Lumbar epidural anaesthesia prevented prostaglandin E1 — induced diuretic effect in enflurane anaesthetized patients

Prostaglandin E₁, (PGE,) is used to induce deliberate hypotension during anaesthesia. The purpose of this study was to compare the PGE₁ induced diuretic effect in anaesthetized patients with and without lumbar epidural anaesthesia. The changes in haemodynamic variables, urinary flow, one-hour creatinine clearance (Ccr), and fractional excretion of sodium (FE_Na) during injection of PGE₁, or a vehicle were compared in 42 surgical patients during enflurane anaesthesia with lumbar epidural anaesthesia (EPI group) with those in 44 surgical patients during enflurane anaesthesia alone (GA group). Patients in the GA group demonstrated increases in urinary flow (114 ± 46%) (mean ± SE), Ccr (74 ± 26%), and FE_Na (54 ± 23%) during PGE₁, infusion, which were not observed in the patients in the EPI group. Mean arterial pressure decreased during PGE₁, infusion from 92 ± 3 to 70 ± 2 mmHg in the GA group (P < 0.01) and from 85 ± 2 to 65 ± 1 mmHg in the EPI group (P < 0.01). Plasma antidiuretic hormone concentration during surgery was 12.5 ± 2.6 U. L^?1 in the GA group and 2.3 ± 0.8 U· L^?1 in the EPI group (P < 0.001). It is concluded that PGE₁ induced diuresis was prevented by lumbar epidural anaesthesia.     

Postoperative patientcontrolled epidural analgesia with opioid bupivacaine mixtures

Purpose

To determine the efficacy and safety of patient-controlled epidural analgesia of morphine or fentanyl in combination with bupivacaine for postoperative pain relief.

Methods p]Forty ASA 1–11 patients scheduled for major abdominal surgery were studied. After insertion of a lumbar epidural catheter, patients were given a non-opioid general anaesthetic. After surgery patients complaining of pain, received a loading dose of 2 mg morphine (Group I) or 50 μg fentanyl (Group II). For continuing pain, 1 mg morphine in 4 ml bupivacaine 0.125% (0.25 mg·ml^?1 morphine and 1 mg·ml^?1 bupivacaine, Group I) or 20 μg fentanyl in 4 ml bupivacaine 0.125% (5 μg·ml^?1 fentanyl and 1 mg·ml^?1 bupivacaine Group II) were administered. Blood pressure, heart rate, respiratory rate and SpO₂ were monitored. Assessments of pain (VAS), nausea-vomiting, motor block, pruritus and sedation were recorded for 24 hr.

Results

No difference in pain or sedation was observed between groups, The 24 hr postoperative opioid consumption was 15.50 ± 7.53 mg morphine and 555.10 ± 183.85μg fentanyl. Total bupivacaine 0.125% consumption was 58.00 ± 30.14 ml in Group I and 101.05 ± 36.77 ml in Group II. One patient in Group II complained of motor weakness in one leg. The incidence of nausea (Group I 45%, Group II 10%P < 0.05) and pruritus (Group I 30%, Group II 5%P < 0.05) was less in patients receiving fentanyl. Conclusion: Both methods were effective in the prevention of pain but, because of fewer side effects, fentanyl may be preferable to morphine.     

Epidural and intravenous bolus morphine for postoperative analgesia in infants

Purpose

To compare two doses of bolus epidural morphine with bolus iv morphine for postoperative pain after abdominal or genitourinary surgery in infants.

Methods

Eighteen infants were randomly assigned to bolus epidural morphine (0.025 mg · kg^?1 or 0.050 mg · kg^?1) or bolus iv morphine (0.050–0.150 mg · kg^?1). Postoperative pain was assessed and analgesia provided, using a modified infant pain scale. Monitoring included continuous ECG, pulse oximetry, impedance and nasal thermistor pneumography. The CO₂ response curves and serum morphine concentrations were measured postoperatively.

Results

Postoperative analgesia was provided within five minutes by all treatment methods. Epidural groups required fewer morphine doses (3.8 ± 0.8 for low dose [LE], 3.5 ± 0.8 for high dose epidural [HE] vs. 6.7 ± 1.6 for iv, P < 0.05) and less total morphine (0.11 ± 0.04 mg · kg^?1 for LE, 0.16 ± 0.04 for HE vs 0.67 ± 0.34 for iv, P < 0.05) on POD1 Dose changes were necessary in all groups for satisfactory pain scores. Pruritus, apnoea, and haemoglobin desaturation occurred in all groups. CO₂ response curve slopes, similar preoperatively (range 36–41 ml · min^?1 · mmHg ETco ₂ ^?1 · kg^?1) were generally depressed (range, 16–27 ml · min^?1 · mmHg ETco ₂ ^?1 · kg^?1) on POD1. Serum morphine concentrations, negligible in LE (<2 ng · ml^?1), were similar in the HE and iv groups (peak 8.5 ± 12.5 and 8.6 ± 2.4 ng · ml^?1, respectively).

Conclusion

Epidural and iv morphine provide infants effective postoperative analgesia, although side effects are common. Epidural morphine gives satisfactory analgesia with fewer doses (less total morphine); epidural morphine 0.025 mg · kg^?1 is appropriate initially. Infants receiving epidural or iv morphine analgesia postoperatively need close observation in hospital with continuous pulse oximetry.     

Prostaglandin E1 attenuates the hypertensive response to tracheal extubation

Purpose

Tracheal extubation causes hypertension and tachycardia, which may cause imbalance between myocardial oxygen demand and supply in patients at risk of coronary artery disease. We conducted a randomized, controlled study to evaluate the effects of 0.05 or 0.1 μg · kg^?1 · min^?1 prostaglandin E₁, (PGE₁) iv on haemodynamic variables occurring during tracheal extubation and emergence from anaesthesia and compared them in patients receiving either lidocaine or saline.

Methods

Eighty ASA physical status I patients undergoing elective surgery were enrolled in the current study. Anaesthesia was maintained with sevoflurane 1.0%–2.5% (ET concentration) and nitrous oxide 60% in oxygen. Muscle relaxation was achieved with vecuronium. The patients were randomly assigned to receive one of four treatments (n = 20 each): saline (control), 0.05 μg · kg^?1 · min^?1 PGE₁, 0.1 μg · kg^?1 · min^?1 PGE₁, or 1 mg · kg^?1 lidocaine. PGE₁ was infused from completion of surgery until five minutes after tracheal extubation. Changes in heart rate (HR) and blood pressure (BP) were measured during and after tracheal extubation.

Results

In the control group, the HR, systolic BP, and diastolic BP increased during tracheal extubation. Administration of 0.1 μg · kg^?1 · min^?1 PGE₁ and 1 mg · kg^?1 lidocaine attenuated the increases in BP although 0.05μg · kg^?1 · min^?1 PGE₁ failed to do so. The inhibitory effect of the 0.1 μg · kg^?1 · min^?1 PGE₁ on BP was similar to that of lidocaine 1 mg · kg^?1 iv. The increase in HR was attenuated by lidocaine but not by PGE₁.

Conclusion

The intravenous infusion of 0.1 μg · kg^?1 · min^?1 PGE₁ given during emergence from anaesthesia and tracheal extubation is a useful method for attenuating the hypertension associated with noxious stimuli during this period.     

Comparison of renal function under deliberate hypotension during epidural plus light-enflurane anesthesia and during enflurane anesthesia

We compared the effects of deliberate hypotension induced with trimethaphan on renal function and renal tubular damage under combined epidural and light-enflurane anesthesia (epidural group) and enflurane anesthesia alone (enflurane group). The mean arterial blood pressure was maintained at 50–55 mm Hg for 2.5 h in both groups using continuous infusion of trimethaphan. The urine volume and free water clearance were significantly greater in the epidural group than in the enflurane group [1.8±1.8 (SD)vs 0.4±0.3 ml·kg⁻¹·h⁻¹ and 0.81±1.30vs −0.15±0.22 ml·min⁻¹, respectively] (P<0.05). The creatinine clearance and fractional sodium excretion rate did not differ significantly between the two groups. Urinary excretion of norepinephrine was significantly less in the epidural group than in the enflurane group (P<0.05); however, epinephrine excretion did not differ. Urinary excretion ofN-acetyl-β-d-glucosaminidase was significantly less in the epidural group than in the enflurane, group (4.2±2.5vs 12.2±4.6 U·g⁻¹ CR) (P<0.01). The plasma antidiuretic hormone concentration was significantly lower in the epidural group compared to the enflurene group (13±23vs 57±42 pg·ml⁻¹) (P<0.05). No significant difference in plasma atrial natriuretic peptide concentration was found between the groups. We conclude that renal function during trimethaphan-induced hypotension is better maintained under epidural plus light-enflurane anesthesia than under enflurane anesthesia alone.     

Patient-controlled epidural analgesia in labour: varying bolus dose and lockout interval

This double-blind prospective study was designed to determine the best dose variables for patient-controlled epidural analgesia (PCEA) and to compare bolus-only PCEA with continuous infusion epidural analgesia (CIEA) during the first stage of labour. Five groups of parturients self-administered 0.125% bupivacaine with 1:400,000 epinephrine and fentanyl 2.5 μg·ml^?1 using PCA pumps programmed as follows: Group A, 2 ml bolus/10 min lockout interval (LI); Group B, 3 ml bolus/15 min LI; Group C, 4 ml bolus/20 min LI; Group D, 6 ml bolus/30 min LI; Group E, 8 ml·hr^?1 continuous infusion. Hourly assessments included: VAS scores for pain and satisfaction, sensory and motor block, bupivacaine and fentanyl consumption. Blood samples were collected at birth for maternal and fetal fentanyl concentrations. Data from 68 patients showed no differences among groups in pain relief or maternal satisfaction. Most patients received excellent analgesia and those requiring extra epidural supplements were evenly distributed across groups. There was higher consumption of bupivacaine and fentanyl in Group E than in any of the other four groups: bupivacaine mg·hr^?1, mean (SD), 9.4 (2.7) in Group E vs 5.2 (1.7) in Groups A-D inclusive (P<0.0001); fentanyl μg·hr^?1, 19.6 (4.6) in Group E vs 12.6 (7.5) in Groups A-D inclusive (P<0.05). Motor block was minimal, whereas sensory levels were higher at the 3- and 4-hour assessments in Groups D and E than in all other groups (P<0.05). Plasma fentanyl concentrations were <0.5 ng·ml^?1 in all samples and no sequelae from fentanyl were observed, apart from mild pruritus. Bolus-only PCEA is a safe and effective alternative to CIEA during the first stage of labour irrespective of the initial dose variables selected.     

Thoracic epidural block attenuates cardiovascular response to apnea in rabbits

Purpose

Apnea is one of the potential complications during anaesthesia. If sympathetic nerve activity is blocked by epidural anaesthesia, circulatory responses to apnea might change. Our objective was to assess the potential modifying effects of epidural anaesthesia on the cardiovascular responses to apnea in the animals.

Methods

Twenty rabbits anaesthetised with pentobarbital (25 mg·kg^?1 iv, 8 mg·kg^?1·hr^?1) and pacuronium bromide (0.2 mg·kg^?1·hr^?1 iv) were randomly assigned to one of two groups: control (n = 10) and epidural (n = 10). In the control group, 0.6 ml saline, and in the epidural group, 0.6 ml lidocaine 1% was injected into the epidural space respectively. After mechanical ventilation with FIO₂ 0.4, apnea was induced by disconnecting the anaesthetic circuit from the endotracheal tube, and mean arterial pressure (MAP), heart rate (HR), and time to cardiac arrest were measured.

Results

Before apnea MAP was lower in the epidural than in the control group (73 ± 10vs 91 ± 10 mmHg,P < 0.05). Heart rate was not different between groups (264 ± 36vs 266 ± 24 bpm). Mean arterial pressure increased in the control group after apnea, but not in the epidural group. The time to cardiac arrest was less in the epidural group than in the control group (420 ± 67vs 520 ± 61 sec,P < 0.05). Heart rate decreased markedly after apnea in the control group whereas it decreased gradually in the epidural group.

Conclusion

Thoracic epidural anaesthesia attenuated cardiovascular response to apnea and reduced the time to cardiac arrest.     

Methylprednisolone inhibits increase of interleukin 8 and 6 during open heart surgery

It has been reported that interleukin 8 (IL-8) and interleukin 6 (IL-6) are two of the chemical mediators causing myocardial injury. It is not clear whether treatment with corticosteroids in vitro in these patients can prevent the production of interleukin 8 and 6. This prospective study was conducted to investigate whether methylprednisolone (MP) pretreatment (30 mg · kg^?1 before CPB and before declamping of aorta) influenced the production of IL-8 and 6 in the peripheral circulation in 27 patients undergoing elective coronary artery bypass surgery. The IL-8 and IL-6 concentrations were measured by ELISA kit. We also studied the effect of MP pretreatment on postoperative cardiac Junction. Serum concentration of IL-8 in non-MP-treated patients (37 ± 44 pg · ml^?1 preoperatively) increased to 169 ± 86 pg · ml^?1 60 min after declamping of the aorta (P < 0.001). The increase was greater than the increase from 22 ± 8.9 pg · ml^?1 to 52 ± 35 pg · ml^?1 in the MP-treated patients (P < 0.01). Serum IL-6 concentration in non-MP-treated patients increased from the preoperative value of 59 ± 30 pg · ml^?1 to 436 ± 143 pg · ml^?1 60 min after declamping of the aorta (P < 0.001). The increase was greater than the increase from 36 ± 15 pg · ml^?1 to 135 ± 55 pg · ml^?1 in the MP-treated patients (P < 0.01). Furthermore, postoperative cardiac index in MP-treated patients (3.6 ± 1.1 L · min^?1· m^?2) was higher than 2.3 ± 0.8 L · min^?1 · m^?2 of non MP-treated patients (P < 0.05). The levels of IL-8 max during surgery correlated negatively with postoperative cardiac index (γ = ?0.67). These results suggest that methylprednisolone suppresses production of IL-8 and 6.     

Effects of olprinone on hepatosplanchnic circulation and mitochondrial oxidation in a porcine model of endotoxemia

Purpose This study was performed in order to assess the effects of olprinone, a phosphodiesterase III inhibitor, on hepatic oxygen delivery (DO₂H), oxygen consumption (VO₂H), and mitochondrial oxidation in the liver of a porcine endotoxemia model. Methods Fourteen pigs received continuous infusion of endotoxin via the portal vein for 240 min. From t = 150 to t = 240 min, animals were randomly divided into two groups to receive saline (control [CONT]; n = 7), or olprinone (OLP; n = 7) via the central vein. Results In the OLP group, prior to olprinone treatment at 150 min, endotoxin induced significant decreases in the cardiac index (CI; from 120 ± 31 to 65 ± 13 ml·kg⁻¹·min⁻¹; P < 0.01) and DO₂H (from 3.58 ± 0.81 to 1.55 ± 0.49 ml·kg⁻¹·min⁻¹; P < 0.01), while VO₂H was maintained. After administration of olprinone (from t = 150 to t = 240 min), CI was unchanged, while DO₂H increased from 1.55 ± 0.49 to 1.93 ± 0.38 ml·kg⁻¹·min⁻¹ (P < 0.01) and VO₂H increased from 0.42 ± 0.28 to 0.69 ± 0.38 ml·kg⁻¹·min⁻¹ (P < 0.01). At t = 240 min, the oxidation level of cytochrome aa3 was significantly higher in the OLP group than in the CONT group (OLP, 66.2 ± 19.3% vs CONT, 26.4 ± 17.3%; P < 0.01). Conclusion Our data for this porcine endotoxemia model suggest that olprinone may have beneficial therapeutic effects in restoring not only systemic and hepatic circulation but also mitochondrial oxidation in the liver.     

Comparison between epidural infusion of fentanyl/bupivacaine and morphine/bupivacaine after orthopaedic surgery

Purpose

To compare epidural infusions of bupivacaine-fentanyl and bupivacaine-morphine mixtures for postoperative pain relief after total hip replacement.

Methods

In a prospective, randomized, double-blind study, 30 ASA physical status I–II patients undergoing total hip replacement were studied. Anaesthesia was provided by combined general/epidural anaesthesia without epidural opioids. Postoperative epidural analgesia was by continuous infusion of bupivacaine 0.125% (4 ml·hr^?1) with either 0.05 mg·ml^?1 morphine (morphine, n = 15) or 0.005 mg·ml^?1 fentanyl (fentanyl, n = 15). Visual analogue pain scale (VAS), sedation (fourpoint scale), respiratory rate, pulse oximetry, rescue analgesics and supplemental oxygen were recorded by a blind observer at 1,3, 6, 9, 12 and 24 hr after surgery.

Results

No differences in pain relief, sedation, or non-respiratory side effects were observed between the two groups. Rescue analgesics were required in three patients in the fentanyl group (20%) and in two receiving morphine (13.3%) (P:NS). Two patients in the fentanyl group and three in the morphine group required oxygen due to SpO₂ < 90% (P:NS). Both opioid/bupivacaine mixtures decreased haemoglobin oxygen saturation compared with preoperative values. The mean ± SD SpO₂ values measured at 3,6, 12 and 24 hr were 94.4 ± 1, 92.6 ± 0.9, 92 ± 0.8, and 92.8 ± 1 in the morphine group, 95.3 ± 0.5, 95 ± 0.5, 94.6 ± 1.2, and 95.6 ± 1 in the fentanyl group (P < 0.05).

Conclusion

Continuous epidural infusion of bupivacaine-morphine or bupivacaine-fentanyl mixtures provided similar pain relief. Patients receiving morphine showed a more marked decrease in SpO₂ than those receiving fentanyl. However, the average SpO₂ remained > 90% in both groups.     

Haemodynamic changes during induced hypotension — comparison of trimethaphan with prostaglandin E1 assessed using transoesophageal echocardiography

Haemodynamic changes during induced hypotension depend upon the hypotensive agent used. We investigated if, using transoesophageal echocardiography (TEE), we could identify the haemodynamic differences between trimethaphan and prostaglandin E₁. Twenty-nine patients undergoing total hip replacement were selected for study. Hypotension was induced to a mean arterial pressure of 8.0– 9.3 kPa with either trimethaphan (5–20 μg · kg^?1 min^?1) or prostaglandin E₁ (0.5–2.0 μg · kg^?1 min^?1). The left atrial dimension, cardiac output, fractional shortening, pulmonary venous flow and mitral valve flow were evaluated using TEE. During induced hypotension, left atrial dimension decreased in both trimethaphan and prostaglandin E₁ groups (P < 0.05). In the trimethaphan-treated patients systolic velocity in pulmonary venous flow decreased from 41.9 ± 4.8 cm · sec^?1 before induced hypotension to 27.8 ± 4.2 cm · sec^?1 by 30 min after stable hypotension had been established (P < 0.01). The late/early ratio of peak velocity in mitral blood flow decreased in prostaglandin E₁ treated patients. Cardiac output increased from 4.2 ± 0.5 L · min^?1 to 5.3 ± 0.4 L · min^?1 during 30 min hypotension with prostaglandin E₁ administration (P < 0.05), but cardiac output decreased from 5.0 ± 0.5 to 3.5 ± 0.4 L · min^?1 with trimethaphan (P < 0.01). The differences in haemodynamic variables could be attributed to the venule dilatation effect of trimethaphan. We conclude that it was possible to detect the haemodynamic differences between trimethephan and prostaglandin E₁ using TEE.     

The inhibitory effect of esmolol on human plasmacholinesterase

Esmolol, a new cardioselective beta adrenergic blocker inhibits plasmacholinesterase activity in vitro. The concentration of esmolol hydrochloride that inhibits by 50 per cent the hydrolysis of 50.0 µnol·L^?1 benzoylcholine hydrochloride by 1:200 diluted, heparinized pooled plasma of six healthy volunteers at 37° C and 240 nm, determined by the ultraviolet spectrophotometric method of Kalow, was 50 µmol·^?1. Esmolol’s primary metabolite, 3-(4-(2-hydroxy-3-(isopropylamino)propoxy)-phenyllpropionic acid, had an l₅ = 190 µnol·L^?1 . The benzoylcholine hydrolysis rates in the plasma of ten patients who received an esmolol infusion of 500 µg·kg^?1. min^?1 for 4 minutes were 58.6 ± 6.2 µmol·hr^?1·ml^?1 (mean ± SE) before and 55.1 ± 6.6 µmol·hr^?1·ml^?1 after the infusion. The benzoylcholine hydrolysis rates in the plasma of ten patients who received an esmolol infusion of 500 µg·kg^?1·min^?1 for two minutes and 200 µg·kg^?1·min^?1 for an additional two minutes were 70.2 ± 8.9µmol·hr^?1·ml^?1 before and 69.1 ± 9.5 µmol·hr^?1. ml^?1 after the infusion. The pre- and post-infusion plasmacholinesterase activities were not significantly different. Since plasmacholinesterase is responsible for the hydrolysis of succinylcholine and that of the ester-type local anaesthetics this lack of in vivo interaction of esmolol with the hydrolysis of these drugs should be further confirmed by experiments with these combinations in man.     

A comparison of lumbar epidural and intravenous fentanyl infusions for post-thoracotomy analgesia

This double-blind randomised study compared the analgesic efficacy, respiratory effects, side effects, and pharmacokinetic disposition of 24 hr lumbar epidural and intravenous infusions of the same dosage regimen of fentanyl (1.5 μg · kg^?1 bolus then 1 μg · kg^?1 · hr^?1 infusion) in 50 patients after thoracotomy. Patients received either epidural fentanyl and intravenous normal saline, or epidural normal saline and intravenous fentanyl, for postoperative analgesia, after a standard low-dose alfentanil and isoflurane general anaesthetic. Visual analogue pain scores were lower in the epidural group (P < 0.05) only at two hours postoperatively, and there was no difference in the amount of supplementary morphine self-administered by patient-controlled analgesic pump. A mainly spinal analgesic effect probably occurred in the first few hours since fentanyl was not detectable in the plasma of patients in the epidural group until two hours after bolus injection; its concentration was less at that time than after intravenous injection (P < 0.05). Thereafter there was no difference in the plasma concentration profiles between the two groups. Seven patients in the epidural group and ten patients in the intravenous group received naloxone for PaCO₂ > 50 mmHg, and one patient in the intravenous group had the infusions stopped because of PaCO₂ elevation and somnolence. In patients who did not receive naloxone, the epidural route produced better analgesia throughout the study period (P < 0.01). Indices of respiratory centre function (apnoeas > 15 sec, slow respiratory rate < 10 min^?1, oxyhaemoglobin desaturation < 90% and PaCO₂) spirometric measures of pulmonary function, haemodynamic variables, morbidity, and other side effects, were similar in both groups, irrespective of naloxone therapy. Patients who had no respiratory depression and did not require naloxone had better analgesia with epidural fentanyl. However, this advantage did not result in better pulmonary function.     

Pulmonary gas exchange effects by nitroglycerin,dopamine and dobutamine during one-lung ventilation in man

The effects of nitroglycerin, dopamine and dobutamine on pulmonary gas exchange were determined in 21 adult patients during two-lung and one-lung ventilation. Nitroglycerin, in I μg·kg^?1·min^?1, decreased cardiac index (CI) andPaO₂ during both two-and one-lung ventilation, and increased in Qs/Qt during one-lung ventilation. There were no significant changes in the measured variables during infusion of dopamine, 5 μg·kg^?1·min^?1. Dobutamine, 5μg·kg^?1·min^?1, increased Cl and PaO₂ did not change during two-lung ventilation. During one-lung ventilation, PaO₂ increased from (mean value ±SD) 168 ± 46 to 201 ± 52 mmHg (P < 0.01) with dobutamine infusion. Qs/Qt decreased from 29.2 ± 7.0 to 26.0 ± 6.2 per cent (P < 0.05) without any change in pulmonary vascular resistance index during one-lung ventilation. We conclude that dobutamine has advantages over dopamine and nitroglycerin during one-lung ventilation.     

Free and total bupivacaine plasma concentrations after continuous epidural anaesthesia in infants and children

We measured free and total venous bupivacaine plasma concentrations in fourteen infants and children aged 6 days (2800 g) to 9 years (27 kg) undergoing epidural anaesthesia. An initial bolus of 0.5 ml·kg^?1 bupivacaine 0.25% was followed by a continuous infusion administered one h after bolus over a period of seven h (first hour 0.25 ml·kg^?1·h^?1 0.25%; then reduced to 0.125%). Although total bupivacaine plasma concentrations were within acceptable limits (<1.5 μg·ml^?1), four of the seven infants showed adverse reactions. Maximum plasma concentrations of free bupivacaine were significantly higher in infants (P<0.05) than in older children. We conclude that toxicity may be underestimated when only measuring total bupivacaine concentrations. In young infants the bupivacaine dose administered for continuous epidural anaesthesia should be further lowered below recommended concentrations and the patients closely observed for possible adverse reactions.     

Stress hormone responses to major intra-abdominal surgery during and immediately after sevoflurane-nitrous oxide anaesthesia in elderly patients

We studied the responses of plasma epinephrine, norepinephrine, adrenocorticotropic hormone (ACTH), cortisol, and antidiuretic hormone (ADH) during and immediately after sevoflurane-nitrous oxide anaesthesia supplemented with vecuronium in seven elderly patients (mean 76.6 ± 1.7 SEM) who underwent major intra-abdominal surgery. The plasma concentrations of norepinephrine, ACTH, cortisol, and ADH increased in response to surgical procedures (P <0.05). The plasma concentration of ADH increased to a peak concentration of 189.1 ± 20.7 pg · ml^?1 30 min after skin incision (P < 0.05). the plasma concentrations of epinephrine, norepinephrine, ACTH, and cortisol increased to peak concentrations of 408.6 ± 135.5 pg · ml^?1, 635.7 ± 167.8 pg · ml^?1, 222.6 ± 48.0 pg · ml^?1, and 113.6 ± 67.5 μg · dI^?1, respectively immediately after tracheal extubation (P <0.05). We conclude that, in the elderly patients, the responses of stress hormones to major intraabdominal surgery were preserved during sevoflurane-nitrous oxide anaesthesia sufficient to prevent increases in arterial pressure and heart rate. The strongest responses of epinephrine, norepinephrine, ACTH, and cortisol were elicited immediately after treacheal extubation.     

Antinociceptive effects of epidural and intravenous ketamine to somatic and visceral stimuli in rats

Purpose

To evaluate the antinociceptive effect of epidural and intravenous ketamine on somatic and visceral stimuli and to address the emergency reaction.

Methods

Rats were randomly allocated into nine groups (n = 6); five groups with chronically implanted epidural catheters received saline or 0.5, 1, 2 and 4 mg · kg^?1 ketamine epidurally, four groups received saline, or 1, 5 and 10 mg · kg^?1 ketamine iv. To assess somatic and visceral antinociceptive effects, tail flick (TF) test and colorectal distension (CD) test were carried out, respectively. Emergence reactions were graded. Maximal possible effects (% MPE) were calculated.

Results

Epidural ketamine increased % MPE in both tests in a dose-dependent fashion for 30 min (vs saline group, P < 0.05). Epidural ketamine 0.5 mg · kg^?1 produced an increase in % MPE in the CD test (P < 0.05) but failed in the TF test. Intravenous ketamine, 10 mg · kg^?1, produced 100 ± 0 (mean ± SE) % MPE in the CD test but 36 ± 15 % MPE in the TF test. Dose response curves indicated greater visceral antinociception than somatic. All rats showed emergence reactions following intravenous ketamine 10 and 5 mg · kg^?1.

Conclusion

Both epidural and intravenous ketamine produce greater antinociceptive effects to visceral than to somatic stimulation, and that epidural ketamine has a low incidence of emergence reactions.     

Isoflurane anaesthesia (0.6 MAC) and hypoxic ventilatory responses in humans

In order to evaluate the difference between poikilo-capnic (no CO₂ added to inspired gas) and iso-capnic (CO₂ added to keep end-tidal CO₂ constant) hypoxic ventilatory responses (HVR) awake and during 0.6 MAC isoflurane anaesthesia, seven cardio-pulmonary healthy patients were investigated. Pneumotachography and capnography were used before and during hypoxia (end-tidal O₂ tension approx. 7 kPa). In the awake stale, poikilo-capnic hypoxic challenges resulted in an increased HVR as indicated by a V?_E that on average increased by 1.4 ± 1.0 (mean ± s.d.) 1 · min^?1, whereas the iso-capnic hypoxic challenges resulted in a V?_E increase that was 4.7 ± 2.3 1 · min^?1 on average. In the anaesthetized state, the corresponding value during poikilocapnia was 1.3 ± 0.8 1 · min^?1 (88% of the awake responses, n.s.) and during iso-capnia 2.3 ± 1.4 1 · min^?1 (49% of the awake, P < 0.02). Awake HVR was achieved by greater tidal volumes during poikilocapnia as well as during isocapnic challenges, while respiratory rates were unchanged. In the anaesthetized state, during poikilocapnia, however, HVR was mediated by an increased respiratory rate, (from 17.5 ± 1.7 breath · min^?1 to 20.2 ± 2.2) and during isocapnia by a combination of increased rate (from 17.1 ± 1.9 breath · min^?1 to 19.1 ± 1.8) and tidal volume (from 496 ± 80 to 560 ± 83 ml). It is concluded that poikilocapnic HVR is maintained at 0.6 MAC isoflurane whereas iso-capnic HVR is depressed by 50%. In addition, both poikilo- and iso-capnic HVR were accomplished by greater tidal volumes at unchanged respiratory rates in the awake state while the opposite occurred during isoflurane anaesthesia. The more dominating chronotropic HVR during hypoxic challenge under anaesthesia will have to be further clarified in experimental studies.     

Decreased hypothalamic prostaglandin D2 and prostaglandin E2 contents during isoflurane anaesthesia in rats

This study was undertaken to evaluate the effect of isoflurane anaesthesia on the hypothalamic contents of both prostaglandin D₂ and E₂ which affect the sleep-wakefulness cycle. Sixty-three Wistar rats were divided into three equal groups, control, iso-flurane and recovery groups. Twenty-one rats of the control did not receive isoflurane. In the other groups 21 rats received isoflurane 2% far 30 min and 21 received isoflurane 2% for 30 min and were allowed to recover their usual behaviours, including righting reflex, spontaneously. The hypothalamus was removed and the contents of PGD₂ and PGE₂ were measured by enzyme immunoassay. The PGD₂ content in the hypothalamus was 397.9 ± 226.0 pg· g^{? 1} for the control group, 134.2 ± 41.2 pg· g^?1 for the isoflurane group and 269.1 ± 124.6 pg · g^?1 for the recovery group, respectively. The hypothalamic PGE₂ contents were 381.4 ± 139.0 pg · g^?1 for the control group, 183.3 ± 26.4 pg · g^?1 for the isoflurane group and 312.2 ± 96.0 pg · g^?1 for the recovery group, respectively. The hypothalamic PGD₂ and PGE₂ contents in the isoflurane group were lower (P < 0.05) than those in the control and recovery groups, while both the PGD₂ and PGE₂ contents of the control and the recovery groups were similar. We conclude that decreased hypothalamic PGD₂ and PGE₂ contents may be related to some manifestations of general anaesthesia with isoflurane.     

Adrenocorticotrophic hormone,cortisol and catecholamine concentrations during insulin hypoglycaemia in dogs anaesthetized with thiopentone

Glucose homeostasis is maintained by complex neuroendocrine control mechanisms. Increases in plasma concentrations of various glucose-raising hormones such as glucagon, catecholamines, adrenocorticotrophic hormone (ACTH), and cortisol are observed under certain conditions associated with stress (haemorrhage and hypoglycaemia). The purpose of this study was to determine the effect of thiopentone anaesthesia on the cathecholamine, ACTH and cortisol response to insulin hypoglycaemia in dogs. Blood sugar (BS), plasma cathecholamine, and ACTH, and serum cortisol concentrations were measured during the course of (1) an intravenous insulin test (ITT) and (2) an ACTH test in conscious and in anaesthetized fasted dogs. During the ITT, the anaesthetized dogs showed a moderate resistance, compared with conscious dogs, to the hypoglycaemic action induced by insulin (blood sugar concentration 30 min after insulin injection: 2.91 ± 0.25 vs 1.93 ± 0.12 mM · L^?1; P < 0.01). In addition, decreased epinephrine (220 ± 27 vs 332 ± 32 pg · ml^?1 ACTH (65 ± 6 vs 90 ± 5 pg · ml^?1) and cortisol (4.48 ± 0.3 vs 6.25 ± 0.5 μg · ml^?1) concentrations were detected 60 min after insulin injection (P < 0.01). The norepinephrine response to hypoglycaemia was not altered by anaesthesia (273 ± 33 vs 325 ± 25 pg · ml^?1). Anaesthetized dogs showed a decreased cortisol response to ACTH at 45 min (5.68 ± 0.54 vs 8.87 ± 0.47 μg · ml^?1) when compared with control dogs (P < 0.001). Haemodynamic variables during anaesthesia showed little changes (P < NS); while respiratory rate was altered (P < 0.01 between 60 and 105 min). Arterial pH was decreased (7.29 ± 0.03 vs 7.36 ± 0.04; P < 0.05) and PaCO₂ was increased (6.8 ± 0.3 vs 5.2 ± 0.3; P < 0.01) at 30 min from induction of anaesthesia but little change was seen after the beginning of the ITT and ACTH tests. We conclude that thiopentone anaesthesia provokes a moderate resistance to the hypoglycaemic action of insulin. This does not appear to be related to increases in plasma concentrations of cathecholamines, cortisol or ACTH. Since the hyperglycaemic effects of cathecholamines and glucagon are synergistic it is possible that glucagon plays an important role in the altered blood sugar response to insulin administration.