mean _b/g was 1.66 (SD 0.06) for halothane, 0.92 (0.04)for isoflurane, and 0.47 (0.03) for sevoflurane. The _b/g valueswere all significantly lower than in humans (P<0.001). Nocorrelation was found between _b/g and weight, age, haematocrit,plasma triglycerides, cholesterol or total bilirubin. The changein isoflurane solubility per 1 °C temperature increase was–2.63 (0.13)%. Conclusion. The _b/g values of halothane, isoflurane and sevofluranein fasted horses are significantly lower than those reportedin humans. The _b/g for halothane in this study agrees with valuesreported in the literature but a positive correlation with plasmatriglycerides could not be confirmed. Knowledge of _b/g can refinemodels of anaesthetic uptake. Br J Anaesth 2003; 91: 276–8     

Effects of different concentrations of sevoflurane and desflurane on subcortical somatosensory evoked responses in anaesthetized, non-stimulated patients

Twenty-four patients were recruited and given either sevofluraneor desflurane as their sole anaesthetic. Each patient was givensequentially increasing or decreasing doses at 0.5 MAC intervals,and the median nerve somatosensory evoked response recordedafter an equilibration at each concentration. The N₂₀-P₂₅ andP₂₅-N₃₅ amplitudes decreased with increasing agent concentration.However, for both agents the P₁₅-N₂₀ amplitude response wasquadratic in shape. The peak inflection points were at 3.2%for sevoflurane and 4.9% for desflurane. There were no differencesbetween the ascending and descending groups. This increase inactivity in the midbrain at ‘surgical’ end-tidalanaesthetic concentrations suggests more complex neuroelectricalresponses to anaesthesia than simple global suppression. Br J Anaesth 2001; 86: 59–62     

Effects of sevoflurane on dopamine, glutamate and aspartate release in an in vitro model of cerebral ischaemia

Release of excitatory amino acids and dopamine plays a centralrole in neuronal damage after cerebral ischaemia. In the presentstudy, we used an in vitro model of ischaemia to investigatethe effects of sevoflurane on dopamine, glutamate and aspartateefflux from rat corticostriatal slices. Slices were superfusedwith artificial cerebrospinal fluid at 34°C and episodesof ‘ischaemia’ were mimicked by removal of oxygenand reduction in glucose concentration from 4 to 2 mmol litre^–1for     

Comparison of the effects of sevoflurane and propofol on cooling and rewarming during deliberate mild hypothermia for neurosurgery

Background. Because the time available for cooling and rewarmingduring deliberate mild hypothermia is limited, studies of therate of the cooling and rewarming are useful. The decrease incore hypothermia caused by heat redistribution depends on theanaesthetic agent used. We therefore investigated possible differencesbetween sevoflurane and propofol on the decrease and recoveryof core temperature during deliberate mild hypothermia for neurosurgery. Methods. After institutional approval and informed consent,26 patients were assigned randomly to maintenance of anaesthesiawith propofol or sevoflurane. Patients in the propofol group(n=13) received propofol induction followed by a continuousinfusion of propofol 3–5 mg kg^–1 h^–1.Patients in the sevoflurane group (n=13) received propofol inductionfollowed by sevoflurane 1–2%. Nitrous oxide and fentanylwere also used for anaesthetic maintenance. After inductionof anaesthesia, patients were cooled and tympanic membrane temperaturewas maintained at 34.5°C. After surgery, patients were activelyrewarmed. Results. There was no difference in the rate of decrease andrecovery of core temperature between the groups. There was alsono difference in skin surface temperature gradient (forearmto fingertip), heart rate and mean arterial blood pressure betweenthe groups. Conclusions. Sevoflurane-based anaesthesia did not affect coolingand rewarming for deliberate mild hypothermia compared withpropofol-based anaesthesia. Br J Anaesth 2003; 90: 32–8     

Analysis of the composition of 'original' and generic sevoflurane in routine use

BACKGROUND: Original sevoflurane (Sevofrane) contains a small amount of water, which can inhibit the production of hydrofluoric acid. Hydrofluoric acid is highly pungent, and sevoflurane that contains a high concentration of hydrofluoric acid is not suitable for volatile induction of anaesthesia. Recently, generic sevoflurane (Sevoness) has become available in some countries. The generic product is produced by a different method and kept in a different kind of bottle. We questioned whether the original and generic sevoflurane differed in their composition and thus might differ in their resistance to degradation. METHODS: Sevoflurane from groups of three bottles of Sevofrane and three bottles of Sevoness was kept in the bottle at 24-37 degrees C for 2 weeks or in two kinds of vaporizer for 3 days, and the resulting contents measured by gas chromatography. RESULTS: Both products contained sevoflurane concentrations exceeding 99.998%. Fluoride ion concentration did not differ between the products (0.043 ppm). The original sevoflurane contained more (0.07% w/v) water than the generic anaesthetic (0.003% w/v). Original sevoflurane contained 5 ppm compound A, 10 ppm sevomethylether, and 5 ppm of unknown materials. Generic sevoflurane contained 32 ppm hexafluoroisopropanol and 12 ppm of unknown materials. While stored in a vaporizer for 3 days, the water content in the original sevoflurane decreased by two-thirds but the water in the generic sevoflurane increased by a factor of three-fold. CONCLUSIONS: Generic sevoflurane contains high-quality sevoflurane and only a small amount of fluoride ions, making it comparable with the original sevoflurane product.     

Effects of chronic angiotensin II receptor antagonist and angiotensin-converting enzyme inhibitor treatments on neurohormonal levels and haemodynamics during cardiopulmonary bypass

Background. Chronic treatment with renin-angiotensin system(RAS) antagonists frequently causes deleterious hypotensionduring anaesthesia. We compared the effects of angiotensin IIreceptor antagonists (ARA) and angiotensin-converting enzymeinhibitors (ACEI) on neurohormonal levels and haemodynamicsduring cardiopulmonary bypass (CPB). Methods. Forty-four patients undergoing mitral valvular surgerywho were treated with either ARA (ARA group, n=14) or ACEI (ACEIgroup, n=15) over 12 weeks or who were not treated with anyRAS antagonist (control group, n=15) were enrolled. The plasmalevels of epinephrine, norepinephrine, arginine vasopressin(AVP) and angiotensin II, and haemodynamic variables were measuredbefore (T1) and 15 min after (T2) the start of CPB, before aorticunclamping (T3) and at skin closure (T4). Mean arterial pressure(MAP) was maintained above 60 mm Hg with phenylephrine administrationduring CPB. Results. The plasma epinephrine, norepinephrine, AVP and angiotensinII levels increased during CPB in all groups. Compared withthe control group, the AVP level was lower at T1 in the ARAgroup and at T2 in the ARA and ACEI groups. The angiotensinII level was higher at T1, T2 and T3 in ARA group compared withACEI and control groups. There were no significant differencesin the epinephrine and norepinephrine levels among the threegroups. The amount of administered phenylephrine during CPBwas greater and MAP was lower in the ARA group compared withthe ACEI and control groups. Conclusions. Chronic ARA treatment resulted in more profoundhypotension than ACEI treatment during CPB, and this may beassociated with the blockade of angiotensin II receptors byARA.      

Sex and oestrous cycle differences in visceromotor responses and vasopressin release in response to colonic distension in male and female rats anaesthetized with halothane{dagger}

Visceromotor responses and vasopressin release before and aftercolonic visceral distension were compared between male (n=5(n=4 for vasopressin)) and female rats and between females duringthe oestrous cycle (proestrus n=6, oestrus n=5, metestrus n=5,diestrus n=6) at a controlled depth of anaesthesia. Pre-stimulationvasopressin and blood pressures demonstrated oestrous cyclevariability. The mean (SEM) colonic balloon pressure triggeringvisceromotor responses was significantly higher in males (64(4) mm Hg) than females (41 (1) mm Hg), P=0.002 and within females,proestrus rats had the lowest thresholds, (29 (1) mm Hg, P<0.01).Post-stimulation, vasopressin concentrations increased significantlyin all groups (males 1.34 (0.39) to 2.24 (0.74) pmol litre^–1;females 1.54 (0.24) to 2.88 (0.58) pmol litre^–1; P=0.002).Within groups statistically significant differences were measuredin proestrus 2.06 (0.56) to 3.42 (1.12) and oestrus 1.16 (0.38)to 2.76 (0.60) pmol litre^–1 (P<0.05). High vasopressinconcentrations coupled with low-pressure stimulation duringproestrus shows sex-hormone dependent integration of the neuroendocrineresponse to noxious visceral stimulation. Br J Anaesth 2000; 85: 907–10     

Effect of nitrous oxide on cerebrovascular reactivity to carbon dioxide in children during sevoflurane anaesthesia

Background. Sevoflurane and nitrous oxide have intrinsic cerebralvasodilatory activity. To determine the effects of nitrous oxideon cerebrovascular reactivity to carbon dioxide (CCO₂R) duringsevoflurane anaesthesia in children, middle cerebral arteryblood flow velocity (V_mca) was measured over a range of end-tidalcarbon dioxide concentrations (E'_CO2), using transcranial Doppler(TCD) ultrasonography. Methods. Ten children aged 1.5–6 yr were anaesthetizedwith sevoflurane and received a caudal block. Patients wereallocated randomly to receive either air–nitrous oxideor nitrous oxide–air. Further randomization determinedthe sequence of E'_CO2 (25, 35, 45, and 55 mm Hg) and sevoflurane(1.0 then 1.5 MAC or 1.5 then 1.0 MAC) concentrations. Oncesteady state had been reached, three measurements of V_mca, meanarterial pressure (MAP), and heart rate (HR) were recorded. Results. Cerebrovascular carbon dioxide reactivity was reducedin the 25–35 mm Hg E'_CO2 range on the addition of nitrousoxide to 1.5 MAC, but not 1.0 MAC sevoflurane. A plateau inCCO₂R of 0.4–0.6% per mm Hg was seen in all groups betweenE'_CO2 values of 45 and 55 mm Hg. Mean HR and MAP remained constantthroughout the study period. Conclusions. Cerebrovascular carbon dioxide reactivity is reducedat and above an E'_CO2 of 45 mm Hg during 1.0 and 1.5 MAC sevofluraneanaesthesia. The addition of nitrous oxide to 1.5 MAC sevofluranediminishes CCO₂R in the hypocapnic range. This should be takeninto consideration when hyperventilation techniques for reductionof brain bulk are being contemplated in children with raisedintracranial pressure. Br J Anaesth 2003; 91: 190–5