Haemodynamic effects of induction of general anaesthesia with propofol during epidural anaesthesia

PURPOSE: To clarify whether propofol administration during thoracic or lumbar epidural anaesthesia intensifies the haemodynamic depression associated with epidural anaesthesia. METHODS: Patients (n = 45) undergoing procedures of similar magnitude were randomly divided into three study groups: a control group (n = 15) receiving general anaesthesia alone and two study groups undergoing thoracic (n = 15) and lumbar epidural anaesthesia (n = 15) before induction of general anaesthesia. All patients received 2 mg.kg-1 propofol at a rate of 200 mg.min-1, followed by a continuous infusion of 4 mg.kg-1.hr-1. Mean arterial blood pressure (MAP) and heart rate (HR) were measured at baseline, three minutes after induction, and one minute after tracheal intubation in all three groups and at 20 min after epidural anaesthesia was established in the thoracic and lumbar groups. RESULTS: Following epidural anaesthesia, MAP decreased from 94 +/- 14 (SD) at baseline to 75 +/- 11 mmHg (P < 0.0001) in the thoracic group and from 92 +/- 12 to 83 +/- 15 mmHg in the lumbar group. After propofol administration, MAP decreased further in the thoracic group to 63 +/- 9 mmHg (P = 0.0077) and to 67 +/- 10 mmHg (P = 0.0076) in the lumbar group. The MAP following propofol induction in the thoracic group (P < 0.0001) and in the lumbar group (P = 0.0001) was lower than MAP in the control group (81 +/- 9 mmHg). HR decreased only in response to thoracic epidural anaesthesia (P = 0.0066). CONCLUSION: The hypotensive effects of propofol are additive to those of epidural anaesthesia, resulting in a profound decrease in mean arterial pressure.     

Halothane, enflurane and isoflurane anaesthesia for adenoidectomy in children, using two different premedications

In 48 children subjected to adenoidectomy, comparisons of airway problems, heart rates, cardiac arrhythmias, ventilation and stress hormone reactions were studied during halothane, enflurane and isoflurane anaesthesia. Sixteen children were anaesthetized with either of the three agents and eight patients in each group received diazepam 0.25 mg kg-1 and atropine 0.015 mg kg-1 rectally (DA) as premedication and the remainder diazepam 0.5 mg kg-1, morphine 0.15 mg kg-1 and scopolamine 0.01 mg kg-1 (DMS) rectally. All children were intubated and breathing spontaneously. Equianaesthetic inspired concentrations of halothane, enflurane and isoflurane were used. Airway problems were of the same magnitude during halothane and isoflurane anaesthesia but were less frequent with both agents compared with enflurane anaesthesia. DMS reduced the number of airway reactions in all groups. Respiratory rates were uninfluenced by anaesthesia, intubation and surgery during enflurane anaesthesia. Cardiac arrhythmias were less frequent with enflurane and isoflurane than with halothane. Plasma ACTH and cortisol were similar with all three agents. During induction of anaesthesia in the DA-premedicated halothane group, however, plasma catecholamines were higher than in the group which received DMS, in contrast to the findings during enflurane and isoflurane anaesthesia. The DMS premedication decreased the response of plasma ACTH, cortisol and plasma catecholamines to surgery.     

Atropine vs Glycopyrrolate During Reversal of Pancuronium Block in Patients Anaesthetized with Halothane

Atropine 0.015 mg kg-1 and glycopyrrolate 0.0075 mg kg-1 were compared as antimuscarinic agents during reversal of pancuronium block with neostigmine 0.03 mg kg-1 in 30 patients anaesthetized with thiopental-N2O-halothane and undergoing minor surgery. In patients treated with atropine-neostigmine, the frequencies of bradycardia and junctional rhythm were relatively high and about the same as those reported by us previously in patients anaesthetized with thiopental-N2O-fentanyl. As in our previous study, glycopyrrolate seemed to have advantages over atropine during reversal of pancuronium block: the incidences of bradycardia and junctional rhythm were significantly less in patients treated with glycopyrrolate. Recovery from anaesthesia, as assessed by the awakening after discontinuation of N2O and halothane administration, and the incidence of postoperative nausea and vomiting, were not significantly different between the atropine and glycopyrrolate groups.     

Effects of dopamine on intestinal hemodynamics and motility during epidural analgesia in the cat

The effects of dopamine on intestinal blood flow (IBF) and intestinal contraction rate (ICR), and on mean arterial pressure (MAP) and heart rate (HR) were studied in eight cats before and during epidural analgesia (EDA). Before EDA, dopamine 5 and 10 micrograms.kg-1.min-1 had no effect on IBF, MAP and HR, but the higher infusion rate decreased ICR by 71 +/- 19% (mean +/- 1 s.e.mean) (P less than 0.01). EDA significantly increased IBF when intestinal arterial pressure was maintained at an unchanged level by means of a pump, and transiently increased ICR and intestinal tone, but reduced MAP by 46 +/- 8% (139 +/- 11 to 75 +/- 9 mmHg, P less than 0.01) and HR by 26 +/- 3% (248 +/- 7 to 184 +/- 8 beats.min-1, P less than 0.01). During EDA, dopamine increased IBF further, the response being similar at both infusion rates. 5 micrograms.kg-1.min-1 increased HR by 26 +/- 7 beats.min-1 (P less than 0.01) and MAP by 19 +/- 9 mmHg (ns). The corresponding values at 10 micrograms.kg-1.min-1 were 65 +/- 14 beats.min-1 (P less than 0.01) and 35 +/- 8 mmHg (P less than 0.01), respectively, Vascular autoregulation appeared to be unaffected by dopamine and EDA. The effect of dopamine on ICR was not significantly different to what was seen before EDA. It is concluded that the effects of dopamine on IBF, MAP and HR were markedly different during EDA as compared to before the block and that ICR was reduced by dopamine, while it was transiently increased by EDA.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of halothane,enflurane and isoflurane on the end-systolic pressure-length relationship

Myocardial contractility was measured using the end-systolic pressure-length (ESPL) relationship in dogs subjected to increasing concentrations of halothane (0.5-2 per cent), enflurane (0.77-2.6 per cent) or isoflurane (0.70-2.13 per cent), combined with an infusion 7 micrograms X kg-1 X min-1 of fentanyl, after induction of anaesthesia with 15 mg X kg-1 thiopentone. The relationship between the concentrations of the different drugs and contractility (ESPL) can best be described by ESPL = a + b/(MAC fraction) where "a" is a constant and "b" is the slope of the curve relating ESPL to MAC. At 1.0 MAC values, the ESPL for halothane (69.04 +/- 25.83 mmHg X mm-1) did not differ from that of isoflurane (63.19 +/- 17.36 mmHg X mm-1). However, the myocardial contractility during 1.0 MAC halothane and isoflurane anaesthesia was better preserved than that of enflurane (38.66 +/- 9.73 mmHg X mm-1: p less than 0.01, p less than 0.05 respectively).     

Haemodynamic effects of atropine during halothane or isoflurane anaesthesia in infants and small children

In this study, two-dimensional and pulsed Doppler echocardiography were used to measure cardiovascular changes before and after IV atropine in 31 infants and small children during halothane (n = 15) or isoflurane (n = 16) anaesthesia. Prior to induction of anaesthesia heart rate (HR), mean blood pressure (MBP), and two0dimensional echocardiographic dimensions of the left ventricle and pulmonary artery bloodflow velocity were measured by pulsed Doppler echocardiography. Cardiovascular measurements were repeated while anaesthesia was maintained at 1.5 MAC halothane (n = 15) or isoflurane (n = 16). Atropine 0.02 mg·kg⁻¹ IV was then administered and two minutes later, a third set of cardiovascular data was obtained. Heart rate decreased during halothane anaesthesia but did not change significantly during isoflurane anaesthesia. Mean blood pressure, cardiac output (CO) and stroke volume (SV) decreased similarly during 1.5 MAC halothane or isoflurane anaesthesia. Ejection fraction (EF) decreased and left ventricular end-diastolic volume (LVEDV) increased significantly in bothgroups, but decreases in EF (32 ± 5 percentvs18 ± 5 per cent) and increases in LVEDV (18 ± 7 per cent vs7 ± 5 per cent) were significantly greater during halothane than during isoflurane anaesthesia. Following atropine, HR increased more in the patients maintained with halothane (31 ± 6 per cent), than during isoflurane anaesthesia (18 ± 5 per cent). Atropine increased CO in both groups of patients, but SV and EF remained unchanged. When compared with awake values, HR increased similarly and significantly (18 ± 4 per cent) following atropine in both groups, and CO returned to control levels. Halothane decreased EF and increased LVEDV more than isoflurane at 1.5 MAC end— expired anaesthetic levels. Atropine did not diminish the myocardial depression produced by halothane or isoflurane. The increase in CO following atropine during halothane and isoflurane anaesthesia in infants and small children is the result of increases in HR alone. Nous avons utilisé un appareil à échocardiographie bi-dimensionnelle couplé à un Doppler pulsé chez des bébés et de jeunes enfants pour évaluer l’impact hémodynamique de l’halothane (n = 15) et de l’isoflurane (n = 16) et la modification possible de ces effets par l’atropine. Nous avons mesure la frequence cardiaque (FC), la pression artérielle moyenne (PAM), la dimension de la cavité ventriculaire gauche (par écho bi-dimensionnelle) et la vélocité du flot sanguin pulmonaire (par Doppler) et ce, en trois occasions soit avant l’induction, après l’instauration de 1.5 MAC d’halothane ou d’isoflurane et finalement, deux minutes après l’injection IV de 0.02 mg·kg⁻¹ d’atropine. On ne nota une baisse de la frequence cardiaque qu’avec l’halothane tandis que la PAM, le débit cardiaque (DC) et le volume d’éjection (VE) diminuaient autant avec l’un ou l’autre anesthésique. La diminution de la fraction d’éjection (FE) et l’augmentation du volume télédiastolique du ventricule gauche (VTDVG) significatives pour les deux groupes, étaienl plus marqué avec l’halothane qu’avec l’isoflurane: FE 32 ± 5 pour cent vs18 ±5 pour cent; VTDVG 18 ± 7 pour cent vs 7 ± 5 pour cent. Avec l’atropine, la FC monta plus dans le groupe halothane (31 ± 6 pour cent) que dans le groupe isoflurane (18 ± 5 pour cent), le DC augmentant dans les deux groupes, alors que le VE et la FE demeuraient inchangés. Comparée aux mesures pré-induction, l’atropine amenait une hausse significative de la FC, semblable dans les deux groupes (18 ± 4 pour cent) et restaurait le DC. Donc, chez les bebes et les jeunes enfants, a 1.5 MAC, l’halothane diminue la FE et augmente le VTDVG plus que ne le fait l’isoflurane. L’atropine ne modifie pas la depression myocardique et elle ne restaure le DC que par une hausse de la FC.

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Supported by PHS Grant No. 8507300 from the College of Medicine, University of Iowa Hospital, Iowa City, IA.     

Continuous infusion of atracurium in children

Atracurium infusion requirements were determined in 28 children anesthetized with N2O:O2 narcotic, N2O:O2 halothane (1% inspired), and N2O:O2 enflurane (2% inspired). When the patient was recovering from a bolus dose of 0.4 mg/kg atracurium, a continuous infusion of atracurium was started and the rate was adjusted to maintain 90-99% muscle twitch depression. Patients receiving enflurane anesthesia required atracurium at an infusion rate of 4.9 +/- 0.3 micrograms X kg-1 X min-1 which was a significantly lower rate (P = 0.0001) than those anesthetized with halothane (8.3 +/- 0.4 micrograms X kg-1 X min-1) or with N2O:O2 and narcotic (9.3 +/- 0.5 micrograms X kg-1 X min-1). At the onset of neuromuscular blockade, the twitch response disappeared faster after train-of-four stimulation repeated every 10 s than after single twitch rates of stimulation at 0.1 Hz. In children, during halothane anesthesia after 0.4 mg/kg atracurium, the response of the adductor of the thumb was ablated in 2.0 +/- 0.3 min with train-of-four stimulation, and in 3.7 +/- 0.4 min with single twitch stimulation. The authors recommend the use of a nerve stimulator during continuous infusion of atracurium because of the marked interpatient differences in infusion-rate requirements.     

The control of hypertension with dibutyryl cyclic AMP

The effects of the rapid infusion of large doses of dibutyryl cyclic AMP (DBcAMP) were studied to clarify the clinical usefulness of its vasodilating action in 32 middle-aged patients, who underwent various types of surgery and developed systolic hypertension of over 160 mmHg during general anaesthesia. DBcAMP was given i.v. with an infusion pump at a rate of 0.6 mg kg-1 min-1 for 20 min. In all patients just after the infusion, systolic arterial pressure decreased from 174.0 +/- 20.7 to 129.0 +/- 23.9 mmHg, diastolic pressure decreased from 93.1 +/- 13.4 to 64.8 +/- 13.3 mmHg, heart rate increased from 81.2 +/- 15.7 to 91.5 +/- 19.5 beats min-1, and urine volume increased from 69.4 +/- 54.8 to 182.7 +/- 143.5 ml h-1. In three patients, cardiac index increased from 3.44 to 4.24 l min-1 m-2. In seven patients, tachycardia exceeding 120 beats min-1 developed. DBcAMP was also effective in patients with a history of hypertension. The strongest antihypertensive effect was observed in patients anaesthetized with nitrous oxide-oxygen and enflurane. We speculate that DBcAMP is useful to control hypertension and may be particularly indicated in patients with cardiac failure, renal disorders and essential hypertension.     

Oral clonidine blunts the heart rate response to intravenous atropine in humans.

Clonidine, recently introduced into anesthesia practice, may cause bradycardia. Whether this bradycardia is reversible with atropine is not known. Accordingly, we studied heart rate (HR) responses to intravenous atropine in 80 patients assigned randomly to either a control group, who received no medication (n = 20), or a clonidine group, who received oral clonidine of approximately 1.2 micrograms.kg-1 (n = 20), 2.5 micrograms.kg-1 (n = 20), or 5 micrograms.kg-1 (n = 20). All patients received incremental doses of atropine, 2.5, 2.5, and 5 micrograms.kg-1, at 2-min intervals (total dose 10 micrograms.kg-1). Positive chronotropic response to the cumulative atropine dose of 10 micrograms.kg-1 was attenuated significantly only in patients given clonidine 5 micrograms.kg-1 (7 +/- 1 beats per min, mean +/- standard error) when compared with those given smaller doses of clonidine (15 +/- 2, 16 +/- 2 beats per min) or no clonidine (19 +/- 2 beats per min) (P less than 0.05). To determine whether HR hyporesponsiveness to atropine induced by clonidine can be overcome by a larger dose of atropine, the authors studied 30 additional patients given clonidine 5 micrograms.kg-1 or no medication. In all patients not receiving clonidine (n = 15), HR increased by more than 20 beats per min when atropine of 15 micrograms.kg-1 was administered, whereas in only 5 patients (33%) receiving clonidine did the HR increase by 20 beats per min after atropine 15 micrograms.kg-1 (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Halothane, but not isoflurane or enflurane, protects against spontaneous and epinephrine-exacerbated acute thrombus formation in stenosed dog coronary arteries

Occlusive platelet thrombi periodically form in mechanically stenosed dog coronary arteries producing cyclical blood flow reductions occurring over 4-7 min. Cyclical coronary flow reductions are exacerbated by IV epinephrine 0.4 microgram.kg-1.min-1 for 15 min. These flow reductions can be abolished by known inhibitors of platelet function. This study assesses the effect of halothane, isoflurane, and enflurane on spontaneous- and epinephrine-exacerbated cyclical coronary flow reductions. Twenty-three open-chest dogs [1% halothane (n = 5), 0.5% halothane (n = 5), 0.25% halothane (n = 3), 1.5% isoflurane (n = 5), and 2.0% enflurane (n = 5)] with a mechanically stenosed coronary artery showed cyclical blood flow reductions. With 1.0% halothane administration, spontaneous cyclical blood flow reductions were abolished (n = 5), whereas during administration of isoflurane 1.5% (n = 5) and enflurane 2.0% (n = 5) cyclical flow reductions and myocardial ischemia continued. Subsequent administration of halothane in the isoflurane and enflurane groups showed abolition of coronary flow reductions in all animals (n = 10). In eight animals a 15-min epinephrine infusion (0.4 microgram.kg-1.min-1) was given following a control period and again following abolition of coronary flow reductions by halothane 0.5% (n = 5) and halothane 0.25% (n = 3). The magnitude of cyclical blood flow reductions (difference between initial and final coronary flow level of each flow reduction) changed from 52 +/- 11 to 61 +/- 12 ml/min (NS), and frequency increased from 0.37 to 0.57/min (P less than 0.05, n = 8) during epinephrine infusion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Carbon dioxide elimination in anaesthetized children

Carbon dioxide elimination (VCO2) was measured in 186 anaesthetized, spontaneously breathing infants and children with body weights ranging from 2.8 to 26.5 kg. They all underwent minor paediatric surgical procedures. The influence on VCO2 of age, operation, premedication, caudal anaesthesia, and different volatile anaesthetic agents was investigated. The volume of exhaled gas, during three- to five-minute collection periods, was measured and the fraction of exhaled CO2 was determined by a CO2 meter. Under basal anaesthetic conditions, the average output before operation followed the equation: VCO2 (ml.min-1) = -1.25X + 13.0X2, in which X = lne (body weight, kg). Expressed on a weight basis, the youngest infants (weighing less than 5 kg) had the lowest VCO2. Higher values were measured up to a body weight of 10 kg above which a negative correlation occurred between VCO2 (ml.min-1.kg-1) and body weight. The use of premedication resulted in a more variable VCO2 during operations than when opioid premedication was not used. The combination of a general anaesthetic and caudal anaesthesia stabilized VCO2. Also, children anaesthetized with halothane had a higher VCO2 than those who were anaesthetized with enflurane or isoflurane (P less than 0.05). The variable VCO2 emphasizes the need for increased monitoring of VCO2 during routine anaesthesia and operation in infants and children.     

Efficacy of an epidural test dose in children anesthetized with halothane

The effect of an intravenous (iv) injection of lidocaine with epinephrine was studied to determine if such a test dose would cause a reliably detectable increase in heart rate and systemic blood pressure in children anesthetized with halothane and nitrous oxide. The effect of the injection of atropine before the test dose on these parameters was also determined. Sixty-five children 1 month to 11 yr of age and weighing 3.9-35 kg were studied. The children were assigned to one of four groups, each of which was anesthetized with 1% halothane and 50% nitrous oxide. Group 1 (n = 20) received 10 micrograms/kg atropine followed 5 min later by an iv dose of 0.1 ml/kg 1% lidocaine with 1/200,000 epinephrine (0.5 micrograms/kg) to simulate an intravascularly administered epidural test dose. Group 2 (n = 21) was identical to group 1 but did not receive atropine prior to the simulated intravascular test dose. Groups 3 (n = 12) and 4 (n = 11) were identical to groups 1 and 2, but the simulated intravascular test dose did not contain epinephrine: group 3 received atropine prior to the test dose and group 4 did not. The simulated intravascular test dose increased heart rate in group 1 (with atropine) at each time period from 15 to 120 s, but only at 45 and 60 s in group 2 (without atropine). Following the iv test dose, 6 of 21 children in group 2 had an increase in heart rate of less than 10 beats/min, while only one child in group 1 had an increase in heart rate of less than 10 beats/min. Intravenous test doses that did not contain epinephrine (groups 3 and 4) had no effect on heart rate or blood pressure. Atropine, 10 micrograms/kg, improves the reliability of an epidural test dose in children anesthetized with halothane and nitrous oxide but does not ensure total reliability in detecting an intravascular injection.     

Effect of pre-treatment with intravenous atropine or glycopyrrolate on cardiac arrhythmias during halothane anaesthesia for adenoidectomy in children

We studied the effect of anticholinergics on the incidence of cardiac arrhythmias during paediatric anaesthesia. ASA I-II children (n = 77) undergoing adenoidectomy were randomly allocated to three groups. Intravenous atropine 0.02 mg kg-1 was given in group A (n = 25), glycopyrrolate 0.004 mg kg-1 in group G (n = 27) and physiological saline in group P (n = 25) 3 min before the induction of anaesthesia. The children breathed spontaneously under halothane anaesthesia with 66% nitrous oxide in oxygen after induction with thiopentone and succinylcholine. Perioperative monitoring of the ECG (Holter recordings) and oxygen saturation was carried out. Ventricular tachycardia occurred in 16.0%, 18.5% and 12.0% of the children in groups A, G and P respectively (ns). The incidence of ventricular arrhythmias (ventricular tachycardia, ventricular bigeminy, ventricular premature beats > 10) was 20.0% in group A, 44.4% in group G and 36.0% in group P (ns). Bradycardia (< 70 beats min-1) was observed in 0.0%, 14.8% and 24.0% of patients in groups A, G and P respectively (A vs P, P < 0.05). The use of anticholinergics did not influence the incidence of ventricular arrhythmias during halothane anaesthesia in children. Bradycardia was more common in the placebo group than in the atropine group.      

Comparison of Halothane and Enflurane Anaesthesia for Tonsillectomy in Adults

Halothane and enflurane in combination with N₂O/O₂ were compared in 103 adults undergoing tonsillectomy. Anaesthesia was induced with thiopental, and intubation was facilitated with suxamethonium. During halothane anaesthesia the mean heart rate ranged from 91 to 106 beats/min and the mean systolic arterial pressure from 111 to 127 mmHg. The values did not diifer significantly from the corresponding values during enflurane anaesthesia. Electrocardiographic changes occurred in 56% and 31% of the patients anaesthetized with halothane or enflurane, respectively. The incidence of junctional rhythm, the most common ECG change, was 46% in the halothane group and 29% in the enflurane group. 19% of the patients in the halothane group and 31% in the enflurane group responded to surgical stimulus by swallowing or coughing. The responses were mostly short-lasting and did not much disturb the surgeon. The incidence of laryngospasm was 6% after halothane and 2% after enflurane anaesthesia. The mean total recovery score (0—10) was 6.1 after halothane and 6.3 after enflurane at arrival in the recovery room and 9.8 in both groups 30 min later. After halothane, nausea and vomiting occurred in 8 and 12% of the patients, respectively. The corresponding figures after enflurane were 2 and 8%. It is concluded that both halothane and enflurane arc suitable anaesthetics for tonsillectomy in adults. The most striking difference between the anaesthetics was the significantly more common occurrence of ECG changes during halothane than enflurane anaesthesia.     

A formula for determining the distance from the skin to the lumbar epidural space in infants and children

In paediatric epidural anaesthesia, the distance from the skin to the epidural space is of special importance because of the great differences in size of the patients. We measured the distance from the skin to the lumbar epidural space (L3/4) in 355 paediatric patients. The epidural space was punctured using a midline approach under general anaesthesia, and was identified by the micro-drip infusion technique. There was a good correlation between the distance to the epidural space and body weight. A clinically useful formula for estimating the distance from the skin to the lumbar epidural space was derived as follows: D = (W+10) × 0.8 where D = distance from the skin to the lumbar epidural space (L3/4) (mm) and W = body weight (kg).     

Vomiting, retching, headache and restlessness after halothane-, isoflurane- and enflurane-based anaesthesia: An analysis of pooled data following ear, nose, throat and eye surgery

Background: Isoflurane has exceeded halothane and enflurane in usage. A literature search, however, revealed no data comparing the effects on emesis, headache and restlessness of these three agents.
Methods: With hospital ethics committee approval and patient consent, a prospective, randomised, double-blind study of 556 patients undergoing ENT and eye surgery was undertaken to evaluate the effects of halothane, isoflurane and enflurane on vomiting, retching, headache and restlessness until 24 h after anaesthesia. Balanced general anaesthesia was administered comprising benzodiazepine premedication, induction with thiopentone-atracurium-morphine (ENT patients) or fentanyl (eye patients), controlled ventilation and maintenance with either halothane 0.4–0.6 vol% (n = 186), isoflurane 0.6–0.8 vol% (n = 184) or enflurane 0.8–1 vol% (n=186) in nitrous oxide 67% and oxygen.
Results: The three study groups were comparable, and comprised comparable subgroups having ear, nose, throat, intraocular and non-intraocular surgery. During early recovery from anaesthesia, the respective requirements for halothane, isoflurane and enflurane for analgesia (7%, 9% and 10%), frequency of emesis (6%, 8% and 8%), antiemetic requirements (1%, 1% and 2%), restlessness-pain scores and time spent in the recovery ward (27 SD 10, 31 SD 12 and 26 SD 9 min) were similar. During the ensuing 24-h postoperative period, patients who had isoflurane experienced emesis less often than those who had halothane (36% vs 46%, P <0.025) but did so with similar frequency to those who had enflurane (46% vs 41%). Antiemetic requirements were least in those given isoflurane (isoflurane 12%, halothane and enflurane 23% each, P <0.005), but headache and analgesic requirements were similar.
Conclusion: Isoflurane induces less postoperative emesis than halothane, but headache is similarly frequent after anaesthesia with any of these agents.     

Epidural anaesthesia blocks changes in peripheral lymphocytes subpopulation during gastrectomy for stomach cancer

To examine the effects of surgery and anaesthesia on cell-mediated and humoral immunity, we investigated changes in subpopulations of peripheral T cells and B cells during gastrectomy. Twenty-one patients with gastric cancers who underwent total or subtotal gastrectomy were randomly assigned to receive thiopental/N₂O general anaesthesia supplemented with either epidural (epidural group, n =12) or enflurane(enflurane group, n =9). The changes in peripheral lymphocyte subpopulations were detected and quantified using single and double label analysis of monoclonal antibodies against lymphocyte membrane surface markers (Leu series). Subpopulations were measured before induction, and 1 and 2 hours after skin incision. In the enflurane group, B cells (Leu12⁺), total T cells (Leu4⁺), inducer T cells (CD4⁺, Leu8⁺) and the CD4/CD8 ratio decreased and suppressor T cells (CD8⁺, Leu15⁺) increased significantly after skin incision. Whereas, the epidural group showed no change in the number of B cells and each T cell subpopulation during the study. These data suggest that epidural anaesthesia blocks the effect of stress induced by major surgery on fluctuation of peripheral lymphocyte subpopulations which may be associated with suppression of immunity.     

Endocrine Stress Response during General and Epidural Anaesthesia for Elective Caesarean Sections

In 17 patients scheduled for elective caesarean sections, the influence of general (GA, n = 9) and epidural anaesthesia (EA, n = 8) on maternal and umbilical vein blood plasma concentrations of ACTH, Cortisol, 17-α-hydroxyprogesterone (OHP) and blood glucose (BG) was studied. Mean blood pressure (MBP mmHg) and heart rate (HR beats min^-1) were also followed during the operation and Apgar scores were evaluated in all neonates. With epidural anaesthesia, an MBP of 102±6.5 mmHg and an HR of 87 ±4.9 beats min^-1 was found at hysterotomy (HT). With general anaesthesia, the corresponding values were 143 ±6.9 mmHg (P<0.01) and 108 ±6.3 beats min^-1 (P<0.05). The plasma concentration of ACTH at HT was higher during GA than during EA (P<0.01), while the plasma concentration of Cortisol during GA was higher 30 min alter HT (P<0.05). Maternal ACTH and Cortisol levels at HT were higher than umbilical vein levels, while OHP was 2–3 times higher in the umbilical vein than in maternal blood at HT. Umbilical vein Cortisol concentration was higher in the EA than in the GA group (P<0.01). With epidural anaesthesia, neonates had higher Apgar scores than with general anaesthesia (P<0.01). The increased umbilical vein Cortisol concentration with epidural anaesthesia challenged the assumption of a higher fetal stress response. The results might have a bearing on the choice of the most suitable anaesthetic method in complicated pregnancies.     

The effects of preanesthetic oral clonidine upon heart rate response to intravenous atropine in patients during general anesthesia]

In awake subjects the positive chronotropic effect of intravenously administered atropine 10 micrograms.kg-1 has been demonstrated to be blunted by preanesthetic medication of oral clonidine 5 micrograms.kg-1. The aim of the present study is to investigate whether general anesthesia could alter the clonidine-induced attenuation of positive chronotropic effect by atropine. Thirty-two patients were randomly assigned to one of the two groups; patients of the clonidine group received oral clonidine 5 micrograms.kg-1 (n = 12), whereas those of the control group received no clonidine. General anesthesia was induced with intravenous thiamylal 4-5 mg.kg-1, and was maintained with enflurane and nitrous oxide in oxygen after endotracheal intubation. Following the stable circulatory period of 10 min, hemodynamic measurements were made at 1 min intervals for 10 min after atropine 10 micrograms.kg-1 was administered intravenously as a bolus in both groups. A significant attenuation in heart rate response to intravenous atropine 10 micrograms.kg-1 was observed in patients receiving clonidine 5 micrograms.kg-1, as compared with that in the control group (P less than 0.01); maximal increases in heart rate were 15 +/- 8 and 22 +/- 6 beats.min-1 (mean +/- SD) in the clonidine and control groups, respectively. It is concluded that clonidine 5 micrograms.kg-1 blunts the heart rate response to intravenous atropine 10 micrograms.kg-1 in patients anesthetized with enflurane and nitrous oxide in oxygen.     

Thoracic epidural anaesthesia decreases the incidence of ventricular arrhythmias during acute myocardial ischaemia in the anaesthetized rat

The aim of the present investigation was to study the effect of high thoracic epidural anaesthesia (TEA) on the incidence of ventricular arrhythmias after ligation of the left coronary artery in chloralose-anaesthetized rats. Forty animals were randomly assigned to receive either 40-50 microliter of bupivacaine (5 mg/ml) or saline in implanted thoracic epidural catheters. TEA decreased mean arterial pressure (MAP) from 118 +/- 5 mmHg to 72 +/- 4 mmHg and heart rate (HR) from 450 +/- 9 to 387 +/- 8 beats/min, while epidural saline did not affect MAP and HR. In both groups coronary artery ligation induced a transient decrease in MAP within the first 5-10 min after ligation. In the control group HR increased, during the 30-min post-ligation period, from 453 +/- 9 to 474 +/- 10 beats/min (P less than 0.05) while no significant change was seen in the TEA group. In both groups the mortality rate was 10%. In the TEA group 30% and in the control group 0% had normal sinus rhythm during the recording period (P less than 0.001). The incidence of ventricular fibrillation and/or tachycardia was significantly lower (P less than 0.05) in the TEA group (20%) compared to the control group (53%). The incidence of ventricular extrasystoles did not differ between the two groups. We conclude that TEA-induced blockade of sympathetic afferents and efferents may offer protection against malignant ventricular arrhythmias in the early phase of acute myocardial infarction.