bluuebunny/crossref_metadata_2025_split huggingface dataset:
A large simple randomized trial of rocuronium versus succinylcholine in rapid‐sequence induction of anaesthesia along with propofol
Authors: Andrews J. I. , Kumar N. , Van Den Brom R. H. G. , Olkkola K. T. , Roest G. J. , Wright P. M. C. 
Published: March 2003

Background: Rocuronium has an onset of action more rapid than other non‐depolarizing neuromuscular blocking agents, but it is unclear whether it and succinylcholine give equivalent intubating conditions during rapid‐sequence induction of anaesthesia. We performed this study to answer the question – are there clinically relevant differences between the use of rocuronium and succinylcholine to secure acceptable intubating conditions during rapid‐sequence induction of anaesthesia with propofol?Methods: Anaesthesia was induced using propofol 2.5 mg/kg in 349 ASA physical status grade I–IV patients who were undergoing either elective or emergency surgery. Propofol was followed immediately by either rocuronium 0.6 or 1 mg/kg or succinylcholine 1.0 mg/kg (randomly selected). Fifty seconds after the end of muscle relaxant injection laryngoscopy was performed and intubating conditions were graded by an experienced anaesthetist blind to the muscle relaxant allocation. This study design was selected so that a 10% difference in clinically acceptable intubating conditions between drugs would be detectable.Results: In this setting rocuronium 1.0 mg/kg provided superior intubating conditions compared with rocuronium 0.6 mg/kg. The incidence of clinically acceptable intubating conditions with rocuronium 1.0 mg/kg and succinylcholine 1.0 mg/kg was 93.2% and 97.1% respectively, the difference being −3.9% (95% C.I. −9.7% to 1.9%).Conclusion: Rocuronium 1.0 mg/kg given along with propofol in a rapid‐sequence induction of anaesthesia is clinically equivalent to succinylcholine 1.0 mg/kg.
Time dependency of the ratio of umbilical vein/maternal artery concentrations of vecuronium in caesarean section
Authors: Iwama H. , Kaneko T. , Tobishima S. , Komatsu T. , Watanabe K. , Akutsu H. 
Published: March 2003

Background: The ratio of umbilical vein (UV) and maternal artery (MA) concentrations of vecuronium may more accurately determine the placental transfer ratio during caesarean section. This ratio potentially correlates with the time from induction of anaesthesia to delivery (I‐D time). The aim of this study was to determine the UV/MA ratio of vecuronium and its relationship with the I‐D time.Methods: Eighteen pregnant women at full term undergoing caesarean section were studied. The parturient was given intravenously 0.01 mg/kg vecuronium as a priming dose, followed 180 s later by 0.11 mg/kg vecuronium as an intubation dose and 4 mg/kg thiamylal. The time from the injection of the intubation dose to the clamping of the umbilical cord was regarded as the I‐D time. At the time of clamping the umbilical cord, blood samples were collected and the UV and MA of vecuronium were measured.Results: The UV/MA ratio and the I‐D time, expressed as the mean (SD), were 0.056 (0.016) and 280 (57) s, respectively. The regression equation indicated y=0.0083+0.00017×(R2=0.381, r=0.617, P=0.0063, I‐D time (s)=x, UV/MA=y).Conclusion: The present study demonstrated that the UV/MA ratio of vecuronium as an index of the placental transfer becomes smaller as the delivery time after injection of this drug becomes shorter during caesarean section.
Clinical evaluation of low‐flow sevoflurane anaesthesia for paediatric patients
Authors: Igarashi M. , Watanabe H. , Iwasaki H. , Namiki A. 
Published: March 2003

Background: Sevoflurane expenditure, inspired gas humidity, temperature, soda lime temperature, and compounds A and B were measured during high and low fresh gas flow anaesthesia in paediatric patients.Methods: Sixty ASA 1 or 2 paediatric patients were randomly allocated to two groups: low‐flow circle anaesthesia (LFA) patient group (n=30) and high‐flow circle anaesthesia (HFA) patient group (n=30). Initial fresh gas flow (FGF) was 4 l · min−1 of nitrous oxide and 2 l · min−1 of oxygen in both groups. This FGF of 6 l · min−1 was maintained in the HFA group. After 10 min of HFA, the FGF was reduced to 600 ml · min−1 (nitrous oxide and oxygen 300 ml · min−1 each) in the LFA group.Results: Sevoflurane expenditure during LFA was about 1/7 of that during HFA (3.3±0.2 ml · h−1 · vol.%−1 compared to 22.8±0.6 ml · h−1 · vol.%−1, mean±SEM, respectively). Absolute humidity in the LFA patients was 4 times higher than that in the HFA patients (22.8±2.4 g · m−3, 5.6±3.4 g · m−3 respectively). There was no significant difference in the inspiratory gas temperature between the LFA (28.5±0.6°C) and HFA (26.9±1.3°C) groups. There was significant difference in the mean highest soda lime temperature between the LFA (35.5±1.2°C) and HFA (28.7±1.2°C) groups. The mean highest concentration of compound A was 12.2±3.8 ppm in the LFA group. The mean highest concentration of compound B was less than 1 ppm. Compounds A and B were below detectable level in the HFA group.Conclusion: In conclusion, sevoflurane used for paediatric patients in a circle system with a fresh gas flow of 0.6 l · min−1 resulted in a significantly reduced sevoflurane expenditure, higher inspired absolute humidity, but not temperature, compared to a fresh gas flow of 6 l · min−1. Low levels of compounds A and B were detected.
The effects of tramadol on postoperative nausea, vomiting and headache after ENT surgery. A placebo‐controlled comparison with equipotent doses of nalbuphine and pethidine
Authors: Van Den Berg A. A. , Halliday E. , Kisembo Lule E. , Baloch M. S. 
Published: March 2003

Background: Opioids given as adjuncts to balanced inhalational anaesthesia augment postoperative nausea and vomiting (PONV). Tramadol, equipotent to pethidine, does not depress respiration, but can cause an increase in blood pressure and headache via its monoaminergic actions. Nalbuphine, ten times as potent as pethidine, has a ceiling respiratory depressant and ceiling analgesic effect at >0.3 mg · kg−1. We compared the effects of equipotent doses of tramadol and nalbuphine (3.0 and 0.3 mg · kg−1, respectively) given as analgesic with induction of anaesthesia on emesis during recovery from anaesthesia and on PONV and headache until 24 h after ENT surgery, using saline (0.2 ml · kg−1) and an equipotent dose of pethidine (1.5 mg · kg−1) as controls.Method: The study population (N=281) comprised 4 comparable subgroubs (N=69 to 71 each). Anaesthetic medications were standardised. Emesis during recovery from anaesthesia and nausea, vomiting, retching, headache and administrations of antiemetic and analgesics until 24 h after surgery were recorded.Results: Emesis and antiemetic requirements during recovery from anaesthesia were similar and infrequent in each group, as were the incidences of nausea alone (3 to 5%), vomiting alone (17 to 31%), and nausea with vomiting (10 to 22%) during the first 24 h after surgery. However, any complaint of PONV was least frequent in the saline and pethidine groups (32% and 37%, respectively) and most frequent in the tramadol and nalbuphine groups (49% and 52%, respectively; P<0.05 versus saline, both comparisons; P=NS versus pethidine, both comparisons). The times to onset and severity of PONV were similar in each group, but patients given nalbuphine most frequently (P<0.025) needed rescue antiemetic to treat PONV. Headache occurred with similar frequency in each group.Conclusion: It is concluded that tramadol, nalbuphine and pethidine have similar emetic effect in the doses and manner used, and that tramadol does not increase the incidence of postoperative headache when used as peroperative analgesic.
Does preoperative night pulse oximetry provide a reliable baseline?
Authors: Rasmussen L. S. , Kjær M. , Vogt K. , Moller J. T. 
Published: March 2003

Background: Postoperative hypoxaemia may be detected by pulse oximetry monitoring of the arterial haemoglobin saturation (SpO2). The SpO2‐values obtained on the preoperative night are presumed to represent baseline values for the patients. The aim of this study was to evaluate the possible difference between nocturnal SpO2‐values in the patient’s home and in the hospital before operation.Methods: We included 20 patients, 60 years or older, who underwent continuous monitoring of SpO2 on one night in the patient’s home and on the night following hospitalisation before surgery. The alarms were turned off and the values were not accessible to the hospital staff. The SpO2 value was stored every 10 s. We described the general oxygen saturation level using the median of all valid values and we calculated the number of valid SpO2‐values at 3 levels: above 90%, between 86 and 90%, and below 86%.Results: The number of valid SpO2‐values at home and in the hospital were 2186 and 2330, respectively; the median value was 96% on both occasions. Only 0.36% of the values were below 91% on the two occasions and there were no statistically significant differences between the number of SpO2‐values at any of the considered levels.Conclusion: Arterial oxygen saturation values measured on the preoperative night in the hospital seem reliable as baseline values for elderly patients.
Effect of experience with spinal anaesthesia on the development of post‐dural puncture complications
Authors: Flaatten H. , Berg C. M. , Brekke S. , Holmaas G. , Natvik C. , Varughese K. 
Published: March 2003

Background: This clinical study was conducted in order to investigate the effect of operator experience with spinal anaesthesia (SA) on development of postural post‐dural puncture headache (PPDPH) and postoperative backache.Methods: The study was a cohort study of the first 100 SA performed by each of 5 trainees in anaesthesiology at the very beginning of their training period. SA was conducted with assistance and guidance according to usual departmental practice. In each SA, data regarding level of puncture, needle size, number of punctures, use of introducer and infiltration anaesthesia were recorded. In addition, usual problems and complications connected with dural puncture were registered. A visual analogue scale was used to record how difficult the procedure was experienced by the trainees. Postoperatively, the patients were contacted by the same trainee, usually by telephone. A semi‐structured interview was conducted where occurrence and duration of headache, backache and other complaints were recorded. Headache was classified as PPDPH or non‐PPDPH, and intensity of the headache was registered using a numerical rating scale (NRS) from 0 to 10.Results: Five hundred SA in 495 patients with a mean age of 61.3 years were included in the study. Of these, 394 patients were completely followed‐up postoperatively; the main reason for the drop‐out was patient‐related factors such as advanced age and dementia. Headache occurred in 56 patients postoperatively. PPDPH was diagnosed in 33 and non‐PPDPH occurred in 23 patients. Postoperative backache was experienced by 27 patients. No significant effect experience with SA could be found regarding the occurrence of postoperative complications; 16 compared to 17 patients with PPDPH were found in the first and the last half of patients. A marked inter‐individual difference in the occurrence of PPDPH was found in the patients treated by the 5 trainees.Conclusions: We could not demonstrate an effect of experience and training on development of complications after SA with regard to PPDPH and backache.
Intra‐articular buprenorphine after knee arthroscopy
Authors: Varrassi G. , Marinangeli F. , Ciccozzi A. , Iovinelli G. , Facchetti G. , Ciccone A. 
Published: March 2003

Background: Demonstration of peripheral opioid receptors in inflamed synovia supports the concept of peripheral opioid analgesia. The aim of this study was to evaluate the analgesic effect of intra‐articular administration of buprenorphine after knee arthroscopy.Methods: In a double‐blind randomised trial, 48 patients were assigned to four groups: group A patients received buprenorphine 100 μg i.a. and NaCl 0.9% i.m., group B patients received bupivacaine 0.25% 50 mg i.a. and NaCl 0.9% i.m., group C patients received NaCl 0.9% i.a. and buprenorphine 100 μg i.m., and group D patients received NaCl 0.9% i.a. and NaCl 0.9% i.m. Intensity of postoperative pain was evaluated by VAS at recovery (T0) and 1, 3, 6, 12, 24 h after operation (T1, T2, T3, T4, T5), at rest and during passive 10° knee flexion. Total analgesic requirements and side effects related to study drugs were recorded.Results: The VAS scores were significantly higher in groups C and D than in group A and B patients. The differences were significant at T0, T1, T2 and T3. At T1, group C and D patients had greater analgesic requirement than groups A and B. No patients developed side effects.Conclusion: Intra‐articular buprenorphine and i.a. bupivacaine, both produced equally good postoperative pain control and allowed a significant reduction of analgesic requirement after knee arthroscopy.
Intestinal and hepatic perfusion and metabolism in hypodynamic endotoxic shock. Effects of nitric oxide synthase inhibition
Authors: Dahm P. L. , Thörne J. , Myhre E. , Grins E. , Mårtensson L. , Blomquist S. 
Published: March 2003

Background: Inhibition of nitric oxide synthase (NOS) has been claimed to be beneficial in septic shock. We investigated the overall and regional effects of a NOS‐inhibitor on perfusion and metabolism during severe endotoxic shock.Methods: Nineteen anaesthetised pigs were catheterised and ultrasonic flow‐probes were placed around the portal vein, the hepatic artery, and the superior mesenteric artery. Thirteen animals were given a 3‐h infusion of endotoxin; in 6 of these an infusion of NG‐nitro‐L‐arginine‐methyl‐ester (L‐NAME) was started an hour after the start of endotoxin while 7 animals served as controls and received endotoxin only. Six animals were sham operated with no further intervention.Results: Endotoxin produced a hypodynamic shock with pulmonary hypertension. L‐NAME did not increase arterial blood pressure, but deepened the fall in cardiac output and enhanced the increase in systemic and pulmonary vascular resistance. The infusion of endotoxin caused a decrease in flows in all regions. The addition of L‐NAME induced a further decrease in the mesenteric artery flow only. L‐NAME had no additional effect on hepatic artery flow ratio, while a transient decrease was seen in mesenteric flow ratio. Portal flow ratio decreased in the control group only. Global as well as regional oxygen extraction increased in both groups, more so in the L‐NAME group. Lactate levels increased with no differences between the groups.Conclusion: In hypodynamic endotoxic shock, L‐NAME infusion enhanced pulmonary vasoconstriction and increased left ventricular afterload. The resulting hypoperfusion caused an increase in mortality. The effects of L‐NAME on global and mesenteric blood flow and metabolism were similar, while L‐NAME had no additional effects on hepatic hypoperfusion or oxygen extraction. Thus, nitric oxide does not seem to be a major factor in the preservation of hepatic perfusion during unresuscitated endotoxic shock.
Segmental pulmonary vascular responses to changes in pH in rat lungs: role of nitric oxide
Authors: Gao Y. , Tassiopoulos A. K. , Mcgraw D. J. , Hauser M. C. , Camporesi E. M. , Hakim T. S. 
Published: March 2003

Background: Respiratory or renal failure is associated with changes in blood pH. Changes in pH may have profound effects on vascular tone and reactivity. Site of action of acidosis in the pulmonary vasculature and the role of nitric oxide production remain unclear.Methods: We utilized isolated rat lung preparation perfused with autologous blood (Hct=20%, flow rate=33 ml/min), and investigated the effect of acidosis and alkalosis (induced by ventilation with high and low inspired CO2) on vascular resistance and the role of nitric oxide during resting and elevated tone conditions. Changes in resistance were described in terms of small and large arteries and veins, using the vascular occlusion technique.Results: Acidosis (PCO2=66.7±0.7 mmHg, pH=7.17±0.01, PO2=255±3 mmHg) caused vasoconstriction under resting and increased vascular tone conditions (U46619‐induced). The changes in resistance occurred primarily in the small arteries. In contrast, alkalosis (PCO2=20.1±0.3 mmHg, pH=7.61±0.01, PO2=244±3 mmHg) caused vasodilation only at elevated tone conditions. Nitrow‐L‐arginine (LNA), an inhibitor of nitric oxide synthase, increased vascular resistance slightly but did not modulate the responses to pH, suggesting that such responses are not nitric oxide dependent. During KCl‐induced contraction, the effects of pH were abolished.Conclusions: We conclude that in rat lung, acidosis causes an increase in pulmonary vascular resistance at normal and elevated tone conditions. Furthermore, the response is limited primarily to the small arteries, and is not mediated by nitric oxide. Alkalosis tends to cause the opposite effects. The effects of acidosis and alkalosis were abolished when vascular tone was elevated with a low dose of KCl, suggesting that vascular response to pH may involve changes in membrane potential.
The direct effect of halothane on myocardial contraction in rat myocytes with poorly developed gap junctional intercellular communication
Authors: Kanaya N. , Kimura H. , Nakayama M. , Tsuchida H. , Ohshika H. , Namiki A. 
Published: March 2003

Background: The gap junction channel plays an important role in synchronous beating in the heart, and the reduction in the amount of gap junctional intercellular communication (GJIC) is thought to be the main arrhythmogenic factor in diseased heart. However, the effect of halothane on myocardial contraction in heart tissue with less GJIC is not well known. The purpose of the present study is to examine the direct effect of halothane on myocardium with poorly expressed GJIC.Methods: Ventricular myocytes were obtained from neonatal rats by enzymatic digestion with collagenase and then cultured for 3 or 7 d. We have previously reported that the number of gap junctions at 3 d is approximately 10% of that at 7 d (1). The myocytes were stabilized in serum‐free medium, and the spontaneous beating rate and amplitude were measured by a fiberoptic sensor.Results: Heptanol (2 mM), an inhibitor of GJIC, abolished synchronized beating in myocytes cultured for 7 d. Halothane decreased the beating rate and amplitude in both groups of myocytes in a concentration‐dependent manner (P<0.05). Halothane at 1 and 2 MAC (adult rat MAC) decreased the beating rate more in myocytes cultured for 3 d than in myocytes cultured for 7 d (P<0.05). Halothane reduced beating amplitude equally in both groups. Asynchronous contraction developed more frequently among myocytes cultured for 3 d than for those at 7 d.Conclusion: Halothane may block the GJIC channels, and when the number of these channels is reduced, exposure to halothane may cause asynchronous beating and decrease the beating rate. However, the halothane‐induced decrease in amplitude is probably not due to blockade of GJIC because reducing the number of GJIC channels did not alter halothane’s depressant effect.
Perioperative ST‐segment depression and troponin T release
Authors: Rapp H.‐J. , Rabethge S. , Luiz T. , Haux P. 
Published: March 2003

Background: Patients undergoing major vascular surgery are at constant risk of developing perioperative myocardial complications, especially myocardial infarction. The following study was performed to answer the question whether ST segment changes, analysed by Holter monitoring and ST segment analysis, are accompanied by release of cardiac troponin T, a highly specific marker of myocardial damage.Methods: Tventy patients undergoing elective aortic resection were studied by performing Holter ECG, including ST segment analysis, beginning on the evening before surgery until the third postoperative day. Within this period serum levels of cardiac troponin T were determined at 8 timepoints.Results: A total of 8/20 of the patients (40%) showed significant ST depressions (range −0.17/−0.68 mV), without any clinical symptom, with a median of 9 episodes (range 2–24). In 3 of the 8 patients, each with repetitive periods of ST depression, elevated troponin T levels were found (0.45/0.52/1.69 μg/l). No troponin T release nor cardiac events were noticed in the remaining patients. No dependancy could be found between troponin T release and the magnitude of ST depression or the number of ST depression episodes.Conclusion: Haemodynamic changes, oxygen imbalance and stress during major vascular surgery frequently lead to an ischaemic burden, which is indicated by ST segment changes during ECG ST analysis. Longlasting ST depression reaching an individual critical cut‐off limit followed by structural myocardial damage may be verified by elevated levels of cardiac troponin T. Prolonged periods of ST depression should be followed by determination of cardiac troponin T.
Neuroprotective properties of propofol and midazolam, but not pentobarbital, on neuronal damage induced by forebrain ischemia, based on the GABAA receptors
Authors: Ito H. , Watanabe Y. , Isshiki A. , Uchino H. 
Published: March 2003

Background: The mechanism of the neuroprotective effects of propofol was compared to two other types of intravenous (i.v.) anesthetics (i.e., benzodiazepine; midazolam and barbiturate; pentobarbital) using Mongolian gerbils focusing on GABA receptor subtypes.Methods: Neuronal injury was induced by a 4‐min occlusion of the common carotid arteries followed by reperfusion. One week after occlusion, animals were transcardially perfused for histochemistry. Neuronal death in four brain regions was evaluated by direct visual counting of acidophilic neurons.Results: Seven days after this ischemic episode, severe neuronal injury was measured in the hippocampal CA1 area (>98% of total cells damaged) and parietal cortex (>35%). Also lateral thalamus and caudate putamen were damaged but to a lesser extent (about 10%). The neuronal injury in these areas was significantly attenuated by propofol, midazolam and the GABAA agonist, muscimol, intraperitoneally administered 15 min prior to ischemia. This neuroprotective property, however, was lacking with pentobarbital and GABAB agonist baclofen. Concomitant pretreatment with subthreshold doses of propofol and muscimol significantly reduced the amount of cell death induced by brain ischemia. On the other hand, pretreatment with the GABAA antagonist bicuculline significantly inhibited the neuroprotective effects of propofol. However, a GABAB antagonist, phaclofen, was without effect on neuronal damage and on neuronal protection of propofol.Conclusion: These results indicate that activation of GABAA receptors, which include the specific binding subunits for propofol and midazolam, but not pentobarbital, plays a role in the inhibition of neuronal death induced by brain ischemia.