Comparison of two esmolol bolus doses on the haemodynamic response and seizure duration during electro-convulsive therapy

Twelve ASA physical status I-III patients were enrolled in a double-blind, prospective, randomized, three-way, within-patient crossover study designed to determine the effect of two standard esmolol bolus doses (100 and 200 mg) on the haemodynamic response and seizure duration during electro-convulsive therapy (ECT). Esmolol or placebo was administered one minute prior to induction of anaesthesia and exactly two minutes before ECT. Both the 100 and 200 mg bolus doses significantly blunted the maximum increase in heart rate (HR) and mean arterial pressure (MAP) following ECT in comparison with placebo. Compared with placebo, esmolol 100 mg decreased maximum HR by 23 +/- 3%, maximum MAP by 17 +/- 7% and maximum rate-pressure product (RPP) by 40 +/- 9%. Esmolol 200 mg decreased maximum HR by 25 +/- 3%, maximum MAP by 19 +/- 3% and maximum RPP by 42 +/- 5%. No significant difference was found between the two esmolol doses at corresponding measurement points before and after ECT. Treatment with esmolol 200 mg resulted in a significantly shorter mean seizure duration than with placebo. As the 200 mg dose caused a shorter seizure duration and the haemodynamic effects of 100 mg and 200 mg doses were similar, it was concluded that the 100 mg esmolol bolus dose was the better dose for ECT.     

Randomized comparison of outcome after propofol-nitrous oxide or enflurane-nitrous oxide anaesthesia in operations of long duration

A randomized, prospective, comparative study was performed to evaluate induction characteristics, haemodynamic changes and recovery in 60 ASA I-II patients undergoing mainly gynaecological laparotomies with either propofol or thiopentone-enflurane anaesthesia. The propofol group (n = 30) received 2 mg.kg-1 propofol for induction of anaesthesia followed by propofol infusion. The thiopentone-enflurane group (n = 30) received thiopentone 4 mg.kg-1 for induction followed by enflurane (0.5-2 per cent). All patients received nitrous oxide (66 per cent] in oxygen begun one minute after tracheal intubation, and fentanyl (1.5 micrograms.kg-1) four minutes prior to induction. Other drugs administered during or after anaesthesia were similar among the groups. Haemodynamic measurements were similar between propofol and enflurane groups except after tracheal intubation when the mean arterial pressure was lower in the propofol group (P less than 0.05). The propofol group had significantly less (P less than 0.01) emesis in the recovery room than the enflurane group. The propofol group experienced significantly less (P less than 0.05) dizziness, depression/sadness and hunger than the enflurane group in the postoperative period as assessed with a visual analogue questionnaire. We conclude that propofol provided better outcome than enflurane in terms of these nonvital but annoying outcome measures after relatively long intra-abdominal operations.     

A comparison of esmolol and labetalol for the treatment of perioperative hypertension in geriatric ambulatory surgical patients

This is an open randomized study comparing the efficacy and safety of i.v. esmolol and labetalol in the treatment of perioperative hypertension in ambulatory surgery. Twenty-two elderly patients undergoing cataract surgery under local anaesthesia were studied. The main inclusion criteria were development of systolic blood pressure greater than 200 mmHg or diastolic greater than 100 mmHg. Esmolol was given as a bolus 500 micrograms.kg-1 i.v. followed by a maintenance infusion (150-300 micrograms.kg-1.min-1). Labetalol was given as a bolus of 5 mg i.v. followed by 5 mg increments as needed up to a maximum of 1 mg.kg-1. Esmolol and labetalol both produced reductions in systolic and diastolic blood pressure (P less than 0.05) within ten minutes of administration which lasted for at least two hours. Reduction of blood pressure by esmolol was accompanied by a decrease in HR (P less than 0.05). Two patients developed extreme bradycardia (HR less than 50 beats.min-1) and esmolol had to be discontinued. Labetalol, in contrast, induced only a moderate decrease in HR. None of the patients treated with labetalol experienced any prolonged side effects such as orthostatic hypotension. In conclusion, esmolol may produce considerable bradycardia in elderly patients when hypertension is not accompanied by tachycardia. Labetalol was easier to administer in the ambulatory setting and one-tenth the cost of esmolol.     

A comparison of fentanyl,esmolol, and their combination for blunting the haemodynamic responses during rapid-sequence induction

The purpose of this randomized, double-blind study was to compare the ability of a combination of fentanyl and esmolol to blunt the haemodynamic effects of intubation with that of either agent alone. Patients received fentanyl or saline four minutes before, and esmolol or saline two minutes before rapid-sequence induction of anaesthesia. The F2 group (n = 24) received fentanyl 2 micrograms.kg-1, the E2 group (n = 24) received esmolol 2 mg.kg-1, the F2/E2 group (n = 25) received a combination of fentanyl 2 micrograms.kg-1 and esmolol 2 mg.kg-1, and the F5 group (n = 26) received fentanyl 5 micrograms.kg-1. Following tracheal intubation, the maximum percent change from baseline heart rate was less in the F2/E2 and F5 groups (12% and 16% respectively) than in the E2 group (34%)(P < 0.05). The maximum percent changes from baseline systolic blood pressure in the F2/E2 and F5 groups (15% and 6% respectively) were less than in the F2 and E2 groups (24% and 33% respectively) (P < 0.05). The combination of a low dose of fentanyl and esmolol provides an alternative to a higher dose of fentanyl for blunting the haemodynamic responses to laryngoscopy and tracheal intubation during rapid-sequence induction in healthy patients.     

Bolus doses of esmolol for the prevention of perioperative hyper-tension and tachycardia

The effectiveness of esmolol, an ultra short-acting cardioselective beta blocker, in the prevention and treatment of post-intubation haemodynamic perturbations, was investigated. Forty-eight ASA physical status I and II patients undergoing hysterectomy were randomly assigned to receive a single intravenous bolus of placebo, esmolol 100 mg, or esmolol 200 mg in a double-blind fashion. This was administered over 15 sec, and immediately followed by thiopentone 3-5 mg.kg-1, succinylcholine 1.5 mg.kg-1, and tracheal intubation 90 sec later. The heart rate following induction of anaesthesia was lower in the esmolol 200 mg group (P less than 0.01); following intubation, the increase in heart rate in the placebo group was greater than in the esmolol groups (P less than 0.05). The systolic blood pressure post-induction was lower in the esmolol 200 mg group (P less than 0.05); following intubation, however, no significant differences were seen among groups in systolic, diastolic, or mean blood pressures. Following tracheal intubation, the incidence of ventricular arrhythmias was lower in the esmolol groups (P less than 0.05). In summary, esmolol in 100 mg and 200 mg doses was effective in mitigating the haemodynamic response following tracheal intubation.     

Induction reflex actions with intravenous nalbuphine as an adjunct to isoflurane

Ninety unpremedicated patients undergoing mask anaesthesia were assigned to one of three groups according to the volatile anaesthetic and the acute intravenous premedication administered. Group I received saline placebo as premedication and halothane by inhalation. Group II received saline placebo and isoflurane by inhalation. Group III received nalbuphine 0.1 mg.kg-1 IV as premedication and isoflurance by inhalation. Mean time to loss of consciousness (71 sec) did not differ among groups. The dosage of thiopentone required to induce loss of consciousness was decreased by 15 per cent (from 3.9 to 3.3 mg.kg-1) by nalbuphine premedication (P less than 0.05), and time to induction of surgical anaesthesia using isoflurane was decreased by 15 per cent (P less than 0.05). The incidence of reflex actions (coughing, laryngospasm, breath holding, hiccoughs and movement) during induction was no different in the saline-premedicated halothane or isoflurane groups. Acute intravenous nalbuphine premedication decreased significantly the incidence of reflex actions during induction of isoflurane anaesthesia from 77 per cent to 37 per cent (P less than 0.02). Desaturation episodes (SaO2 less than 90 per cent) were more frequent with isoflurane inductions compared with halothane (55 per cent vs 17 per cent, P less than 0.01). Apnoeic episodes accounted for the majority of desaturations associated with nalbuphine premedication, while excitatory reflexes (coughing and laryngospasm) accounted for more desaturations with isoflurane alone.     

Pharmacokinetics and cardiovascular dynamics of pipecuronium bromide during coronary artery surgery

The haemodynamic effects of 200 micrograms.kg-1 pipecuronium and pancuronium were compared under etomidate/piritramide anaesthesia in 20 patients scheduled for elective coronary artery surgery. Following the completion of the haemodynamic measurements (ten minutes), anaesthesia was maintained by etomidate/sufentanil infusion. The mean changes in cardiac output were approximately -19 and -2 per cent and in heart rate -1 and +26 per cent for pipecuronium and pancuronium respectively. Plasma and urine concentrations of pipecuronium were also measured and the pharmacokinetic variables obtained indicated rapid initial decrease in plasma concentration (t1/2 = 7.6 minutes) followed by a longer terminal phase (t1/2 = 161 minutes). The central compartment volume was 102 +/- 24 ml.kg-1 and plasma clearance was 1.8 +/- 0.4 ml.kg-1 min-1. Approximately 56 per cent of the dose was recovered from the urine within 24 hours of administration and about 25 per cent of this was the metabolite, 3-desacetyl pipecuronium. High-dose pipecuronium administration under the anaesthetic regimen employed did not produce deleterious haemodynamic effects. The pharmacokinetic variables after bolus injection of pipecuronium did not deviate from those reported under normothermic conditions.     

Denitrogenation in pregnancy

This study measured nitrogen washout in ten pregnant and nine non-pregnant women to understand better how pregnancy effects denitrogenation. Nitrogen concentration was monitored continuously while the women breathed 100 per cent O2 for three minutes and took four deep breaths of 100 per cent O2 using a circle anaesthesia system and 8 L.min-1 fresh gas flow. Parturients achieved 95 per cent denitrogenation significantly (P less than 0.0005) faster than non-pregnant women (54.5 +/- 17.8 vs 110.8 +/- 35.7 sec). In parturients, denitrogenation for three minutes lowered expired N2 concentration to 1.0 +/- 0.2 per cent while four deep breaths lowered it to 5.1 +/- 1.7 per cent (P less than 0.0001). This difference, while statistically significant, is predicted to supply only 10-15 sec of extra protection against hypoxaemia, and thus is probably not clinically significant. The authors conclude that either two minutes of tidal breathing or four deep breaths of 100 per cent O2 provide adequate denitrogenation and similar protection against apnoeic hypoxaemia in normal parturients.     

Plasma lidocaine concentrations during continuous epidural infusion of lidocaine with and without epinephrine

Plasma lidocaine concentrations were measured over a five-hour period in 20 patients following continuous epidural infusion of lidocaine for surgical anaesthesia. Patients were divided into two groups: Group I received plain lidocaine; Group II received lidocaine with epinephrine. Patients initially received 10 ml followed by a constant infusion of 10 ml.hr-1 of two per cent lidocaine. The mean plasma concentrations of lidocaine were significantly higher for the first 40 min in Group I than in Group II. However, from one to five hours, there was no significant difference between the groups. These results demonstrate that the addition of epinephrine to lidocaine does not decrease the plasma concentration of lidocaine during continuous epidural infusion for long operations.     

Disposition of propofol infusions for caesarean section

The disposition of propofol was studied in women undergoing elective Caesarean section. Indices of maternal recovery and neonatal assessment were correlated with venous concentrations of propofol. After induction of anaesthesia with propofol 2.0 mg.kg-1, ten patients received propofol 6 mg.kg-1.hr-1 with nitrous oxide 50 per cent in oxygen (low group) and nine were given propofol 9 mg.kg-1.hr-1 with oxygen 100 per cent (high group). Pharmacokinetic variables were similar between the groups. The mean +/- SD Vss = 2.38 +/- 1.16 L.kg-1, Cl = 39.2 +/- 9.75 ml.min-1.kg-1 and t1/2 beta = 126 +/- 68.7 min. At the time of delivery (8-16 min), the concentration of propofol ranged from 1.91-3.82 micrograms.ml-1 in the maternal vein (MV), 1.00-2.00 micrograms.ml-1 in the umbilical vein (UV) and 0.53-1.66 micrograms.ml-1 in the umbilical artery (UA). Neonates with high UV concentrations of propofol at delivery had lower neurologic and adaptive capacity scores 15 minutes later. The concentrations of propofol were similar between groups during the infusion but they declined at a faster rate in the low group postoperatively. Maternal recovery times did not depend on the total dose of propofol but the concentration of propofol at the time of eye opening was greater in the high group than the low group (1.74 +/- 0.51 vs 1.24 +/- 0.32 micrograms.ml-1, P less than 0.01). The rapid placental transfer of propofol during Caesarean section requires propofol infusions to be given cautiously, especially when induction to delivery times are long.     

Low-dose sufentanil in major surgery

The purpose of this study was to assess the efficacy of sufentanil 1 micrograms.kg-1 during N2O-O2 and intermittent isoflurane anaesthesia in major non-cardiac surgery. Thirty-one patients (18 females, 13 males; mean age 47 yr), undergoing cholecystectomy received a 1 microgram.kg-1 bolus of sufentanil before the induction of anaesthesia with thiopentone. On average, three sufentanil increments were administered, to a total (bolus + maintenance) dose of 1.5 micrograms.kg-1. Cardiovascular stability was not achieved in eleven patients who then were given isoflurane. The arterial pressure decreased after sufentanil (P less than 0.05), reaching a nadir (mean 108/65 mmHg, heart rate 63 bpm) at one minute post-incision. Clinically important hypertension or hypotension did not occur in any patient. One patient, receiving beta-blocker therapy, required atropine to control bradycardia. Postoperative respiratory depression did not occur in patients who received less than one micrograms.kg-1.hr-1 with the last increment being given more than 20 minutes before the end of anaesthesia. Slight respiratory depression in the recovery room was reported in one patient, who had received a total of 1.3 micrograms.kg-1.hr-1 of sufentanil, and the last sufentanil increment 24 min before the end of surgery. The most frequently reported side-effects were nausea (35 per cent) and vomiting (23 per cent). Induction, maintenance and recovery from anaesthesia were rated as "good" in 87, 87, and 74 per cent of the cases, respectively, and "satisfactory" in the remainder. We conclude that this technique is valuable to assure good protection of the cardiovascular system without undue respiratory depression during recovery.     

Epidural epinephrine and the systemic circulation during peripheral vascular surgery

This study was designed to determine the haemodynamic effects of epidural epinephrine, 5 micrograms.ml-1, added to bupivacaine, 0.75 per cent, in elderly patients with cardiac disease undergoing peripheral vascular surgery (PVS). The effect of epidural epinephrine on the plasma concentration of bupivacaine was also measured. Twenty patients with a history and/or ECG evidence of myocardial ischaemia requiring PVS were randomly assigned to two groups. The patients were monitored with a modified V5 ECG, oscillometric BP monitor and a PA catheter. After control haemodynamic measurements, 12 ml of bupivacaine, 0.75 per cent, +/- epinephrine, 5 micrograms.ml-1, was injected over five minutes into the epidural space at L3-4. Supine haemodynamic measurements were repeated at 15 and 45 min after injection. At 15 min after epidural injection, compared with control values, patients receiving epidural epinephrine showed a significantly greater decrease in mean blood pressure and systemic vascular resistance, and a significantly greater increase in cardiac output than patients receiving plain epidural bupivacaine (79.3 +/- 11.6 per cent vs 94.6 +/- 16.8 per cent, 61.6 +/- 9.0 vs 91.6 +/- 19.2 per cent, 130.8 +/- 23 vs 105 +/- 20.8 per cent, respectively). These differences were not present at 45 min after epidural injection. Heart rate was not significantly different between groups at either time. The presence of epidural epinephrine reduced the peak plasma concentration of bupivacaine from 0.86 +/- 0.20 to 0.64 +/- 0.33 micrograms.ml-1 and increased the time to achieve this concentration from 16.1 +/- 11.2 to 33.7 +/- 20.1 min.     

Left ventricular regional wall motion and haemodynamic changes following bolus administration of pipecuronium or pancuronium to adult patients undergoing coronary artery bypass grafting

The objective of this study was to compare the haemodynamic and myocardial effects of pipecuronium and pancuronium in patients undergoing coronary artery bypass grafting (CABG) during benzodiazepine/sufentanil anaesthesia. Twenty-seven ASA III–IV patients received lorazepam (1–3 mg) po and midazolam (<0.1 mg · kg^?1) iv before induction of anaesthesia with sufentanil (3–8 μg · kg^?1). Vecuronium (0.1 mg · kg^?1) was administered to facilitate tracheal intubation. According to random allocation, each patient received either pipecuronium (150 μg · kg^?1) or pancuronium (120 μg · kg^?1) after stemotomy but before heparinization. Mean arterial pressure, central venous pressure (CVP), pulmonary artery pressure (PAP), ST segment position and ECG (leads HI, V₅, AVF) were monitored continuously throughout the procedure. Thermodilution determinations of CO in triplicate were made immediately before, and at two and five minutes after muscle relaxant administration. Multiplane transoesophageal echocardiography (TEE, midpapillary short axis views of the left ventricle) images were continuously recorded from ten minutes before until ten minutes after muscle relaxant administration and graded by two experienced echocardiographic readers. Heart rate, MAP and CO increased after administration of pancuronium (by 13.6 beats · min^?1, 10.8 mmHg and 1.0 L · min^?1 respectively) but not after pipecuronium (P < 0.05). Evidence of myocardial ischaemia was not detected in any patients using ECG ST segment analysis or TEE assessment of left ventricular wall motion. We conclude that pancuronium caused increases in HR, MAP and CO but that neither pancuronium nor pipecuronium caused myocardial ischaemia.     

Oral clonidine premedication attenuates the haemodynamic effects associated with ketamine anaesthetic induction in humans

Induction of anaesthesia is often associated with undesirable variations in blood pressure and heart rate. Clonidine has been demonstrated to attenuate many of these undesirable effects when used as a premedicant. Other alpha₂ adrenergic agonists have been used to ameliorate the cardiostimulatory effects of ketamine in animals but there are few data on the use of this combination in humans. The effect of oral clonidine premedication, 5 μg · kg^?1 on the haemodynamic changes induced by iv ketamine was studied in 42 patient volunteers. Ninety minutes before surgery, patients randomly received clonidine (C), diazepam (D), or a placebo (P) in a double-blinded fashion. Anaesthesia was induced with a ketamine infusion of I mg · kg^?1· min^?1 until loss of consciousness. Heart rate and phasic blood pressure were measured noninvasively prior to induction, before and up to seven minutes after tracheal intubation. There were no differences in demographics or baseline vital signs among the three groups. With ketamine administration, increases in heart rate and blood pressure were less in those patients given C preoperatively than in those who received either D or P. The peak increase in mean blood pressure was 39% (C) versus 70% (D) and 55% (P) (P < 0.01). Heart rate increased by a maximum of 20% (C) versus 41% (D) and 46% (P) (P < 0.01). We conclude that oral clonidine attenuates the hyperdynamic effects of anaesthetic induction with iv ketamine.     

Neuromuscular and cardiovascular effects of mivacurium chloride in surgical patients receiving nitrous oxide-narcotic or nitrous oxide-isoflurane anaesthesia

The neuromuscular and cardiovascular effects of mivacurium chloride were studied during nitrous oxide-oxygen narcotic (fentanyl) (n = 90) and nitrous oxide-oxygen isoflurane (ISO) anaesthesia (n = 45). In addition, a separate group (n = 9) received succinylcholine during fentanyl anaesthesia to compare its neuromuscular effects with mivacurium. Mivacurium was initially administered as a single bolus in doses from 0.03 mg.kg-1 to 0.25 mg.kg-1 to study the dose-response relationships, as well as the cardiovascular effects of mivacurium. Neuromuscular block (NMB) was measured by recording the twitch response of the adductor pollicis muscle following ulnar nerve stimulation (0.15 Hz, 0.2 ms supramaximal voltage). The ED95 values for mivacurium were estimated to be 0.073 mg.kg-1 and 0.053 mg.kg-1 in the fentanyl and ISO groups respectively. The duration of block (time from injection to 95 per cent recovery) for a dose of 0.05 mg.kg-1 mivacurium was 15.3 +/- 1.0 min and 21.5 +/- 1.3 min for fentanyl and ISO anaesthesia, respectively. The recovery index (25-75 per cent) between initial bolus dose (6.1 +/- 0.5 min), repeat bolus doses (7.6 +/- 0.6 min), mivacurium infusion (6.7 +/- 0.7 min) and succinylcholine infusion (6.8 +/- 1.8 min) were not significantly different. There was minimal change in mean arterial pressure (MAP) or heart rate (HR) following bolus doses of mivacurium up to 0.15 mg.kg-1. Bolus administration of 0.20 mg.kg-1 or 0.25 mg.kg-1 of mivacurium decreased MAP from 78.2 +/- 2.5 to 64.0 +/- 3.2 mmHg (range 12-59 per cent of control) (P less than 0.05). The same doses when administered slowly over 30 sec produced minimal change in MAP or HR.     

Premedication of children with oral midazolam

In a randomized, double-blind, placebo-controlled study, the safety, efficacy and feasibility of oral midazolam premedication in children were evaluated in an ambulatory surgery unit. Eighty unmedicated children (ASA PS I or II, ages 1-6 yr) were randomly assigned to one of four groups receiving midazolam 0.5, 0.75, or 1.0 mg.kg-1 or a placebo 30 min before separation from parents. Heart rate, systolic blood pressure, arterial oxygen saturation, respiratory rate, sedation and anxiolysis scores were recorded before premedication, every five minutes for 30 min and then during induction of anaesthesia and recovery. We found that heart rate, systolic blood pressure, arterial oxygen saturation and respiratory rate were unchanged during the study. Sedation and anxiolysis scores in the midazolam-treated groups were greater than those in the placebo group and that anxiolysis at the time of separation from the parents was judged excellent in 80-90% of the children who received midazolam. However, sedation and anxiolysis did not differ among the three midazolam groups. Mean times to discharge from hospital were similar for all four groups. The side effects, loss of balance and head control, blurred vision and dysphoric reactions were observed only in the 0.75 and 1.0 mg.kg-1 midazolam groups. We conclude that oral midazolam 0.5 mg.kg-1 is a safe and effective premedication and that 0.75 and 1 mg.kg-1 while offering no additional benefit, may cause more side effects.     

Comparaison de l’incidence sur le saignement de deux techniques anesthésiques midazolam-alfentanil versus propofol-alfentanil lors de la cure d’otospongiose

This study was performed to compare the incidence of bleeding associated with two anaesthetic techniques during otolaryngological microsurgery. Twenty-eight venous interpositions for otospongiosis have been carried out at random either under local anaesthesia combined with light sedation (midazolam 0.1 mg.kg-1 and alfentanil 0 micrograms.kg-1) or using general anaesthesia (propofol 2.5 mg.kg-1, then 9 mg.kg-1.hr-1 and alfentanil 30 micrograms.kg-1, then 15 micrograms.kg-1). The patients' lungs were mechanically ventilated. Every ten minutes, heart rate, arterial blood pressure and FETCO2 were observed. Bleeding was assessed on a four-point scale and evaluated according to its duration and the annoyance that it caused. General anaesthesia was clinically better tolerated. Heart rate and arterial blood pressure were lower than with general anaesthesia. The end-expiratory CO2 was 4.7 +/- 0.2 per cent. Bleeding was less frequent, lasted less time, but when it occurred the surgical disturbance was identical in the two groups. General anaesthesia produced a less bloody operating field and local anaesthesia required the cooperation of the patient.     

Halothane inhibits hypoxic pulmonary vasoconstriction in the presence of cyclooxygenase blockade

Using an isolated lung the effects of halothane on hypoxic pulmonary vasoconstriction (HPV) were studied in the presence of cyclooxygenase blockade. The pulmonary vasculature can be divided into arterial, middle and venous segment resistances. Analysis of the vascular pressure-flow relationship further separates resistance into a flow dependent resistance (1/slope) and a zero-flow pressure intercept (PCRIT). We ventilated six lobes with control (35 per cent O2) and hypoxic (three per cent O2) gas mixtures with the addition of either 0, 0.5, 1.0, or 2.0 per cent halothane. We found that after addition of indomethacin (5 mg.kg-1), ventilation with three per cent O2 increased total resistance by 87 per cent over baseline with the increase primarily in the middle vascular segment. During normoxic ventilation PCRIT was 7.9 cm H2O and this increased significantly with hypoxia to 11.5 cm H2O). Only 2.0 per cent halothane blocked the increases in middle segment resistance and in PCRIT. We conclude that following cyclooxygenase blockade, halothane inhibits HPV by acting on middle segment vessels.     

A comparison of the cerebral pressure-flow relationship for halothane and isoflurane at haemodynamically equivalent end-tidal concentrations in the rabbit

The cerebral pressure-flow relationship for halothane and isoflurance was studied at end-tidal concentrations which resulted in similar baseline mean arterial pressure (MAP). Two groups of New Zealand white rabbits (n = 8; each group) were studied with five regional blood flow determinations in each animal. Blood flow was determined by injecting radioactive microspheres during the following conditions: injection 1: after stable 2.05 per cent end-tidal isoflurane (1.0 MAC) Group I; or after stable 0.74 +/- 0.04 per cent end-tidal halothane (0.53 MAC) Group H. Injections 2-5: after MAP was increased 20, 40, 60, and 80 per cent respectively above baseline MAP by phenylephrine infusion. Baseline MAP was the same for both groups (64.3 +/- 3.1 vs 67.2 +/- 2.0 mmHg; mean +/- SEM; Group I and H respectively). Baseline total CBF (tCBF; 0.68 +/- 0.03 vs 0.86 +/- 0.05) and hemispheric CBF (hCBF; 0.64 +/- 0.03 vs 0.96 +/- 0.06) were significantly greater in Group H; no significant difference between groups was seen for baseline posterior fossa CBF (pCBF; 0.79 +/- 0.06 vs 0.75 +/- 0.04). For each experiment a pressure-flow curve was generated by curvilinear regression analysis. Significantly greater phenylephrine concentrations were required for injections 2-5 in Group H. Mean slopes and intercepts were derived for each group. Within each group comparison of the pressure-flow curves for hCBF vs MAP and pCBF vs MAP showed autoregulation was less impaired in posterior fossa structures (cerebellum and brain stem) for both anaesthetic agents (P less than or equal to 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Tussive effect of a fentanyl bolus

The aim of this study was to investigate the incidence of pre-induction coughing, after an iv bolus of fentanyl. The study sample was 250 ASA physical status I-II patients, scheduled for various elective surgical procedures. The first 100 were randomly allocated to receive 1.5 micrograms.kg-1 fentanyl via a peripheral venous cannula (Group 1), or an equivalent volume of saline (Group 2). Twenty-eight per cent of patients who received fentanyl, but none given saline, coughed within one minute (P less than 0.0001). The second 150 patients were then randomly assigned to three equal pretreatment groups. Group 3 received 0.01 mg.kg-1 atropine iv one minute before fentanyl. Groups 4 and 5 received 0.2 mg.kg-1 morphine im, and 7.5 mg midazolam po, respectively, one hour before fentanyl. Thirty per cent of patients in Group 3, 6% in Group 4, and 40% in Group 5, had a cough response to fentanyl. Fentanyl, when given through a peripheral cannula, provoked cough in a considerable proportion of patients. This was not altered by premedication with atropine or midazolam, but was reduced after morphine (P less than 0.01). Coughing upon induction of anaesthesia is undesirable in some patients, and stimulation of cough by fentanyl in unpremedicated patients may be of clinical importance.