Wakefulness during the induction with high-dose fentanyl and oxygen anesthesia

The purpose of this study was to investigate the state of wakefulness during the induction of anesthesia with high-dose fentanyl using the isolated forearm technique. Ten patients scheduled for elective cardiovascular surgery were premedicated with morphine (0.15mg/kg) and scoploamine (0.3–0.4mg) intramuscularly one hour before induction. The induction of anesthesia was performed by intravenous administration of 100µg/kg of fentanyl in 15min or over. The pneumatic tourniquet applied on the left upper arm was inflated to 220–240mmHg after 10µg/kg of fentanyl was given and then pancuronium was administered. Verbal commands were given to the patient after 25, 50, 75 and 100µg/kg of fentanyl was administered. Eight patients out of 10 responded to the verbal commands after administration of 25µg/kg of fentanyl. Six patients also responded after administration of 100µg/kg of fentanyl and diazepam 5mg was given to prevent tachycardia and rigidity during endotracheal intubation. Muscle rigidity and tachycardia were noticed in three and four patients respectively. These complications disappeared by diazepam administration.It was noted that wakefulness frequently occurred during the induction by high-dose fentanyl and oxygen anesthesia. To prevent such wakefulness therefore, it is necessary to use anesthetic supplements which do not cause cardiovascular depression.(Watanabe A, Namiki A, Ujike Y et al.: Wakefulness during the induction with high-dose fentanyl and oxygen anesthesia. J Anesth 2: 165–169, 1988)     

Fentanyl antagonizes diazepam on carotid sinus baroreflex control of circulation in rabbits

To investigate the effects of a combination of fentanyl and diazepam on carotid sinus baroreflex in conscious rabbits, we examined the responses of mean systemic arterial pressure (MAP), heart rate (HR) and total peripheral resistance (TPR) to bilateral carotid occlusion (BCO). Seven rabbits were given 0.5mg·kg^–1 of diazepam i.v. followed by 10mg·kg^–1 of fentanyl i.v. at 5min intervals (group 1), and the drugs were given in the reverse order to 5 other rabbits (group 2). BCO was repeated in conscious state (control) and after each drug injection. MAP responses did not differ from control response in either group when both drugs were given. In group 1, however, diazepam decreased HR response to 71.4% of control, and increased TPR response by 36%. Fentanyl administration reversed diazepam-induced changes in BCO responses to the control level. In group 2, fentanyl decreased TPR response to 61.6% of control and increased HR response by 41.5%. Administration of diazepam following fentanyl restored HR and TPR responses to control levels. Carotid sinus baroreflex gain was 3.1 ± 0.4 (mean ± SEM) in control and 3.1 ± 0.4 after administration of both drugs in 12 rabbits. The results suggest that a sedative dose of either fentanyl or diazepam antagonizes the other drugs action on the carotid sinus baroreflex. The combination of fentanyl and diazepam has little influence on carotid sinus baroreflex control of the circulation in rabbits.(Sakamoto M, Ohsumi H, Sumida T, et al.: Fentanyl antagonizes diazepam on carotid sinus baroreflex control of circulation in rabbits. J Anesth 7: 210–217, 1993)     

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)     

Effects of calcium and temperature on tension in isolated canine coronary artery

The effects of calcium and temperature on the tension of isolated canine coronary arterial strips were studied.In 20mEq·l ^–1 K solution, the tension was significantly increased from 0mg with 0mEq·l ^–1 Ca to 33 ± 18mg with 0.2mEq·l ^–1 Ca at 37°C, from –40 ± 18mg with 0mEq·l ^–1 Ca to –17 ± 11mg with 0.2mEq·l ^–1 Ca at 30°C, from –77 ± 19mg with 0mEq·l ^–1 Ca to –52 ± 17mEq·l ^–1 with 1mEq·l ^–1 Ca at 25°C, from –88 ± 13mg with 0mEq·l ^–1 Ca to –41 ± 18mg with 2mEq·l ^–1 Ca at 20°C, from –125 ± 16mg with 0mEq·l ^–1 Ca to –116 ± 13mg with 2mEq·l ^–1 Ca at 15°C. Ca higher than 0.2mEq·l ^–1 produced a dose-dependent increase in tension between 37°C and 15°C. In spite of the presence of 4mEq·l ^–1 Ca, the development of tension was strongly supressed by lowering the temperature below 20°C, and completely inhibited at 10°C. The rate of a decrease in tension caused by cooling was about 5.5mg·°C^–1.This study demonstrated that Ca²⁺ produced a dose-dependent increase in tension in high-K solution, which was suppressed as the temperature was lowered.(Yoshida K, Fujii Y, Ina H, et al.: Effects of calcium and temperature on tension in isolated canine coronary artery. J Anesth 5: 172–176, 1991)     

Erythemas caused by electrodes while monitoring neuromuscular blockade: three cases

Skin erythemas formed in three patients during surgery at the sites where negative electrodes had been attached to stimulate the ulnar nerve for a neuromuscular transmission monitor (Relaxograph). The patients were all women, aged 52, 62, and 74 years, and general anesthesia lasted 8h 20min, 4h 50min, and 8h 45min, respectively. The electrodes used were disposable ECG electrodes in the first two patients and one designed for a neuromuscular monitor in the third; all were carbon-coated and then covered with gel. However, when the electrodes were detached from the lesion, they all showed loss or damage of the carbon coating under the gel. We recommend balancing the merit of monitoring with the risk of complications, even when applying an apparently safe, noninvasive monitor.     

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.     

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)     

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.     

Time-level relationship for nitric oxide and the protective effects of aminoguanidine in experimental spinal cord injury

Summary. Background. The secondary injury process following spinal cord trauma has been shown to involve different mechanisms such as excessive release of excitatory amino-acids, and induction of free radical induced lipid peroxidation. In this experimental study, the time-level relationship of the nitric oxide and the neuroprotective effects of aminoguanidine were investigated in a rat spinal cord trauma model.Methods. The experiments were performed on 63 Wistar albino rats divided into three groups; sham-operated control (Group 1), trauma created control (Group 2) and aminoguanidine group (Group 3). In groups 2 and 3, spinal cord trauma was produced at thoracic level by using weight the drop technique (at a severity of 50gr-cm). After the trauma, the rats in Group 3, received an intraperitoneal injection of 100mg/kg aminoquanidine twice a day for 3 days. The effects of the injury and the efficacy of aminoguanidine were determined based on biochemical parameters (lipid peroxidation and nitric oxide levels in tissue), and on light microscopy findings in cord tissue collected at different times post-injury. Biochemical parameters were performed one hour, three and five days after injury. Functional recovery was assessed at 3, and 5 days after cord trauma with the inclined-plane technique and Tarlovs motor grading scale.Findings. Although there was no statistically significant difference at the 1^st hour, the values of the tissue nitric oxide in trauma created controls were 42% higher on the 3^rd day and 40% higher on the 5^th day when compared with those in sham controls. The levels of the tissue lipid peroxidation in trauma created controls were 88% higher at the 1^st hour and 52.8% higher on the 5^th day when compared with shame controls, but there was no meaningful difference on the 3^rd day. In the trauma created control group, the mean motor function scores decreased to 1.16±0.40 and to 1±0 on the 3^rd and 5^th day, respectively. In this group the mean values of the inclined plane were 39.16±2.04 on the 3^rd day and 37.91±1.02 on the 5^th day. No statistically significant difference was observed in both tissue lipid peroxidation and nitric oxide levels for all time points between the aminoguanidine group and the sham-operated controls (p>0.01). The motor function scores were observed as 2.16±0.40 on the 3^rd day and as 3±0 on the 5^th day in aminoguanidine group. These values were significantly higher than the trauma created controls (p<0.01). Aminoguanidin treatment also improved the inclined plane performance of the rats; In this group, the mean values of the inclined plane scores were 44.58±2.92 and 52.91±1.88 on the 3^rd and 5^th days, respectively. These values were significantly higher than the trauma created controls (p<0.01).Interpretation. This study shows that the nitric oxide level does not increase in the spinal cord tissue during the first hour after the spinal cord trauma. It increases significantly in the spinal cord tissue not only three days but also five days following the trauma. Aminoguanidine treatment, which is started just after the trauma, can prevent both the nitric oxide production and lipid peroxidation in spinal cord tissue and it can improve the functional status of the animals. In this respect, aminoguanidine may have a potential role in the treatment of acute spinal cord injury.     

Enzyme inhibition by analgesic and hypnotic agents on anaerobic dehalogenation of halothane

Enzyme inhibition on anaerobic dehalogenation of halothane by various analgesic or hypnotic agents was investigated in vitro using rat liver microsomal fraction. The production rate of chloro-difluoro-ethylene (CDE) and chloro-trifluoro-ethane (CTE), anaerobic metabolites of halothane, was measured when various concentrations of analgesic or hypnotic agents (fentanyl, morphine, pentazocine, buprenorphine, ketamine, diazepam, chlorpromazine and hydroxyzine) were supplemented. Inhibitor constant (Ki) of each agent was calculated and compared with each other. The activity of NADPH-cytochrome c reductase (fp₂) and NADH-ferricyanide reductase (fp₁) was measured when each agent was added. The values of inhibitor constants (Ki) for CDE and CTE formation were in the following order from large to small values; morphine (656µM and 2570µM), chlorpromazine (49.7µM and 68.1µM), ketamine (24.9µM and 64.4µM), fentanyl (23.9µM and 34.6µM), hydroxyzine (19.2µM and 50.8µM), diazepam (17.0µM and 13.9µM), buprenorphine (11.2µM and 22.4µM), and pentazocine (1.96µM and 6.67µM) respectively. Pentazocine inhibited the formation of CDE 300 fold greater than morphine. The activity of fp₂ and fp₁ did not change by the addition of these analgesic or hypnotic agents. These results indicate that various analgesic or hypnotic agents, which are commonly used with halothane in clinical anesthesia, suppress the anaerobic dehalogenation of halothane in vitro. They also imply that the suppression of production of halothane metabolites is the result of direct enzyme inhibition on cytochrome P-450, since these agents did not affect the activity of fp₂ and fp₁ which are flavoproteins existing in the microsomal electron transport system.(Yamanoue T, Kikuchi H, Fujii K, et al.: Enzyme Inhibition by Analgesic and Hypnotic Agents on Anaerobic Dehalogenation of Halothane. J Anesth 5: 331–337, 1991)     

Induced hypotension for surgical repair of congenital dislocation of the hip in children

The surgical repair of congenital dislocation of the hip was performed under normotensive anaesthesia (23 children) and hypotensive anaesthesia (52 children). Hypotension was induced with infusion of hypotensive agents such as trimetaphan or nitroglycerin during inhalation or neurolept-anaeshesia under careful monitoring of blood pressure, haematocrit and electrocardiogram. Blood replacement was done to keep hematocrit value above 30%. Blood loss was significantly less in hypotensive group (2.53ml/kg/h) than that in normotensive group (4.53ml/kg/h). Twenty one percent of patients in hypotensive group required blood transfusion with the rate of 3.3ml/kg/h compared with 43% of cases in normotensive group with the rate of 4.4ml/kg/h. Depending upon anaesthesia technique blood loss was greater in neuroleptanaesthesia (5.5ml/kg/h) than inhalation (2.3ml/kg/h) or epidural (2.1ml/kg/h) anaesthesia. Urine output and laboratory data for liver and kidney functions were not different between normotensive and hypotensive group. The dose of hypotensive agents required to produce moderate hypotension for paediatric patients was much higher than that for adult. We consider that moderate hypotension is safe procedure if employed by well experienced anaesthetist with careful monitoring of blood pressure, Hct and ECG. Blood loss and requirement of blood replacement are significantly reduced with this technique.(Nam YT, Shin T, Yoshitake J: Induced hypotension for surgical repair of congenital dislocation of the hip in children. J Anesth 3: 58–64, 1989)     

Dose-finding study of intravenous midazolam for sedation and amnesia during spinal anesthesia in patients premedicated with intramuscular midazolam

Purpose We investigated the effective and safe dose of intravenous midazolam for sedation and amnesia during spinal anesthesia in patients premedicated with intramuscular midazolam.Methods One hundred and eighty patients aged 20–50 years scheduled for spinal anesthesia received midazolam 0.06mg·kg^–1 and atropine 0.01mg·kg^–1 intramuscularly 15min before entering the operating room. Spinal anesthesia was performed with 0.5% hyperbaric tetracaine. Five minutes after starting surgery, midazolam 0 (control group), 0.01, 0.02, 0.03, 0.04, or 0.05mg·kg^–1 was intravenously administered (30 patients each). Blood pressure, heart rate, respiratory rate, percutaneous oxygen saturation (S_{p O 2}), verbal response, eyelash reflex, and involuntary body movement were measured every 5min for 30min. Memory during surgery was also investigated.Results The number of the patients with loss of verbal response, with loss of eyelash reflex, and with no memory during surgery were significantly larger in the groups receiving midazolam 0.03mg·kg^–1, 0.04mg·kg^–1, and 0.02mg·kg^–1, respectively. The decrease in blood pressure or increase in respiratory rate with decrease in S_{p O 2} was significantly larger in the groups receiving midazolam 0.03mg·kg^–1 or 0.05mg·kg^–1, respectively.Conclusion For sedation and amnesia of the patients aged 20–50 years in spinal anesthesia with about 1h duration receiving intramuscular midazolam 0.06mg·kg^–1 as a premedication, intravenous midazolam 0.02mg·kg^–1 might be effective and safe.     

Vitamin C may be beneficial in the prevention of paracetamol-induced renal damage

Background There is no specific treatment for paracetamol-induced renal damage. Vitamin C is an outstanding chain-breaking antioxidant and a free radical scavenger. The present study was undertaken to determine whether large doses of vitamin C are useful in the treatment of paracetamol-induced renal damage.Methods Renal injury was induced in rats by the administration of 1g/kg body weight paracetamol intraperitoneally. Some rats received intraperitoneal injections of vitamin C (250, 500, or 1000mg/kg body wt) at 1.5h, 6h, 9h, or 16h after the administration of paracetamol, and the rats were killed 24h after the administration of paracetamol.Results Renal injury was accompanied by a decrease in nonprotein thiol and protein thiol in the kidneys of paracetamol-treated rats. The administration of vitamin C to the paracetamol-treated rats prevented renal damage either completely or partially. Lower doses of vitamin C were beneficial in the prevention of paracetamol-induced renal injury when administered early and higher doses were beneficial when administered later. In the paracetamol-treated rats that responded to vitamin C, renal nonprotein thiol level and protein thiol were restored almost completely. Interestingly, a highly significant inverse correlation was obtained between renal nonprotein thiol level and plasma creatinine.Conclusions Megadoses of vitamin C may be beneficial in the treatment of paracetamol-induced renal damage. The mechanism of protection by vitamin C appears to be the regeneration of nonprotein thiol.     

Changes in venous capacitance during prostaglandin E1-induced hypotension; Comparisons with trinitroglycerin

The purpose of this study was to examine the effects of prostaglandin E₁ (PGE₁) on venous capacitance during controlled hypotension. Trinitroglycerin (TNG) was used as a control agent. In rats anesthetized with ketamine, mean arterial pressure was lowered to 70mmHg and subsequently 50mmHg by intravenous infusion of PGE₁ or TNG. Venous capacitance was assessed before and during induced hypotension by measuring the mean circulatory filling pressure (MCFP). MCFP was measured after briefly arresting the circulation by inflating an indwelling balloon in the right atrium. MCFP was significantly decreased by PGE₁ from 7.9 ± 0.3 to 6.9 ± 0.3mmHg at mean arterial pressure of 70mmHg and to 6.9 ± 0.2mmHg at mean arterial pressure of 50mmHg. The decrease in MCFP by PGE₁ at mean arterial pressure of 70mmHg was not significantly different from TNG. However, the decrease in MCFP by PGE₁ at mean arterial pressure of 50mmHg was significantly less than that by TNG. The results suggest that the venous capacitance may be increased by PGE₁ to a similar degree with TNG at doses to produce a comparable level of moderate hypotension, but the increase in venous capacitance may be less in PGE₁ than TNG at doses to produce deep hypotension.(Liang J, Hoka S, Okamoto H, et al.: Changes in venous capacitance during prostaglandin E₁-induced hypotension; comparisons with trinitroglycerin. J Anesth 7: 303–307, 1993)     

Inhaled Nitric Oxide Therapy After Fontan-Type Operations

Purpose Inhaled nitric oxide (NO) therapy is a newly developed strategy designed to reduce pulmonary vascular resistance after the Fontan-type operation. We reviewed our experience to evaluate its efficacy and true indications.Methods We retrospectively examined 47 children who received inhaled NO therapy after the Fontan-type operation between August 1996 and December 2002. The maximal dose of NO ranged from 5 to 30ppm (median 10ppm), and the duration of inhaled NO therapy ranged from 5h to 52 days (median 2 days).Results Inhaled NO significantly decreased the central venous pressure (CVP), from 16.2 ± 2.2 to 14.6 ± 2.2mmHg (P < 0.0001), and the transpulmonary pressure gradient between the CVP and left atrial pressure, from 9.9 ± 2.9 to 8.4 ± 2.7mmHg (P < 0.0001). It also increased the systolic systemic arterial pressure from 71.9 ± 15.2 to 76.8 ± 14.5mmHg (P < 0.05). In 26 patients with additional fenestration, inhaled NO led to a significant improvement in SaO₂ from 90.1% ± 9.6% to 93.3% ± 7.9% (P < 0.01). However, patients with a CVP <15mmHg or a transpulmonary pressure gradient <8mmHg, or both, after the Fontan-type operation, showed no significant changes in hemodynamics during inhaled NO therapy.Conclusions We propose that a CVP 15mmHg or a transpulmonary pressure gradient 8mmHg, or both, after Fontan-type operations are appropriate indications for inhaled NO therapy.     

Percutaneous and Open Renal Revascularizations Have Equivalent Long-Term Functional Outcomes

Atherosclerotic renal artery stenosis is a significant cause of poorly controlled hypertension and progressive renal dysfunction leading to ischemic nephropathy and other end-organ damage. The optimal treatment of renovascular disease contributing to hypertension and renal dysfunction is not known. This study compares the anatomic and functional outcomes of both open and endovascular therapy for chronic, symptomatic atherosclerotic renal artery disease. We performed a retrospective analysis of records from patients who underwent renal arterial interventions, endovascular or open bypass, between January 1984 and January 2004. Principal indications for intervention were hypertension (51%), chronic renal insufficiency (13%), and hypertension and elevated creatinine (36%). A total of 247 patients (109 males; mean age 69±10, range 44–89 years) underwent 314 interventions (109 open procedures; 205 angioplasties, 71% with stent placement). There was a significant difference in 30-day mortality (4% vs. <1%; p < 0.005) between the open and endoluminal groups, but not at 1, 3, or 5 years. Patients in the open group had a higher primary patency rate at 5 years (83±5% vs. 76±6%; p=0.03), but patients in the endoluminal group had a higher assisted primary patency rate at 5 years (92±5% vs. 84±5; p=0.03). There was no significant difference between both treatment groups in cumulative freedom from presenting symptom or in freedom from dialysis and renal-related death. Patients who presented with hypertension were more likely to have shown improvement in their blood pressure with endoluminal intervention at 1, 3, and 5 (59±6% endoluminal vs. 83±5% open; p=0.01) years. From these results we conclude that open repair and endoluminal repair of atherosclerotic renal artery stenosis have similar immediate and long-term functional and anatomic outcomes. Patients who present with hypertension may have greater benefit with an endoluminal repair.Presented at the Twenty-ninth Annual Meeting of the Peripheral Vascular Surgery Society, Anaheim, CA, June 4-5, 2004.     

Enhancement of lidocaine-induced epidural anesthesia by deoxyaconitine in the rabbit

Purpose.Aconiti tuber has been used in traditional Oriental medicine to alleviate pain. The antinociceptive property of aconiti tuber is due to the action of its extracted alkaloids such as deoxyaconitine. The purpose of this study was to investigate the effect of epidural deoxyaconitine on epidural lidocaine anesthesia. Methods.Five adult rabbits were used. Three different combinations of drugs were injected into the epidural space, in the following order: first (combination A), 1.5ml of 2% lidocaine; second (combination B), 1.5ml of 2% lidocaine and 150µg deoxyaconitine; and third (combination C), 3mg nor-binaltorphimine followed by 1.5ml of 2% lidocaine and 150µg deoxyaconitine 30min later. The latency of onset and the duration of three end-points (sensory loss in the tail, loss of weight-bearing ability, and flaccid paresis of hind limb) were measured. Results.Onset times for the three end-points were not changed by deoxyaconitine or by nor-binaltorphimine. The duration of sensory loss was 27.0 ± 2.7min, the duration of loss of weight-bearing ability was 33.0 ± 2.7min, and the duration of flaccid paresis was 21.0 ± 4.2min in the combination A group. In the combination B group, deoxyaconitine extended the time of sensory loss by 80%, the time of loss of weight-bearing by 50%, and that of flaccid paresis by 60% compared with the combination A group. In the combination C group, this phenomenon was partially antagonized by pretreatment with nor-binaltorphimine, a -opioid antagonist. Conclusions.Based on our observations, deoxyaconitine enhanced epidural lidocaine anesthesia in the rabbit, and this effect seemed to be partly mediated by -opioid receptors.     

Wear of ultra-high-molecular-weight polyethylene cup articulating with 22.225 mm zirconia diameter head in cemented total hip arthroplasty

A number of studies have highlighted the increasing incidence of aseptic cup loosening with increasing depth of cup penetration by the metal head. We present our experience with a 22.225mm diameter zirconia head on a 9–10 taper articulating with an ultra-high-molecular-weight polyethylene (UHMWPE) cup in cemented total hip arthroplasties. We prospectively studied the wear of the UHMWPE cup articulating with a 22.225mm diameter zirconia head in cemented total hip arthroplasties. A total of 339 patients (153 men, 186 women, 373 hips) were included. The patients mean age at surgery was 52 years (17–76 years), with 41% age 50 years or younger. Their mean weight was 72.4kg (24–125kg). At a mean follow-up of 4.3 years (0–8 years) the mean penetration rate of the cup was 0.03mm/year (0–0.51mm/year). Altogether, 289 (77.5%) showed no measurable wear, 38 (10.2%) had a penetration rate of 0.11mm/year or less, 33 (8.9%) had a rate of 0.12–0.2mm/year, and in 13 (3.5%) the rate was more than 0.2mm/year. Ceramic–UHMWPE is the next stage in the evolution of total hip arthroplasty for addressing wear and any possible related issues.     

Comparison of Precuffed and Vein-Cuffed Expanded Polytetrafluoroethylene Grafts for Infragenicular Arterial Reconstructions:A Case-Matched Study

Distal vein cuff interposition is often added to prosthetic infragenicular arterial reconstruction in an attempt to improve hemodynamics and patency rates. The purpose of this study was to compare the outcome of a precuffed expanded polytetrafluroethylene (ePTFE) graft with a vein-cuffed ePTFE graft for infragenicular bypass. We reviewed the clinical outcome of 77 patients with critical limb ischemia without available autologous vein conduits who underwent arterial reconstruction of 80 limbs to below-knee popliteal or tibioperoneal vessels using either ePTFE precuffed graft (precuffed group, 38 patients 40 limbs) or ePTFE vein-cuffed graft (vein-cuffed group, 39 patient, 40 limbs). Precuffed group patients were enrolled in a prospective cohort study. Vein-cuffed group patients consisted of consecutive case-matched patients operated on during the same study period. End points were primary graft patency and limb salvage rates. There were 42 males and 35 females with a mean age of 73.4 years (range, 44-92 years). Both groups were matched to demographics, risk factors for atherosclerosis, previous ipsilateral reconstruction, and location of the distal anastomosis. Proximal anastomosis was to the common (n=68) or superficial (n=12) femoral arteries. Distal anastomosis was to the below-knee popliteal (n=28), anterior tibial (n=12), posterior tibial (n=15) and peroneal (n=25) arteries. Operative mortality was 1.3%. Graft patency at dismissal was 90% and 95% in the precuffed and vein-cuffed groups, respectively. The mean follow-up was 25.7 months (range, 2.4-61 months). Primary patency rates at 1 and 3 years were 70% and 57% in the precuffed group, and 78% and 54% in the vein-cuffed group (p=0.32). Limb salvage rates at 1 and 3 years were 97% and 70% in the precuffed group, and 95% and 81 % in the vein-cuffed group (p=0.49). Overall patient survival at 1 and 3 years was 81 % and 57%, respectively. In this case-control study, results of precuffed ePTFE graft were similar to those obtained with vein-cuffed ePTFE grafts. The precuffed ePTFE graft is an adequate alternative conduit for infragenicular arterial reconstruction in patients with critical limb ischemia and no available autologous veins.Presented at the 32^nd Annual Symposium on Vascular Surgery, Society for Clinical Vascular Surgery, Rancho Mirage, CA, March 10–13, 2004.     

Beneficial Effects of Apolipoprotein A-I on Endotoxemia

Purpose. Although many studies have shown the beneficial effects of lipoproteins on animals with endotoxemia, little is known about the impact of apolipoprotein A-I (apoA-I) on tumor necrosis factor (TNF-) release in response to lipopolysaccharide (LPS). The present study was conducted to determine whether the administration of apoA-I inhibits the release of TNF- and influences the survival rate of rats with endotoxemia.Methods. Forty male Wistar rats were divided randomly into four groups. Rats in the first and second groups were given 1mg/kg LPS intraperitoneally (i.p.) and blood was collected 1h later to measure the serum levels of TNF-. Either 10mg/kg apoA-I or Tris-buffered saline was injected i.p. and the serum TNF- levels were measured again 2h later. Rats in the third and fourth groups were given 5mg/kg LPS. Following the administration of 10mg/kg apoA-I or Tris-buffered saline, animals were observed for 5 days and survival rates were determined.Results. ApoA-I inhibited the release of serum TNF- and improved the survival rates of rats with endotoxemia.Conclusion. The administration of apoA-I suppressed the TNF- release in endotoxemia and decreased the mortality rates of rats.