EnHurane supresses phrenic nerve-diaphragm Transmissionin vivo

We examined the effects of enflurane on the diaphragmatic function in 15 pentobarbital-anesthetized, mechanically ventilated dogs. They were divided into three groups of five animals each, according to the administered concentration of enflurane. The diaphragmatic function was assessed from transdiaphragmatic pressure (Pdi) and integrated diaphragmatic electromyography (Edi) developed at functional residual capacity against an occluded airway during bilateral supramaximal phrenic nerve stimulation at 0.5, 10, 20, 50 and 100Hz under quasiisometric condition. After a control measurement, enflurane was administered at a constant end-expired concentration (0, 0.5 and 1MAC) and the measurement was repeated after 1 hour of exposure. The Pdi amplitude generated by single twitch (0.5Hz) and during 10, 20 and 50Hz stimulation was unchanged between the groups. No change in Pdi during 100Hz stimulation was noted during 0 and 0.5MAC exposure, while it was reduced by 1MAC of enflurane. When the values of Pdi were expressed as % of maximum Pdi (%Pdi,max) that developed during control measurement and analyzed in terms of %Pdi,max—stimulus frequency relationship, a significant decrease in %Pdi,max was noted for 100Hz stimulation in 0.5 and 1MAC groups compared to the control. Similarly, Edi during 100Hz stimulation obtained in 0.5 and 1MAC groups was markedly depressed compared to the control. Edi during 50Hz stimulation was also decreased at 1MAC. Relative changes in Edi following enflurane administration were greater than the corresponding changes of Pdi. These results demonstrate that enflurane impairs diaphragmatic function through its inhibitory effects on neuromuscular transmission.(Kochi T, Ide T, Isono S, et al.: Enflurane supresses phrenic nerve-diaphragm transmission in vivo. J Anesth 5: 260–267, 1991)     

Tracheal dilatation by halothane and enflurane in man

The effect of halothane and enflurane on tracheal tone were studied in 21 patients during the induction of anesthesia. Endotracheal tube cuff pressure was used to measure tracheal tone. Anesthesia, maintained by nitrous oxide 70% in oxygen, was supplimented with succinylcholine drip infusion to immobilize the patient. Ventilation was controlled by a Volume-preset ventilator. In the halothane group, the initial cuff pressure was 14.8 ± 1.3 (mean ± SE) cmH₂O but 10min after 0.15mg/kg of pancuronium injection, it increased to 21.7 ± 2.3cmH₂O (control). Ten min after inhalation of 0.75% of halothane, cuff pressure decreased to 14.7 ± 2.3cmH₂O (34 ± 11% decrease from the control value). In the enflurane group, the initial cuff pressure was 17.6 ± 1.8cmH₂O and it increased to 21.0 ± 1.7cmH₂O (control) 10min after pancuronium injection. Ten min after 1.7% of enflurane inhalation, cuff pressure decreased to 17.1 ± 2.3cmH₂O (23.9 ± 6% decrease from the control value). Halothane and enflurane produced similar tracheal dilatation in healthy individuals.(Yasuda I, Irimada M, Hirano T et al.: Tracheal dilatation by halothane and enflurane in man. J Anesth 2: 46–49, 1988)     

The echocardiographic assessment of left ventricular performance during sevoflurane and halothane anesthesia

The cardiovascular effects of sevoflurane were studied and compared with those of halothane in 30 healthy patients. The patients were assigned to receive 1MAC sevoflurane (n = 10), 2MAC sevoflurane (n = 10) or 1MAC halothane (n = 10) in N₂O 2l·min^–1 and O₂ 4l·min^–1. The changes in left ventricular diastolic and systolic dimension (Dd and Ds), fractional shortening (FS), mean velocity of circumferential fiber shortening (mVcf), left ventricular diastolic and systolic volume (Vd and Vs), stroke volume (SV), ejection fraction (EF) and cardiac index (CI) were evaluated by echocardiography. Sevoflurane produced significant dose-dependent decreases in FS, mVcf, EF and SV, but no significant changes in Dd and Vd. Therefore, the decrease in SV was due mainly to the increase in left ventricular residual volume (Vs). One MAC halothane produced a more significant decrease in FS, mVcf, EF and SV, when compared to values obtained at 1MAC sevoflourane (P 0.01). CI was more significantly decreased with 1MAC halothane than with 1MAC and 2MAC sevoflurane (P 0.01). This was brought about by a slight decrease in HR with halothane and a slight increase in HR with sevoflurane, in addition to a smaller decrease in SV with sevoflurane than with halothane. This study suggests that sevoflurane may better preserve cardiac function as a pump in healthy patients, when compared to halothane.(Kasuda H, Akazawa S, Shimizu R.: The echocardiographic assessment of left ventricular performance during sevoflurane and halothane anesthesia. J Anesth 4: 295–302, 1990)     

Neuromuscular effects of pipecuronium during sevoflurane anesthesia compared with isoflurane and enflurane anesthesia

We evaluated the neuromuscular effects of pipecuronium during anesthesia with equipotent concentrations of either sevoflurane, isoflurane or enflurane.Twenty-seven patients scheduled for minor elective otolaryngeal or plastic surgery were studied and randomly assigned to 3 groups, one group per anesthetic agent. Anesthesia was induced with thiamylal 5mg·kg^–1 and the trachea was intubated with succinylcholine 1mg·kg^–1, then anesthesia was maintained with 60% nitrous oxide in oxygen and sevolfurane, isoflurane or enflurane, depending on the group. Neuromuscular blocking effects were monitored by recording the electromyographic activity of the adductor pollicis muscle from supramaximal stimulation of the ulnar nerve at 10-s intervals. Pipecuronium 40µg·kg^–1 was administered when electromyographic activity had reached a stable state, 30min after succinylcholine administration. The maximum effect (% block of control) and clinical duration (time to 25% recovery) of pipecuronium were 99.1 ± 1.4% and 63.7 ± 14.7min (mean ± S.D.) for sevoflurane, 99.0 ± 2.0% and 60.9 ± 20.5min for isoflurane, and 98.0 ± 2.5% and 62.8 ± 28.7min for enflurane, respectively. There were no significant differences in these values between the anesthetics. Cardiovascular stimulant effects were not observed in any of the groups.We conclude that the effect of pipecuronium under seveflurane anesthesia is similar to that under isoflurane and enflurane anesthesia.(Nakao Y, Ohno M, Imai M, et al.: Neuromuscular effects of pipecuronium during sevoflurane anesthesia compared with isoflurane and enflurane anesthesia. J Anesth 7: 405--410, 1993)     

Effects of lidocaine and verapamil on early afterdepolarizations in isolated rabbit sinoatrial node

The effects of local anaesthetic anti-arrhythmic agents (lidocaine) and Ca antagonists (Verapamil) have been examined on the early afterdepolarizations (EADs) in isolated rabbit sinoatrial (SA) node. In a nominally calcium free and magnesium free solution, strontium (0.5–4.5mM) produced an EAD in small pieces isolated from the SA node. The additional presence of 0.02–0.6mM lidocaine did not abolish the strontium (0.5mM)-induced EAD. 0.6mM lidocaine produced an increase in EAD amplitude and then abolished a prolonged action potential (AP) associated with repetitive EADs. On the other hand, the addition of 4µM verapamil abolished the strontium (0.5mM)-induced EAD but did not abolish the AP.It is concluded that under conditions when the AP is not abolished, EAD blockade by lidocaine is less effective than that by verapamil.(Miyamae S, Matsuda T, Goto K, et al.: Effects of lidocaine and verapamil on early afterdepolarizations in isolated rabbit sinoatrial node. J Anesth 5: 213–220, 1991)     

Blockade of sodium channels by phenytoin protects ultrastructure and attenuates lipid peroxidation in experimental spinal cord injury

Summary Spinal cord injury (SCI) involves a series of pathological events. Abnormal sodium influx has been implicated as one of the key events in the pathophysiology of the SCI. Pharmacological blockade of sodium channels can reduce secondary injury and increase recovery from trauma. The aim of the present study was to show the neuroprotective effect of phenytoin, a sodium channel blocker, after experimental SCI.Control and laminectomy-only groups were not injured. 50g-cm weight drop injury was produced in the trauma group. In the treatment groups, methylprednisolone (30mg/kg) and phenytoin (1mg/kg, 10mg/kg, or 30mg/kg) were given intraperitoneally immediately after injury. Malondialdehyde (MDA) levels in the spinal cord samples were examined for lipid peroxidation. Spinal cord ultrastructure was evaluated and grading system was used for quantitative evaluation.Trauma increased tissue MDA levels. Treatment with methylprednisolone and phenytoin decreased MDA levels compared to trauma in all doses. Significant ultrastructural neuroprotection was observed with 30mg/kg of phenytoin treatment according to general neural score. This ultrastructural neuroprotection of phenytoin was not different from methylprednisolone. Phenytoin appears to protect spinal cord against injury by decreasing lipid peroxidation and lessening neuronal damage associated with SCI in rats.     

Hemodynamic effects of nicardipine-induced hypotension during enflurane/nitrous oxide anesthesia in man

Hemodynamic effects of nicardipine-induced hypotension during enflurane/nitrous oxide were evaluated in 10 surgical patients. An infusion of nicardipine was titrated to maintain mean arterial pressure at 60 to 70mmHg under enflurane 1.5 to 2.0vol% and nitrous oxide 60vol%. Mean arterial pressure was well controlled with the nicardipine infusion, whereas cardiac index increased with decreased systemic vascular resistance. Heart rate increased concomitantly with decreased blood pressure, which indicated that enflurane 1.5 to 2.0vol% did not suppress baroreceptor reflex during nicardipine administration. However, rate-pressure-product was not increased by the nicardipine. Right and left ventricular systolic work indices were not increased by the nicardipine. Right ventricular ejection fraction was not also changed by the nicardipine. Although serum norepinephrine level increased during the nicardipine infusion, the values remained within physiological ranges. Our results suggest that nicardipine-induced hypotension may be safely performed during enflurane/nitrous oxide anesthesia because neither ventricular work nor myocardial oxygen demand was increased by nicardipine.(Okamura A, Kemmotsu O, Morimoto Y, et al.: Hemodynamic effects of nicardipine-induced hypotension during enflurane/nitrous oxide anesthesia in man. J Anesth 6: 401–406, 1992)     

Hospital Readmissions Following Abdominal Aortic Aneurysm Repair

In-hospital outcomes associated with abdominal aortic aneurysm (AAA) repair are well described. However, little is known about post-discharge readmission rates, lengths of stay, associated mortality, and costs. We examined 206 consecutive patients who underwent AAA repair at two American hospitals between 1998 and 2000. Index hospitalization and 6-month readmission data were extracted from a resource and cost accounting system used by both hospitals. Among the 206 patients, 183 survived until discharge (mortality rate 11.2%). Among the surviving patients, 38 (21.0%) were readmitted within 6 months. Half of the readmissions occurred within two weeks of discharge, with patients presenting with a diverse array of complications. Nonelective repair and diabetes mellitus were independent predictors of hospital readmission (OR=2.83, 95% CI=1.25-6.40, p=0.01; OR=6.60, 95% CI=1.02-42.4, p=0.047, respectively). For each readmission, the mean length of stay was 10.7±2.5 days and the mean cost was $13,397±3,381. The cumulative number of hospital days during the 6 months post-discharge was 17.7±3.5 days for each readmitted patient and the mean per-patient total cost was $23,262±5,478. The mortality rate among readmitted patients was 13.2%. Overall, readmissions following AAA repair accounted for a cost >50% over and above the cost of the readmitted patients index hospitalization. Hospital readmissions are common during the 6 months following AAA repair. Patients who are readmitted experience long lengths of stay and high mortality rates, and their care incurs high costs.Dr. Eisenberg is a Physician-Scientist of the Quebec Foundation for Health Research. Dr. Pilote is a Physician-Scientist of the Canadian Institutes for Health Research.     

Correlation of continuously monitored regional cerebral blood flow and brain tissue oxygen

Summary Background. The purpose of this study was to investigate the relationship between continuously monitored regional cerebral blood flow (CBF) and brain tissue oxygen (P_tiO₂).Methods. Continuous advanced multimodal neuromonitoring including monitoring of P_tiO₂ (Licox, GMS) and CBF (QFlow, Hemedex) was performed in eight patients after severe subarachnoid haemorrhage (n=5) and traumatic brain injury (n=3) for an average of 9.6 days. Parameters were measured using a flexible polarographic P_tiO₂-probe and a thermal diffusion CBF-microprobe.Findings. Regarding the whole monitoring period in all patients, the data indicated a significant correlation between CBF and P_tiO₂ (r=0.36). In 72% of 400 analysed intervals of 30 minutes duration with P_tiO₂ changes larger than 5mmHg, a strong correlation between CBF and P_tiO₂ existed (r>0.6). In 19% of intervals a still statistically significant correlation was observed (0.3<r<0.6). During the remaining 9% no correlation was found (r<0.3). Regarding the clinical stability of the monitoring devices, the CBF monitoring system allowed monitoring of CBF in 64% of the time when P_tiO₂ monitoring was possible only. Phases of non-monitoring were mostly due to fever of the patient, when the system does not allow monitoring to avoid overheating of the cerebral tissue.Conclusions. This study suggests a correlation between CBF and P_tiO₂. The level of P_tiO₂ seems to be predominately determined by regional CBF, since changes in P_tiO₂ were correlated in 90% of episodes to simultaneous changes of CBF.     

Comparison of anesthetic effects of epidural and intravenous administration of buprenorphine during operation

Thirty six patients were received epidural anesthesia with or without buprenorphine (BPN) during upper abdominal surgery. They were divided into three groups of 12 patients as follows; G-I received 20ml of 1% lidocaine epidurally, G-II received 20ml of 1% lidocaine epidurally and 0.6mg BPN intravenously, G-III received 20ml of 1% lidocaine with 0.6mg BPN epidurally. Additional 5ml of 1% lidocaine was given to any patient if systolic blood pressure or heart rate increased 10% compared to control value. Trachea was intubated following anesthetic induction with thiopental. The lungs were ventilated with a mixture of N₂O/O₂ (33%) and pancuronium was used for muscle relaxation. The total required doses of lidocaine in G-II and G-III were decreased 60% compared to control group (G-I) (P 0.05). The mean period of time until the first administration of pentazocine for postoperative pain was 13 ± 10hr (mean ± SD) in G-II and 19 ± 24hr in G-III compared to 5 ± 4hr in G-I (P 0.001). The dose of the administration of pentazocine that was required for pain relief during the first 48 postoperative hr in G-III was 54 ± 10mg (mean ± SD) compared to 150 ± 21mg in G-I (P 0.02) and 106 ± 28mg in G-II (P 0.05). Recovery from anesthesia in G-III was more rapid than that in G-I (P 0.05). The Pa_{CO 2} values in G-II and G-III increased 15% compared to control group at about 4hr and 8hr after administration of BPN, but any clinical treatment was not needed for them. Nonrespiratory side effects, e.g., nausea, vomiting, fatigue and headache, were comparably common in all groups. Mild hematuria associated with acute hypotension occurred in two patients in G-II (17%) immediately after the intravenous injection of 0.6mg of BPN. The results showed that 0.6mg of BPN given epidurally demonstrated better anesthetic and more potent postoperative analgesic effects and lesser side effects than 0.6mg of BPN given intravenously in patients undergoing upper abdominal surgery.(Yonemura E, Fukushima K.: Comparison of anesthetic effects of epidural and intravenous administration of buprenorphine during operation. J Anesth 4: 242–248, 1990)     

The N-Methyl-D-aspartate (NMDA) receptor antagonist dizocilpine (MK-801) suppresses enfturane-induced opisthotonus in mice

We determined whether enflurane-induced opisthotonus in ddN mice is mediated by N-methyl-D-aspartate (NMDA) receptor using NMDA receptor antagonists dizocilpine (MK-801) and ketamine. Animals were given intraperitoneal injections of 0.2ml saline (control), 2.5 or 5.0mg·kg^–1 dizocilpine in saline, or 20 or 40mg·kg^–1 ketamine is saline 20min prior to exposure to 2.0% enflurane. Incidence of opisthotonus measured during exposure to enflurane for 20min was 49% (n = 51) in saline (control) group, 6.7 (P 0.01 vs control, n = 30) and 15.0% (P 0.01, n = 40) in 2.5 and 5.0mg·kg^–1 dizocilpine group, respectively, and 43.9 (NS, n = 41) and 40.0% (NS, n = 40) in 20 and 40mg·kg^–1 ketamine group, respectively. These results strongly suggest that enflurane-induced opisthotonus is mediated by NMDA receptor. Ketamine failed to suppress significantly due to possibly small dosages. Further, dizocilpine itself produced severe seizures during preenflurane period (30.0 and 40.0% in 2.5 and 5.0mg·kg^–1, respectively), which may be a novel finding.(Komatsu H, Nogaya J, Anabuki D, et al.: The N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine (MK-801) suppresses enflurane-induced opisthotonus in mice. J Anesth 7: 519–522, 1993)     

Changes of local brain tissue oxygen pressure after vasopressin during spontaneous circulation

Summary. Background. Brain tissue oxygen pressure (PbtO₂) correlates to cerebral blood flow (CBF) during spontaneous circulation, with one important regulator being nitric oxide (NO). Although it is established that arginine vasopressin (AVP) improves CBF and global cerebral oxygenation during cardiopulmonary resuscitation, it is unknown whether similar beneficial effects are present during spontaneous circulation. The purpose of this study was to investigate the effects of AVP with and without pre-treatment with the NO synthase inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME) on local brain tissue oxygenation in a beating heart model.Methods. Following approval of the Animal Investigational Committee, nine healthy piglets underwent general anaesthesia, and were instrumented with a probe in the cerebral cortex to measure PbtO₂. Each animal was assigned to receive AVP (0.4U·kg^–1), and after a wash-out period, L-NAME (25mg·kg^–1 over 20min) followed by AVP (0.4U·kg^–1). After each AVP administration, nitroglycerine (25µg·kg^–1 over 1min) as a NO donor was infused to test the vascular reactivity independently from NOS inhibition.Findings. Three minutes after administration of AVP, PbtO₂ increased significantly (P<.05; mean±SEM, 31±11 versus 43±14mmHg, +39%), compared with baseline. After pre-treatment with L-NAME, the changes of PbtO₂ after AVP were not significant (32±11 versus 28±10, –13%) when compared with the baseline.Conclusion. In this beating heart porcine model, local brain tissue oxygenation was improved after AVP alone, but not after inhibition of NO synthesis with L-NAME.     

Bench test assessment of the new Raumedic Neurovent-P ICP sensor: a technical report by the BrainIT group

Summary. Background. In clinical practice, fiberberoptic and piezo-electric ICP probes are often used for measuring intracranial pressure (ICP). A number of similar technologies, although performing well in bench test studies, have been shown to exhibit unacceptable zero drift, fragility or both during trials conducted under clinical conditions. Recently, a new technology has become available, the Neurovent-P (Raumedic AG+CO, Raumedic, Germany). As a pre-requisite for a clinical trial, we have conducted and report on bench test studies to confirm the manufacturers long term zero-drift performance for this technology.Method. In a test rig static tests (recording of 20mmHg pressure) and dynamic tests, ranging from 5 to 50mmHg have been performed.Findings. 10 ICP probes have been tested for a total of 60 days. All the catheters, after the connection with the ICU monitor displayed a static pressure of 0±1mmHg and did not required pre-insertion alteration. At five days, mean zero drift was 0.6±0.9mmHg. Overall, zero drift ranged from 0 to 2mmHg. At a fixed static pressure of 20mmHg, the mean recorded value was 20.6±0.8mmHg, ranging from 19 to 23mmHg. A regression analysis of the relationship between the applied pressure and the recorded pressure during the dynamic tests of the 10 catheters yielded a correlation coefficient R² of 0.997. Applying the Altman and Bland method to assess the bias and confidence limits for the Raumedic catheter responses during the dynamic tests against the applied gold-standard hydrostatic column pressures, the average bias of –0.66±0.85mmHg, with 95% CLs of –2mmHg and 1mmHg.Conclusions. Mean zero drift, after five days, was very small and long-term continuous recording of a stable pressure was very precise. The response at dynamic tests, i.e. the changes of pressure in a wide range, was excellent. The average bias of the Raumedic catheter compared with the hydrostatic column is very small. After this bench test, the next and most critical step will be to conduct a trial of this promising technology under more demanding clinical environment.     

Comparison of the epinephrine-induced arrhythmogenic effect of sevoflurane with isoflurane and halothane

The effect of sevoflurane on cardiac arrhythmias induced by the infusion of epinephrine into dogs was compared with those of isoflurane and halothane. The arrhythmogenic doses of epinephrine determined in this comparative study were expressed by both infusion rates of epinephrine and the corresponding plasma levels obtained by a series of three-minute epinephrine infusions during sevolurane, isoflurane, and halothane anesthesia at 1.25 MAC. The mean values of the arrythmogenic infusion rates of epinephrine and the corresponding plasma levels were 17.3µg/kg/min and 275.7ng/ml for sevoflurane, 6.7µg/kg/min and 149.2ng/ml for isoflurane and 1.9µg/kg/min and 39.1ng/ml for halothane, respectively. These results indicate that the arrythmogenic doses of epinephrine during sevoflurane and isoflurane anesthesia were significantly higher than those during halothane anesthesia.(Imamura S et al.: Comparison of the epinephrine-induced arrhythmogenic effect of sevoflurane with isoflurane and halothane. J Anesth 1: 62–68, 1987)     

Continuous infusion of vecuronium in children

The average dose of vecuronium required in children continuous infusion to attain a steady state block of 90% was determined. The electromyographic (EMG) response and mechanical response to supramaximal stimulation of the ulnar never recorded simultaneously, were significantly correlated in four children.The steady-state infusion rate requirement of vecuronium was 1.4 ± 0.03µg/kg/min during 2% enflurane anesthesia and 3.1 ± 0.03µg/kg/min during 1% halothane anesthesia. The spontaneous recovery time to 25% of the control by EMG during halothane and enflurane anesthesia was 12.6 ± 1.1 and 10.3 ± 1.5min, respectively, after termination of the infusion. There was no cumultative effect after prolonged vecuronium infusion.(Obara H, Hoshina H, Tanaka O et al.: Continuous infusion of vecuronium in children. J Anesth 2: 8–11, 1988)     

AneuRx Device Migration: Incidence, Risk Factors, and Consequences

Success after endovascular abdominal aortic aneurysm repair (EVAR) is dependent on device positional stability. The quest for such stability has motivated different endograft designs, and the risk factors entailed remain the subject of debate. This study aims at defining the incidence, risk factors, and clinical implications of device migration after EVAR with the AneuRx® endograft. In this study we included all consecutive 109 patients submitted to primary AneuRx placement for infrarenal aortic or aortoiliac aneurysms. Preoperative computed tomography (CT) scans were reviewed for the following anatomic characteristics: neck length, diameter, angulation, calcification, and thrombus load; and sac diameter and thrombus load. Percentage of device oversizing relative to the proximal neck diameter was determined. All postoperative CT scans were reviewed, and the distance between the lowest renal artery and the craniad end of the device was measured. A 5-mm increase in such distance was considered indicative of device migration. Migration cumulative incidence was estimated by the Kaplan-Meier method, and its association with any of the preoperative anatomical characteristics was tested using Cox proportional hazards models. Median follow-up time was 9 (range, 1-31) months. Migration occurred in nine patients, corresponding to a 15.6% estimated probability of migration at 30 months (SE=5.1%). Migration was associated with the risk of proximal type I endoleak (hazard ratio=3.39, 95% confidence interval=1.46-7.87; p=0.007). This type of endoleak occurred in three of the migration-affected patients (33.3%); all of them were resolved by additional cuff placement at the proximal landing zone. No other migration-related reinterventions were performed. The only significant associations between anatomic factors and device migration probability were the protective effects of longer necks (odds ratio [OR]=0.71 for each additional 5 mm, p=0.045) and longer overlapped portions of neck and device (OR=0.56 for each additional 5 mm, p=0.003). There was a trend toward higher probability of migration among reverse-tapered necks (OR=1.75, p=0.109). Percentage of device oversizing correlated with early neck dilation (between preoperative and first postoperative diameters, correlation coefficient=0.4, p < 0.0001), but not with late neck dilatation (between first postoperative and 1.5-year scan diameters, correlation coefficient=0.29, p=0.112). There was a trend toward higher mean percentage of late dilation among migrators (11.4%, standard error of the mean [SEM] 2.6) than nonmigrators (5.7%, SEM=1) (p=0.08), but both groups had similar mean percentages of early dilation (3%, SEM=1.6%, vs. 5.5%, SEM=0.6%; p=0.365). This result indicates that device migration is not a rare event after AneuRx implantation. This phenomenon is associated with proximal type I endoleaks. Deployment of the endograft immediately below the renal arteries might help to prevent migration, since use of greater lengths of overlapped device relative to the proximal neck has a protective effect. Migration seems to be independent of the degree of device oversizing.Presented at the 29th Annual Meeting of the Peripheral Vascular Surgery Society, Anaheim, CA, June 4-5, Sergio M. Sampaio is a recipient of the Edward S. Rogers Clinical Research Fellowship in Vascular Surgery.     

The neuromuscular effects of sevoflurane and isoflurane alone and in combination with vecuronium or atracurium in the rat

Sevoflurane was compared to isoflurane anesthesia alone and in combination with atracurium or vecuronium in 84 rats using the sciatic nerve—anterior tibialis muscle preparation. Both bolus injection and infusion rate techniques were used to evaluate these drug interactions. The ED₅₀ (dose which produced a 50% depression of twitch tension) of atracurium was 311 ± 31 and 360 ± 32µg·kg^–1 during 1.25MAC sevoflurane and isoflurane anesthesia respectively. The ED₅₀ of vecuronium was 190 ± 27 and 149 ± 14µg·kg^–1 during 1.25MAC sevoflurane and isoflurane anesthesia respectively. The mean infusion rates of atracurium and vecuronium required to maintain a 50% depression of twitch tension were 5.04 ± 0.7 and 2.02 ± 0.3mg·kg^–1·hr^–1. These infusion rates were 5.04 ± 0.7 and 2.02 ± 0.3mg·kg^–1·hr^–1 during 1.25MAC sevoflurane and 3.73 ± 0.3 and 1.81 ± 0.4mg·kg^–1·hr^–1 during 1.25MAC isoflurane anesthesia respectively. With both atracurium and vecuronium, the infusion rate required to maintain a 50% depression twitch of tension was inversely related to the concentrations of isoflurane and sevoflurane. The authors conclude that sevoflurane is similar in potency to that of isoflurane in augmenting a vecuronium or atracurium induced neuromuscular blockade in a dose-dependent manner.(Shin YS, Miller RD, Caldwell JE, et al.: The neuromuscular effects of sevoflurane and isoflurane alone and in combination with vecuronium or atracurium in the rat. J Anesth 6: 1–8, 1992)     

Effects of Cilostazol on Human Venous Smooth Muscle

In this study, we evaluated the effect of therapeutic doses of cilostazol on human venous smooth muscle. Saphenous vein rings (two to four per patient sample) were suspended in tissue baths for isometric tension recordings. At the beginning of the experiment, optimal tension for isometric contraction was achieved for each ring in a stepwise fashion in the presence of norepinephrine (10^–2 M). Norepinepherine was then added cumulatively in half-molar increments and isometric tension developed by the rings was measured, thereby obtaining a dose-response curve. Following washout and reequilibration, the rings were precontracted with a 30-50% submaximal dose of norepinepherine determined from the dose-response curve and allowed to contract until a stable plateau was reached. Cilostazol was then added in a cumulative manner (680-2,720 g/L), and the tension generated was recorded. A total of 76 venous rings were tested, and all relaxed in the presence of cilostazol. The amount of relaxation increased as the concentration of cilostazol increased. Relaxation of 15±1.9% (mean±SEM) at low cilostazol doses (680 g/L) to 37±3% at high cilostazol doses (2,720 g/L) was demonstrated. A second finding of this study was demonstrated when the patient samples were divided according to the presence or absence of risk factors for arteriosclerosis. The specific risk factors examined included diabetes mellitus, smoking, hypercholesterolemia, and hypertension. The presence or absence of hypertension (n=52) or hypercholesterolemia (n=18) did not affect the amount of relaxation of the venous rings. Smokers (n=46) had less relaxation 16±2.4% (680 g/L) to 41±3.6% (2,720 g/L) compared to nonsmokers (n=53) who relaxed 22±3.5% (680 g/L) to 48±5.7% (2720 g/L). This did not reach statistical significance at any concentration cilostazol (p=0.11-0.18). Diabetics (n=53) did have statistically significantly less relaxation at every concentration of cilostazol compared to nondiabetics (n=11, p < 0.05). All venous rings relaxed in the presence of cilostazol. Veins of nondiabetics relaxed statistically significantly more than those of diabetics. Smokers had less relaxation than non-smokers, but this was not statistically significant. We are the first to demonstrate that human venous smooth muscle cells undergo relaxation when exposed to therapeutic concentrations of cilostazol.     

Safety of Contrast Venography prior to Caval Interruption in Patients with Renal Insufficiency

We undertook this study to determine whether the use of contrast venography would adversely affect renal function in patients with renal insufficiency requiring caval interruption. We conducted a retrospective review of all inferior vena cava (IVC) filters inserted at our institution over a 2-year period (January 2002 to January 2004). The indication for caval interruption, insertion technique, type of filter used, pre- and postintervention creatinine level, and the presence of diabetes and hypertension were analyzed. A total of 282 IVC filters were inserted, with 38 of them placed in patients with renal insufficiency as defined by a serum creatinine level of > 1.5 mg/dL. Contrast venography with 15 to 30 mL of iohexol (Omnipaque 300) was used in all cases, and no special measures other than proper hydration were used for renal protection. All filters were successfully deployed. The mean±SD preintervention creatinine level was 2.38±0.79 mg/dL. The mean±SD postintervention creatinine levels at 2 and 30 days were 2.26±0.45 mg/dL and 2.12±0.94 mg/dL, respectively. No patients required hemodialysis following caval interruption, and no adverse effect on renal function was noted. Contrast venography accurately delineates venous anatomy and facilitates proper caval filter placement with no apparent adverse effect on renal function. We believe contrast venography is safe even in the presence of renal insufficiency.     

Long-term results of rotational total hip arthroplasty: radiological analysis

We developed a rotational total hip prosthesis that has a 30mm diameter metal-covered head with a polyethylene liner with which it can rotate around the neck of the stem. Long-term results of the rotational total hip arthroplasty with cement were evaluated in 55 hips of 52 patients. The diagnosis was degenerative osteoarthritis in all patients. The mean follow-up was 11.2 years (range 5–19 years). Eight of thirty 7mm thick acetabular components were revised 7.6–14.3 years (mean 10.4 years) afterward. Two of twenty five 9.5mm thick acetabular components and two femoral components were revised at 12 and 15 years, respectively. The mean polyethylene wear in the 9.5mm thick acetabular components was significantly less than that in the 7mm thick components. The mean polyethylene wear inside the rotational head removed during the revision surgeries was 0.01mm in diameter and 0.03mm in depth per year, respectively. Fifty percent of the patients with 7mm thick acetabular components, 9.5mm thick components, and femoral components had surviving prostheses at 13.4, 15.2, and 16.3 years, respectively. It is possible that the rotational system reduces the stress against acetabular and femoral components, but the 30mm diameter head caused high friction torque and required at least 9.5mm thickness in the acetabular component.