Pre-anesthesia Levels Research Articles

Oxidative injury and antioxidants in coronary artery bypass graft surgery: Off-pump CABG significantly reduces oxidative stress

Background Coronary artery bypass grafting (CABG) can now be performed with or without cardiopulmonary bypass. The former entails global ischemia followed by reperfusion after declamping, whereas the latter does not. In view of growing evidence that reperfusion is associated with oxidative stress, we studied the extent of oxidative stress and antioxidant status in patients undergoing on-pump and off-pump CABG to determine whether the latter significantly reduces oxidative stress. Methods Thirty patients were initially enrolled for the study. The inclusion criteria included patients with atherosclerotic triple vessel disease, undergoing elective CABG, with good LV function, no major risk factors for surgery, with all biochemical investigations within normal limits, having stable angina and no history of previous infarct. Patients with valvular heart disease, ventricular aneurysm, heart failure and poor left ventricular function were excluded. These were alternately posted for on-pump and off-pump CABG. Eight patients were excluded as they developed unforeseen complications during the surgery. Out of the remaining 22 patients, 13 underwent off-pump CABG and 9 underwent on-pump CABG. Five blood samples were collected; baseline, 5, 15, 60 min and 24 h after reperfusion. Samples were analyzed for thiobarbituric acid reactive substances (TBARS), glutathione (G-SH) and catalase (CAT). The results were compared with their preanaesthetic levels in both the groups and also with 20 age- and sex-matched normal healthy individuals. Results Lipid peroxidation was significantly increased after reperfusion in patients undergoing on-pump CABG, maximum increase ( p < 0.0001) was seen 1 h after reperfusion, whereas off-pump CABG reduces oxidative stress. The G-SH levels were significantly decreased after reperfusion in on-pump and off-pump CABG patients, maximum decrease ( p < 0.0001) was seen 5 min after reperfusion in on-pump CABG. The catalase activity was significantly increased after reperfusion in on-pump and off-pump CABG patients, maximum increase ( p < 0.0001) was seen 1 h after reperfusion in on-pump CABG. Conclusion Significant increase in oxidative stress was seen in patients undergoing on-pump CABG, whereas oxidative stress was less in off-pump CABG patients. The G-SH levels were decreased and Catalase activity was increased significantly in both on-pump and off-pump CABG patients.

Spinal anaesthesia in a patient with hereditary spastic paraplegia: case report and literature review

We report the use of spinal anaesthesia in a patient with hereditary spastic paraplegia who presented for manual removal of placenta following a normal vaginal delivery. This 18-year-old primigravida had been diagnosed with hereditary spastic paraplegia at 8 years of age when neurological examination revealed mild bilateral lower limb spasticity. A 25-gauge Whitacre spinal anaesthetic needle was inserted at the L3-4 intervertebral space and 0.5% plain bupivacaine 2 mL plus fentanyl 25 microg administered. The procedure was uneventful. At 24 hours postoperatively, there was full neurological recovery to pre-anaesthetic levels. The hereditary spastic paraplegias are a group of neurological disorders characterised by a slowly progressing spastic paraparesis. The neurological disorder and its anaesthetic implications are reviewed.

Alterations in the biochemical markers of renal function after sevoflurane anaesthesia

This study has been carried out to see whether renal function is acutely altered in patients undergoing sevoflurane anaesthesia. For this purpose, the urinary levels of markers of renal tubular function, namely leucine amino peptidase (LAP), gamma-glutamyl transferase (GGT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and beta-2 microglobulin (beta-2M), and urinary albumin as a predictor of renal glomerular function were measured before and after sevoflurane anaesthesia. This study was comprised of 20 patients (11 males and nine females) aged 18-55, who underwent various elective surgical procedures under general anaesthesia. Urine samples of all patients were collected before and 1, 2 and 8 h after the anaesthesia. The levels of LAP, GGT, beta-2M, and albumin were then expressed as factored by urinary creatinine. In all patients, the anaesthesia was maintained with sevoflurane (2% end-tidal) at a high flow-rate (6 L/min). Urinary beta-2M and LAP levels after anaesthesia were unchanged (P > 0.05). While urinary GGT and ALP levels were found elevated in the first hour, LDH levels were higher in the second hour (P < 0.05). They returned to normal levels in the later periods after the anaesthesia. Urinary albumin excretion (UAE) was significantly elevated in the second hour after the anaesthesia (P < 0.001). Although UAE was decreased in the eighth hour after the anaesthesia, it still remained higher than the pre-anaesthesia level (P < 0.001). These results suggest that a 2% end-tidal concentration of sevoflurane at a high flow-rate (6 L/min) acutely alters renal glomerular function but does not have a significant acute effect on biochemical markers of renal tubular damage.

Anaesthetic management of Osler–Weber–Rendu syndrome with coexisting congenital methaemoglobinaemia

A 9-year-old cyanosed child suffering from Osler-Weber-Rendu syndrome with bilateral pulmonary arteriovenous malformations (PAVMs) was posted for cerebral angiography under general anaesthesia. Careful preanaesthetic evaluation led to the diagnosis of coexisting congenital methaemoglobinaemia. There is no previous report of Osler-Weber-Rendu syndrome coexisting with congenital methaemoglobinaemia. This report emphasizes that a second contributory cause of cyanosis must be suspected and meticulously looked for if the symptomatology in a patient cannot be explained by a single established diagnosis. Positive-pressure ventilation was associated with reduction in arterial oxygenation despite an increasing inspired oxygen concentration, which returned to preanaesthetic levels only after extubation and resumption of spontaneous respiration.

Transient and sustained changes in myofilament sensitivity to Ca2+ contribute to the inotropic effects of sevoflurane in rat ventricle

The volatile anaesthetics isoflurane and sevoflurane induce both negative and positive inotropic effects in ventricular myocytes, the mechanisms of which are not fully understood. Previous data suggest that changes in myofilament Ca(2+) sensitivity contribute to their sustained negative inotropic effects. In this study, the role of changes in myofilament Ca(2+) sensitivity in both positive and negative inotropic effects of these agents was examined in intact ventricular myocytes. Contractility and cytosolic Ca(2+) (fura-2) were recorded optically in ventricular myocytes stimulated electrically (1 Hz) at 30 degrees C. Myofilament Ca(2+) sensitivity was assessed from plots of cell length against fura-2 fluorescence ratio (Fr) from individual twitches at various points before, during and after a 1 or 4 min exposure to 0.6 mM anaesthetic. Isoflurane reduced mean (sd) myofilament Ca(2+) sensitivity from 10.3 (1.9) to 5.9 (1.6) microm Fr(-1) (P<0.001) throughout a 1 min exposure, which returned to control on removal. In contrast, on initial exposure to sevoflurane, Ca(2+) sensitivity was reduced from 10.8 (1.3) to 4.3 (0.9) microm Fr(-1) (P<0.001) but this recovered partially towards control over 3 min. On removal, sensitivity was increased above control (to 17.7 (2.2) microm Fr(-1); P<0.001) before preanaesthetic levels were restored. These data show that both isoflurane and sevoflurane reduce apparent myofilament Ca(2+) sensitivity at steady state. However, sevoflurane (but not isoflurane) induced transient changes in apparent myofilament Ca(2+) sensitivity, which would contribute to its inotropic profile.

Cardiovascular responses of Chinook salmon ( Oncorhynchus tshawytscha) during rapid anaesthetic induction and recovery

The effects of three anaesthetics on induction and recovery were compared in Chinook salmon ( Oncorhynchus tshawytscha). Heart rate (HR), cardiac output (Q), dorsal aortic pressure (DAP) and stroke volume (SV) were measured in minimally disturbed salmon during 5 min anaesthetic inductions with approximately equi-potent concentrations of MS222 (100 ppm), metomidate (6–10 ppm) and AQUI-S (60 ppm). MS222 induction caused a steady decline in DAP only, while metomidate induction did not affect any cardiovascular variable. AQUI-S caused a biphasic response, and within 2 min had depressed HR, Q, DAP and SV by between 20 and 50%. In the final 3 min HR returned to pre-anaesthesia levels, and Q and SV climbed to greater than pre-anaesthesia levels. Blood samples taken pre- and post-anaesthesia showed all inductions caused hypoxaemia (oxygen partial pressure of dorsal aortic blood ( Pa o 2): MS222 47 mmHg, metomidate 35 mmHg, AQUI-S 21 mmHg). Haematocrit and plasma adrenaline and noradrenaline levels increased slightly in AQUI-S treated fish only. Recovery was monitored for 6 h post-anaesthesia, and was similar for each anaesthetic. All cardiovascular variables had returned to control levels within 5 min with the exception of DAP, which was initially slightly elevated (up to 20%) but returned to control values within 30 min. Anaesthesia is usually preceded by handling. Netting prior to anaesthesia caused significant increases in HR, Q and SV, which masked any anaesthetic dependent effects. Recovery from anaesthesia combined with surgery was also generally anaesthetic independent and recovery was prolonged, compared to anaesthesia alone. These data suggest limiting fish handling/manipulation is more important in minimising cardiovascular disturbance than the choice of anaesthetic.

Heritable differences in respiratory drive and breathing pattern in mice during anaesthesia and emergence

Postanaesthetic hypoxia and ischaemia can lead to postoperative morbidity and mortality. We studied the effect of isoflurane anaesthesia in two inbred mouse strains known for phenotypic differences in breathing pattern and respiratory drive during carbon dioxide challenge and their first-generation offspring (F(1)). Using whole body plethysmography, we assessed respiratory rate (RR) and pressure amplitude (Amp) in male B6 (high responder to hypercapnia), C3 (low responder), and F(1) mice at rest, during anaesthesia with isoflurane, and during recovery from anaesthesia. At each time point, the magnitude and pattern of breathing were determined during hypercapnic challenge (FI(CO(2)) = 0.08). Data (mean (SD)) were analysed by generalized ANOVA with post hoc Bonferroni's correction (P<0.05). During isoflurane anaesthesia, strain differences between B6 and C3 mice in RR were obscured while differences in Amp persisted. In contrast to baseline RR responses to carbon dioxide were significantly reduced at 0.5 MAC (increase in RR: 175 (33) bpm, 147 (44) bpm, 127 (33) bpm, for B6, C3, and F(1) strains respectively) and completely blocked at 1.5 MAC (change in RR: -3 (10) bpm, -2 (1) bpm, -4 (5) bpm, for B6, C3, and F(1) strains, respectively). During recovery, B6 mice showed a significant increase in RR (77 (33) bpm; P<0.0001) as well as in Amp. This was not observed in either C3 (-22 (31) bpm) or F(1) mice (23 (51) bpm). Isoflurane anaesthesia abolished the strain differences in respiratory drive between B6, C3, and F(1) mice. However, during recovery from anaesthesia, significant strain variation in respiratory drive reappeared and was more pronounced compared with pre-anaesthetic levels. These results suggested, that genetic differences may have minimal contribution to decreased respiratory drive during anaesthesia, but may be a major risk factor for post-operative hypoventilation and the associated morbidity and mortality.

Postoperative changes in visual evoked potentials and cognitive function tests following sevoflurane anaesthesia

We tested the hypothesis that minor disturbance of the visual pathway persists following general anaesthesia even when clinical discharge criteria are met. To test this, we measured visual evoked potentials (VEPs) in 13 ASA I or II patients who did not receive any pre-anaesthetic medication and underwent sevoflurane anaesthesia. VEPs were recorded on four occasions, before anaesthesia and at 30, 60, and 90 min after emergence from anaesthesia. Patients completed visual analogue scales (VAS) for sedation and anxiety, a Trieger Dot Test (TDT) and a Digit Symbol Substitution Test (DSST) immediately before each VEP recording. These results were compared using Student's t-test. P<0.05 was considered significant. VEP latency was prolonged (P<0.001) and amplitude diminished (P<0.05) at 30, 60, and 90 min after emergence from anaesthesia, when VAS scores for sedation and anxiety, TDT, and DSST had returned to pre-anaesthetic levels.

Surgical Stress Induces Endotoxin Hyporesponsiveness and an Early Decrease of Monocyte mCD14 and HLA-DR Expression During Surgery

It is generally accepted that major surgery is associated with severe alterations of the host-defense mechanisms. We investigated the effect of surgical stress on the immune system. Specifically, we studied the relationship between perioperative lipopolysaccharide (LPS) hyporesponsiveness and monocyte human leukocyte antigen-DR (HLA-DR) and CD14 expression during the perioperative period in 20 patients who underwent partial gastrectomy. This study demonstrated that surgical stress rapidly depressed monocyte mCD14 and HLA-DR expression in comparison with preanesthesia levels. Monocyte mCD14 expression recovered to preoperative levels on the first postoperative day, and monocyte HLA-DR expression recovered by the seventh postoperative day. Consistent with our previous study, LPS-induced tumor necrosis factor (TNF)-alpha production ex vivo was significantly suppressed from the beginning of the operation. On the contrary, the plasma interleukin-10 concentration started to increase after the surgical incision was made. LPS hyporesponsiveness was least at the end of the operation and returned to preoperative levels on the first postoperative day. In conclusion, the present study demonstrated that LPS responsiveness, plasma interleukin-10 concentration, and monocytes mCD14 and HLA-DR expression altered from the early period of surgery. These alterations may be related to the impairment of the immune system during the perioperative period. Recent studies demonstrate that surgical stress induces immune dysfunction. We found that surgical stress rapidly decreased monocyte mCD14 and human leukocyte antigen-DR expression, and endotoxin responsiveness. These findings suggest that early changes of the immune system caused by surgical stress contribute to postoperative complications such as sepsis and multiple organ failure.

General versus regional anaesthesia for cataract surgery: effects on neutrophil apoptosis and the postoperative pro-inflammatory state

At clinically relevant concentrations, volatile anaesthetic agents influence neutrophil function. Our hypothesis was that sevoflurane would inhibit neutrophil apoptosis and consequently influence the postoperative pro-inflammatory state. In order to identify selectively the effect of the anaesthetic agent sevoflurane, we studied patients undergoing minimally stimulating (cataract) surgery randomly allocated to receive either sevoflurane (n = 11) or local anaesthesia (n = 12). Venous blood samples were taken immediately prior to anaesthesia and at 1, 8 and 24 h thereafter. The rate of neutrophil apoptosis, plasma concentration of cytokines and differential white cell count were measured. The rates of neutrophil apoptosis and plasma concentrations of IL-1β, TNF-α and IL-8 at each time point were similar in the two groups. IL-6 concentrations increased significantly and to a similar extent compared to preanaesthetic levels at 8 and 24 h. This study demonstrates that sevoflurane does not influence the rate of neutrophil apoptosis, cytokine concentrations and neutrophil count following cataract surgery.

Pulmonary Embolism as a Consequence of Applying Sequential Compression Device on Legs in a Patient Asymptomatic of Deep Vein Thrombosis

INTRAOPERATIVE pulmonary embolism (PE) is an uncommon complication of emergency intraabdominal surgery. Best practice recommendations for longer surgical cases include the fitting of antithrombotic leg devices such as stockings and pneumatic compression devices. 1,2 Although these devices certainly prevent thrombosis in deep vein thrombosis (DVT)-prone surgical patients, 1,2 we were unable to find reports of any significant complications caused by them (besides minor skin bruising, sores, etc.), namely, dislodgment of a pre-existing thrombus, causing a life-threatening PE. Although PE has been observed after tourniquet deflation in orthopedic surgery cases, 3 we report a case of PE possibly related to pneumatic sequential compression device.

Effects of plasma expansion on the pituitary-adrenocortical response to halothane anaesthesia in sheep

The study aimed to investigate the stimulus to adrenocortical activity that is induced by halothane anaesthesia. Groups of 7 sheep were anaesthetised with thiopentone and halothane (TH) or acepromazine, thiopentone and halothane (ATH). During 120 min of anaesthesia hypotension was prevented (mean arterial blood pressure kept at pre-anaesthetic level) by infusion of a modified gelatine plasma replacer given to effect (0.34–1.1 litres with TH and 1.1–3.1 litres with ATH). Pulse rate, arterial blood pressure and gases were measured and sequential samples withdrawn for analysis of plasma cortisol, adrenocorticotrophic hormone (ACTH), arginine vasopressin (AVP), glucose and lactate. Heart rate increased in the ATH but not the TH group. All sheep were well oxygenated but developed hypercapnia and respiratory acidosis. In both groups, cortisol increased more than 2-fold 20 min after the end of anaesthesia but there were no significant changes in ACTH. AVP was measured in the TH group only and increased 3-fold at the end of anaesthesia. Glucose and lactate remained stable except for lactate in the TH group which decreased during anaesthesia. These data indicate that hypotension is a major component of the stimulus inducing adrenocortical activity during halothane anaesthesia. However, maintenance of normotension did not entirely depress the response; halothane itself or decreased perfusion may also contribute.

Inpatient experience with remifentanil.

Inpatient experience with remifentanil.

Endocrine and metabolic responses to plasma volume expansion during halothane anesthesia in ponies.

The study was designed to contribute to identification of the stimulus to adrenocortical activity during halothane anaesthesia in equidae. Two groups of six ponies were premedicated with acepromazine before induction of anaesthesia with thiopentone and maintenance for 120 min with halothane in oxygen. In group H Haemaccel modified gelatine plasma replacer was infused (48+/-13 mL/kg) to maintain mean arterial blood pressure (MABP) close to preanaesthetic values. In group DH, blood pressure was maintained close to preanaesthetic levels with a lower dose of Haemaccel (10 mL/kg) combined with an infusion of dobutamine. Measurements were made before anaesthesia, at 20 min intervals during anaesthesia and 20 and 120 min after anaesthesia. MABP and blood gases, pulse and respiratory rates were measured, and blood was withdrawn for assay of cortisol, adrenocorticotrophic hormone (ACTH), glucose and lactate. Ponies in both groups became hyperoxic, hypercapnic and developed a respiratory acidosis; pulse rate increased in both groups but this was more marked in group H. Haematocrit decreased by 50% in H and by 20% in DH. Cortisol and ACTH did not change significantly during anaesthesia in either group and the area under the time curve (AUC(0-140)) was lower in the DH group. Plasma glucose and lactate remained stable. After the H treatment all ponies had a watery nasal discharge and one pony died from endotoxaemia. This investigation demonstrated that the adrenocortical response to halothane anaesthesia in ponies can be ameliorated by manipulation of ABP using plasma expansion with or without inotrope infusion; however, low dose Haemaccel with dobutamine was safer and more practical. It is suggested that, although hypotension is not the sole stimulus to adrenocortical activity during halothane anaesthesia, it may contribute, probably through an effect on tissue perfusion.

Adrenocortical and metabolic responses to dobutamine infusion during halothane anaesthesia in ponies.

The study investigated whether hypotension in halothane-anaesthetised ponies is the stimulus inducing an endocrine stress response by assessing the effect of maintenance of normotension with a dobutamine infusion. Groups of six ponies were studied. After premedication with acepromazine (0.04 mg/kg) anaesthesia was induced with thiopentone (10 mg/kg) and maintained for 120 min with halothane (group AN). Dobutamine was infused to effect (1.1-4.4 microg/kg/min) to maintain arterial pressure at pre anaesthetic levels. The conscious group (CON) were prepared as for AN and then received only dobutamine infusion 1.0 microg/kg/min for 120 min. Arterial blood pressure, pH, oxygen and carbon dioxide tension, pulse rate, haematocrit, and plasma cortisol, glucose and lactate concentrations were measured before, at 20 min intervals during anaesthesia, and 20 and 120 min after anaesthesia ceased. Blood pressure remained close to control in both groups. The AN group became hypercapnic and acidotic, pulse rate and haematocrit increased, cortisol increased more than twofold and plasma glucose and lactate did not change. All values remained at control in the CON group except for small increases in haematocrit and decreases in pulse rate. Maintenance of normotension during halothane anaesthesia did not blunt the adrenocortical response to anaesthesia nor did the same dose of dobutamine alone increase plasma cortisol. Hypotension appears not to be the sole stimulus to equine adrenocortical activity during halothane anaesthesia.

Interleukin-10 Production During and After Upper Abdominal Surgery

Study Objective: To evaluate the influence of major abdominal surgery on the plasma levels of interleukin-10 (IL-10). Design: Prospective study. Setting: University hospital. Patients: 10 ASA physical status I and II patients undergoing upper abdominal surgery. Interventions: All patients received combined general-epidural anesthesia with isoflurane and nitrous oxide, after insertion of an epidural catheter at T 8–T 9 dosed with 1.5% lidocaine. Measurements and Main Results: Plasma interleukin-6 (IL-6), interleukin-8 (IL-8), and IL-10 levels were determined with an enzyme-linked immunosorbent assay at preanesthesia, 0, 2, and 4 hours during surgery, and at the end of surgery, followed by sampling on the morning of postoperative days 1 (POD1) and 3 (POD3). Before anesthesia and at 0 hours of surgery, IL-10 was not detected. In all ten patients, the plasma levels of IL-10 showed significant elevations and achieved their maximal value 4 hours after the skin incision (p <0.05 vs. baseline). The plasma IL-10 levels returned to preanesthesia levels on POD3. The plasma levels of IL-6 and IL-8 also increased in the perioperative period. The peak cytokine levels correlated (r = 0.915, p = 0.0001 for IL-6 vs. IL-8; r = 0.82, p = 0.025 for IL-6 vs. IL-10; and r = 0.641, p = 0.06 for IL-8 vs. IL-10). The peak plasma IL-10 levels significantly correlated with the amount of intraoperative blood loss (r = 0.69, p <0.05). Conclusions: In patients undergoing major abdominal surgery, plasma IL-10 levels were elevated during and after operation. IL-10 may modulate the inflammatory responses in the perioperative period.

Perioperative transoesophageal echocardiography with low-dose dobutamine stress for evaluation of myocardial viability: a feasible approach?

The feasibility of low-dose dobutamine stress combined with transoesophageal echocardiography (TEE) to detect viable left ventricular myocardium was evaluated in 22 anaesthetised patients prior to sternotomy for elective coronary artery bypass grafting (CABG). After baseline measurements, a dobutamine infusion beginning with 5 micrograms.kg-1.min-1 was started and eventually increased to 10 micrograms.kg-1.min-1. Viability was assessed as visual improvement of left ventricular wall motion (LVWM). The criteria for discontinuation of the infusion were: 1. any changes in LVWM, 2. an increase in preanaesthetic blood pressure exceeding 40 mmHg, and/or a > 20% increase in preanaesthetic heart rate compared to preanaesthetic levels. An off-line evaluation of LVWM was based upon visualisation of the left ventricle in a transgastric short-axis mid-papillary (mid-P) view, and the left ventricle was divided into anterior, septal, inferior, and lateral segments. Moreover, an off-line semiautomatic analysing system was used for assessing regional and global LVWM. With this analysis the effects on LVWM from changes in preload and afterload could be addressed. 19 patients showed a decreased LVWM in one or several segments at baseline. A total of 36 segments exhibited decreased LVWM (an average of 1.9 segments/patient). Of these, 22 segments (61%) improved with dobutamine, while 12 segments (33%) did not, and 2 (6%) became more dysfunctional. Another 6 segments with normal motion at baseline became dysfunctional with dobutamine. According to the off-line semiautomatic analysing system for LVWM, there were no statistically significant changes with dobutamine stimulation. Only one patient showed an increased postoperative aspartateaminotransferase (ASAT) value (3.0 mmol.l-1) but no ECG changes. Since we regard the visual assessment of LVWM as being more applicable for this protocol than the semiautomatic analysis, we conclude that low-dose dobutamine stress echocardiography seems to be a feasible method for detecting viable myocardium in the anaesthetised patient scheduled for elective CABG surgery. However, the semiautomatic analysis complemented our findings, since the variations in pre- and afterload did not significantly change the size of the left ventricle, which hereby would imply LVWM changes.

Spinal Cord Motoneuron Excitability during Isoflurane and Nitrous Oxide Anesthesia

Recent evidence suggests that the spinal cord is an important site of anesthesia that is necessary for surgical immobility, but the specific effect of anesthetics within the spinal cord is unclear. This study assessed the effect of isoflurane and nitrous oxide on spinal motoneuron excitability by monitoring the H-reflex and the F wave. Eight adult patients, categorized as American Society of Anesthesiologists physical status 1 or 2, who were undergoing elective orthopaedic surgery were anesthetized with 0.6, 0.8, 1.0, and 1.2 times the estimated minimum alveolar concentration (MAC) of isoflurane. Nitrous oxide was added in graded concentrations of 30%, 50%, and 70%, whereas the isoflurane concentration was decreased to maintain a total MAC of 1. The H-reflex of the soleus muscle and the F wave of the abductor hallucis muscle were measured before anesthesia and 15 min after each change of anesthetic concentration. Four or more trials of the H-reflex and 18 trials of the F wave were recorded at each concentration of anesthesia. The effect of the anesthetics on the H-reflex and F wave was analyzed using. Dunnett's test. H-reflex amplitude was decreased to 48.4 +/- 18.6% of preanesthesia level at 0.6 MAC isoflurane and to 33.8 +/- 19.1% when isoflurane concentration increased from 0.6 MAC to 1.2 MAC. F wave amplitude and persistence decreased to 52.2 +/- 33.6% and 44.4 +/- 26% of baseline at 0.6 MAC isoflurane, and to 33.8 +/- 26% and 21.7 +/- 22.8% at 1.2 MAC isoflurane. Isoflurane plus nitrous oxide (total 1 MAC) decreased H-reflex amplitude to 30.4-33.3% and decreased F wave persistence to 42.8-56.3% of baseline. Both isoflurane alone and isoflurane plus nitrous oxide decrease H-reflex and F-wave amplitude and F-wave persistence. These effects suggest that isoflurane and nitrous oxide decrease motoneuronal excitability in the human spinal cord. This may play an important role in producing surgical immobility.

The Influence of Various Anesthetics on the Release and Metabolism of Thyroid Hormones

Normal functioning of the thyroid gland during surgery is important, but few data are available on the possible interactions between anesthesia and thyroid hormones.In two independent studies we examined the influence of different types of general anesthesia on the plasma levels of the thyroid hormones. They revealed an intraoperative increase of free thyroxine (fT4) and total thyroxine (tT4) in plasma to approximately 150% of preanesthesia levels when enflurane was used. No increase in thyroid-stimulating hormone (TSH) secretion was noted prior to this. The increase was not due to a quantitative change in the binding proteins. The plasma levels of fT4 and tT4 returned to normal postoperatively; however, no accompanying increase in plasma triiodothyronine levels was observed. Hence we assume the increase to be due to hormone release from thyroid and/or extrathyroidal stores--an intercompartmental shifting. (Anesth Analg 1995;81:612-8)

Augmented Thermic Effect of Amino Acids under General Anaesthesia: A Mechanism Useful for Prevention of Anaesthesia-Induced Hypothermia

1. Intravenous infusion of amino acids stimulates energy expenditure and heat accumulation in normal man. To find out whether such stimulation also occurs during general anaesthesia, thermogenesis was measured in 21 patients before, during and after anaesthesia and surgery. 2. Ten patients received a mixture of 19 amino acids (240 kJ/h) infused intravenously throughout the anaesthesia. The other 11 patients, serving as controls, received saline. Using catheters previously inserted into the pulmonary and a systemic artery, cardiac output, arteriovenous oxygen difference, pulmonary oxygen uptake and mixed blood temperature were measured. 3. During anaesthesia and surgery, the blood temperature fell by 0.67 +/- 0.09 degrees C/h in the control patients and by 0.38 +/- 0.06 degrees C/h in the amino acid-treated patients. Anaesthesia during 34 +/- 4 min before surgery reduced the pulmonary oxygen uptake by 145 +/- 9 ml/min in the control patients and by 81 +/- 10 ml/min in the amino acid-treated patients, corresponding to reductions in total energy expenditure of 47 W in the control group and 26 W in the amino acid-treated group. The difference, 21 W, illustrates the thermogenic action of the amino acids. This value may be compared with that of 4 W, observed in unanaesthetized individuals subjected to 30 min of identical amino acid infusions. 4. At awakening after the anaesthesia, the oxygen consumption rose to 71 +/- 21% above the pre-anaesthesia level in the amino acid-treated patients, who, without shivering, rapidly returned to normothermia, whereas in the control patients the oxygen uptake remained slightly below the pre-anaesthesia level, despite sustained hypothermia and vigorous shivering.(ABSTRACT TRUNCATED AT 250 WORDS)