Fibrinolysis in Living Donor Liver Transplantation Recipients Evaluated Using Thromboelastometry: Impact on Mortality.

BACKGROUND: Inadequate hemostasis during living donor liver transplantation (LDLT) is mainly due to coagulopathy but may also include fibrinolysis. The purpose of this study was to determine the incidence of fibrinolysis and assess its relevance to mortality in LDLT. METHODS: The incidence and prognosis of fibrinolysis were retrospectively studied in 76 patients who underwent LDLT between April 2010 and February 2013. Fibrinolysis was evaluated and defined by maximum lysis (ML) >15% within a 60-minute run time using thromboelastometry (ROTEM). RESULTS: Fibrinolysis was observed in 19 of the 76 (25%) patients before the anhepatic (pre-anhepatic) phase and was developed in 24 (32%) patients during and after the anhepatic (post-anhepatic) phase. In these 43 patients who had fibrinolysis, spontaneous recovery occurred in 29 patients (73%) within 3 hours after reperfusion of the liver graft. Recovery with tranexamic acid was noted in 2 patients with fibrinolysis in the post-anhepatic phase. Thrombosis in the portal vein and liver artery was noted in 14 patients, and the incidence was significantly greater in patients with post-anhepatic fibrinolysis than in those with pre-anhepatic fibrinolysis (P = .0017). Fibrinolysis that developed in the pre-anhepatic phase was associated with increased 30-day and 6-month mortalities (P = .0003 and .0026, respectively). CONCLUSIONS: Fibrinolysis existed and developed in a large percentage of patients during LDLT. Thrombosis in the portal vein and hepatic artery was more common in patients with fibrinolysis in the post-anhepatic phase. Fibrinolysis that developed in the pre-anhepatic phase was associated with increased 30-day and 6-month mortalities.

Diastolic dysfunction of the left ventricle is associated with pulmonary edema after renal transplantation.

BACKGROUND: Post-operative pulmonary complications are associated with high mortality and graft loss in renal transplantation recipients. Left ventricular diastolic dysfunction is not uncommon in patients with chronic renal failure, including those with preserved left ventricular systolic function. The purpose of this study was to determine the relationship between left ventricular diastolic dysfunction and incidence of post-operative pulmonary edema in renal transplantation recipients with preserved left ventricular systolic function. METHODS: Pre-operative left ventricular function and incidence of pulmonary edema were retrospectively studied in 209 patients who underwent living-donor renal transplantation between January 2010 and October 2012. Left ventricular systolic and diastolic functions were evaluated by ejection fraction and E/E' ratio, retrospectively, using transthoracic echocardiography. Pulmonary edema was defined by evidence of pulmonary congestion on the chest X-ray together with PaO2 /FiO2 ratio < 300 mmHg. RESULTS: Eleven out of 190 (5.8%) renal transplantation patients with preserved left ventricular systolic function developed post-operative pulmonary edema. Patients with pulmonary edema had a significantly higher geometric mean (95% confidence interval) of E/E' ratio than those without pulmonary edema [17.8 (14.1-22.5) vs. 11.1 (10.6-11.7), P = 0.001]. CONCLUSION: Pre-operative left ventricular diastolic dysfunction correlated with the development of post-operative pulmonary edema in renal transplantation recipients. Meticulous intraoperative volume therapy is important to avoid post-operative pulmonary edema in such patients.

A double-blind randomized controlled trial of patient-controlled epidural analgesia with or without a background infusion following initial spinal analgesia for labor pain.

BACKGROUND: Patient-controlled epidural analgesia (PCEA) combined with spinal analgesia is an option for pain relief in labor. However, the effect of a CBI on the analgesic requirements of laboring women is still debated. This double-blind study investigated the effect of CBI with PCEA following spinal analgesia on the local anesthetic requirements of parturients during labor. METHODS: Sixty-six nulliparous women were randomly assigned to a standard PCEA protocol (5-mL demand bolus, 10-min lockout) with or without a CBI of 6 mL/h. The epidural solution consisted of 0.1% ropivacaine with fentanyl 2 microg/mL. Labor analgesia was initiated in both groups with intrathecal bupivacaine 2.5 mg plus fentanyl 25 microg. The number of demands per hour and the hourly dose of ropivacaine were calculated for both groups. RESULTS: The median [range] number of analgesic boluses per hour in the PCEA group that were demanded: 2.4 [0.8-12.2] and delivered: 1.6 [0.8-2.6], were significantly greater than those in the PCEA+CBI group: 0.7 [0.4-4.2] and 0.6 [0.2-1.3] (P 0.05). However, the hourly ropivacaine dose in the PCEA group (7.9 [3.9-13.2] mg/h) was not significantly different from that in the PCEA+CBI group (8.4 [6.0-12.5] mg/h). CONCLUSION: In laboring nulliparous patients provided initial labor analgesia with spinal anesthesia, the use of a continuous background infusion decreases PCEA demand dosing, but not the total hourly amount of ropivacaine and fentanyl used.

The effect of hydroxyethylstarch infusion on bupivacaine pharmacokinetics in rats.

BACKGROUND: Bupivacaine is the agent most often used for labor analgesia. However, the risk of accidental intravascular injection of this drug and consequent acute systemic toxicity is ever-present. Although hydroxyethylstarch (HES) is preferred over crystalloid for prevention of hypotension during regional anesthesia, the pharmacokinetics of bupivacaine during fluid preloading has not been studied. METHODS: Twenty-four awake Sprague-Dawley rats were randomly allocated to receive the continuous intravenous infusion of HES 70K, 200K or 400K, or normal saline (NS). After 1 hour of prehydration all animals received bupivacaine, 1mg kg(-1), bolus, followed by a continuous infusion, 0.4mg kg(-1) min(-1) for 15 minutes. After the completion of bupivacaine infusion serial arterial blood samples to determine the plasma bupivacaine concentration were obtained. The plasma concentration-time profile of bupivacaine was fitted to a two-compartment open model, and the estimated intercepts and slopes were used for calculation of standard pharmacokinetic parameters. RESULTS: The mean peak bupivacaine concentration during HES 400K infusion was significantly lower than during NS infusion (1488 +/- 302 ng ml(-1) vs 2388 +/- 582 ng ml(-1)). Mean volume of distribution in each of the three HES groups was greater than in NS group. Mean area under curves (AUC) during HES 200K and HES 400K infusions were significantly lower than during NS infusion (32534 +/- 4180 and 29619 +/- 4431 min ng ml(-1), respectively, vs 39802 +/- 6268 min ng ml(-1)). Mean total clearance of bupivacaine during HES 200K and HES 400K infusions was significantly higher than during NS infusion (115 +/- 14 and 132 +/- 15 ml min(-1) kg(-1), respectively, vs 92 +/- 14 ml min(-1) kg(-1)). CONCLUSION: Our results suggest that the increased volume of distribution during HES infusion could be counterbalanced by the increased total clearance, resulting in unchanged half-life or elimination rate constant of bupivacaine.

Intranasal lidocaine 8% spray for second-division trigeminal neuralgia.

BACKGROUND: Trigeminal nerve block has been widely used for trigeminal neuralgia. This may induce paraesthesia. The second division of the trigeminal nerve passes through the sphenopalatine ganglion, which is located posterior to the middle turbinate and is covered by a mucous membrane. We examined the effectiveness of intranasal lidocaine 8% spray on paroxysmal pain in second-division trigeminal neuralgia. METHODS: Twenty-five patients with second-division trigeminal neuralgia were randomized to receive two sprays (0.2 ml) of either lidocaine 8% or saline placebo in the affected nostril using a metered-dose spray. After a 7 day period, patients were crossed over to receive the alternative treatment. The paroxysmal pain triggered by touching or moving face was assessed with a 10 cm visual analogue scale (VAS) before and 15 min after treatment. Patients used a descriptive scale to grade pain outcome, and were asked to note whether the pain returned and how long after therapy it recurred. RESULTS: Intranasal lidocaine 8% spray significantly decreased VAS [baseline: 8.0 (2.0) cm, 15 min postspray: 1.5 (1.9) cm, mean (SD)], whereas the placebo spray did not [7.9 (2.0) cm, 7.6 (2.0) cm]. Moreover, pain was described as moderate or better by 23 patients of the lidocaine spray and 1 of the placebo group. The effect of treatment persisted for 4.3 h (range 0.5-24 h). CONCLUSIONS: Intranasal lidocaine 8% administered by a metered-dose spray produced prompt but temporary analgesia without serious adverse reactions in patients with second-division trigeminal neuralgia.

Utilization of personal digital assistants (PDA) for intraoperative naming tasks in awake surgery.

The naming task, one of the most important tasks for screening essential language function, is widely used in awake surgery. We employed personal digital assistants (PDA) for the display of objects in three patients performing the naming task during awake surgery for gliomas adjacent to the language area in the left hemisphere. The compact, light-weight, self-illuminated instrument can easily be held close to the patient's face. None had difficulty seeing the screen despite the presence of the surgical drape around the face. The examiner could easily change the displayed objects with a click. However, the PDA screen is too small for use in auditory comprehension tasks such as the Token Test.

Amelioration of hyperalgesia by kinin receptor antagonists or kininogen deficiency in chronic constriction nerve injury in rats.

OBJECTIVE: The present study was designed to examine the involvement of bradykinin in thermal and mechanical hyperalgesia induced by chronic constriction nerve injury (CCI) using B1 and B2 receptor antagonists and mutant kininogen-deficient rats. METHODS: Sprague-Dawley (SD) rats and Brown Norway (B/N-) rats given CCI treatment on day 0, were used as a model of neuropathic pain. Either a kinin B1 antagonist des-Arg9-[Leu8]-bradykinin or the receptor B2 antagonist HOE-140 was constantly infused into the left jugular vein of SD rats on days 15 to 22 after CCI. Vehicle-treated rats and sham-operated rats without nerve injury were also prepared as controls. In all rats, we observed pain behavior, and measured the latency period of paw withdrawal from the thermal stimuli and, with von Frey filaments, the mechanical pain threshold, before surgery and on days 14 and 22 after CCI. B/N-Katholiek rats, which congenitally lack plasma kininogen and release no kinin, were also tested for hyperalgesic parameters. Expression of kinin receptor mRNA in the dorsal root ganglia was detected by RT-PCR. RESULTS: Most of the rats (88%) showed some pain behavior, which was reduced to 67% by a B1 antagonist and to 57% by a B2 antagonist infused between days 15 to 22. Thermal hyperalgesia was significantly reduced from 7.25 +/- 0.41 sec (mean +/- SEM) to 8.36 +/- 0.41 sec in paw withdrawal latency on day 22 by a B1 antagonist and from 7.24 +/- 0.19 sec to 8.23 +/- 0.21 sec by a B2 antagonist (P < 0.05). Mechanical hyperalgesia was also ameliorated from 0.02 +/- 0.007 g force to 0.16 +/- 0.08 g force in pain threshold by a B1 antagonist and from 0.03 +/- 0.007 g force to 0.10 +/- 0.003 g force on day 22 by a B2 antagonist. Moreover, deficient B/N-Katholiek rats showed a low incidence of thermal and mechanical hyperalgesia on day 14. Expression of both B1 and B2 receptor mRNAs was detected in the lumbar dorsal ganglia ipsilateral to the site of the nerve injury. CONCLUSION: These data suggests that kinin were at least partly involved in yielding nociceptor hypersensitivity up to day 14 after CCI. Bradykinin and its B1 and B2 receptors were involved in the maintenance of hyperalgesia.

Intrathecal fentanyl/meperidine combined with low-dose epidural bupivacaine for Cesarean section in a patient with advanced Krukenberg tumors.

This case report demonstrates the anesthetic management of a 41-year-old primiparous parturient with massive ascites due to advanced Krukenberg tumors, undergoing Cesarean section. We chose a combined intrathecal-epidural technique, using intrathecal hypobaric fentanyl and hyperbaric meperidine, and a low dose of epidural bupivacaine in order to avoid hemodynamic instability in this critically ill patient. Surgery was carried out without difficulty under adequate regional anesthesia. The blood pressure was maintained with low doses of phenylephrine and dopamine. Opioid-related complications such as nausea-vomiting, pruritus, drowsiness, and respiratory depression were not observed in this patient. Therefore, intrathecal opioids combined with a low dose of epidural local anesthetics for Cesarean section is suitable for critically ill patients with malignant abdominal tumors, such as a Krukenberg tumor, complicated by massive ascites.

Continuous spinal analgesia for labor and delivery in a parturient with hypertrophic obstructive cardiomyopathy.

Induction of labor under analgesia was planned for a 30-year-old-primiparous patient with hypertrophic obstructive cardiomyopathy (HOCM), as her fetal evaluation revealed intrauterine growth restriction at 38 weeks' gestation. However, regional analgesia during labor may present a potential risk for hemodynamic instability in patients with HOCM due to the possibility of a sympathetic block, as a result of vasodilation associated with the administration of local anesthesia. This case report demonstrates the successful management of the patient with analgesia provided by a continuous spinal catheter dosed with a continuous infusion of fentanyl and supplemental meperidine. Fetal surveillance monitoring included fetal pulse oximetry in addition to conventional cardiotocography, on the basis of which cesarean section was avoided.

[Issues in cancer pain management].

In this article, three aspects of recent issues in cancer pain management such as pain assessment, drowsiness with morphine, and problem in home care setting. First, the assessment of 'impact of pain' is to assess whether the treatment is sufficient for the patient. On the other hand, assessment of 'pain intensity' is the effectiveness of the treatment. Therefore, to reduce the gap in pain evaluations between cancer patients and medical stuffs by assessing the 'impact of pain' in addition to 'intensity of pain'. Second, increasing dosage of morphine often reduces pain, at the same time patients become drowsy. This is often observed soon after starting morphine administration, especially, patients who have renal dysfunction. An active morphine metabolite morphine-6-Glucuronide is excreted into urine, so that, renal dysfunction causes drowsiness. Third, at home care setting, patients tend to be into poor pain control condition. It is necessary that paying attention on patient's knowledge of medications and having support program for pain management for home care setting.

Low-concentration lidocaine rapidly inhibits axonal transport in cultured mouse dorsal root ganglion neurons.

BACKGROUND: Axonal transport plays a critical role in supplying materials for a variety of neuronal functions such as morphogenetic plasticity, synaptic transmission, and cell survival. In the current study, the authors investigated the effects of the analgesic agent lidocaine on axonal transport in neurites of cultured mouse dorsal root ganglion neurons. In relation to their effects, the effects of lidocaine on the growth rate of the neurite were also examined. METHODS: Isolated mouse dorsal root ganglion cells were cultured for 48 h until full growth of neurites. Video-enhanced microscopy was used to observe particles transported within neurites and to measure the neurite growth during control conditions and in the presence of lidocaine. RESULTS: Application of 30 microM lidocaine immediately reduced the number of particles transported in anterograde and retrograde axonal directions. These effects were persistently observed during the application (26 min) and were reversed by lidocaine washout. The inhibitory effect was dose-dependent at concentrations from 0.1 to 1,000 microM (IC50 = 10 microM). In Ca2+-free extracellular medium, lidocaine failed to inhibit axonal transport. Calcium ionophore A23187 (0.1 microM) reduced axonal transport in both directions. The inhibitory effects of lidocaine and A23187 were abrogated by 10 microM KN-62, a Ca2+-calmodulin-dependent protein kinase II inhibitor. Application of such low-concentration lidocaine (30 microM) for 30 min reduced the growth rate of neurites, and this effect was also blocked by KN-62. CONCLUSIONS: Low-concentration lidocaine rapidly inhibits axonal transport and neurite growth via activation of calmodulin-dependent protein kinase II.

Participation of cyclooxygenases in cutaneous thermal nociception under non-inflamed and inflamed conditions.

OBJECTIVE AND DESIGN: Effects of cyclooxygenase inhibitors on noxious thermal stimuli were investigated in non-inflamed and inflamed rats. MATERIALS: Male Sprague-Dawley rats were used in this study. TREATMENT: Cyclooxygenase inhibitors, indomethacin, mofezolac, NS-398, and JTE-522 were administered orally at a dose of 10 mg/kg 1 h prior to and 4 h after the intravenous injection of lipopolysaccharide (1 mg/kg). METHODS: The nociceptive response was evaluated from the escape latency of foot withdrawal to the thermal stimuli with a beam of light. Expression ofcyclooxygenase was examined by reverse transcription-polymerase chain reaction. RESULTS: In normal rat, administration of indomethacin, relatively cyclooxygenase-1-selective inhibitor, mofezolac, or cyclooxygenase-2-selective inhibitors, NS-398 and JTE-522 had no effects on the escape latency against thermal stimuli. Injection of lipopolysaccharide into rat induced the expression of mRNA for cyclooxygenase-2 in the subcutaneous tissue of foot pad. The escape latency at 8 h was significantly shortened by the injection. This hyperalgesia could be reversed by pretreatment of rat with NS-398 or JTE-522, but not with mofezolac. CONCLUSIONS: Cyclooxygenases may have little participation in peripheral skin thermal nociception in non-inflamed condition, although cyclooxygenase-2 could be responsible for the hyperalgesia during inflammation induced by lipopolysaccharide.

Clinical characteristics of perioperative coronary spasm: reviews of 115 case reports in Japan.

PURPOSE: Factors affecting perioperative development of coronary spasm have not been elucidated. A number of case reports describing perioperative coronary spasm have appeared in Japanese anesthesia journals, mostly published in Japanese. The purpose of this study was to investigate the contributing factors affecting perioperative coronary artery spasm by reviewing the published articles. METHODS: Reports were identified by using Medline database (1968-1998) or by manually searching nonindexed Japanese journals. The clinical characteristics of perioperative coronary spasm were analyzed in 115 patients who developed coronary artery spasm during the perioperative period. RESULTS: The mean age of the patients was 64 +/- 9 years (range, 36 to 87 years). There were 97 men (84%) and 18 women (16%). Preoperative risk factors included hypertension (27%), angina pectoris (27%), cigarette smoking (13%), and diabetes mellitus (11%). The attack was related to inadequate depth of general anesthesia (23%), use of vasopressors (22%), vagal reflex (19%), administration of drugs other than vasopressors (17%), and epidural block (15%). About 85% of patients showed no ischemic abnormality on the preoperative electrocardiogram, whereas 56% had significant coronary stenosis on postoperative coronary arteriography. Coronary spasm tended to occur in patients under inhalation anesthesia combined with epidural block. Nitrates alleviated the episode in the majority of cases, whereas defibrillation and cardiac massage were required in 19% of patients. No deaths were reported. CONCLUSION: Perioperative coronary spasm is prevalent in elderly male patients with coronary risk factors who undergo abdominal or thoracic surgery under inhalational anesthesia combined with epidural anesthesia. Instability of the autonomic nervous system and/or vascular hyperreactivity may be the underlying pathogenic mechanisms of perioperative coronary spasm.

Effects of substance P and calcitonin gene-related peptide on axonal transport in isolated and cultured adult mouse dorsal root ganglion neurons.

Substance P and calcitonin gene-related peptide (CGRP) released from primary sensory neurons are known to play important roles in nociception and nociceptive transmission. In the present study, we attempted to clarify the roles of these neuropeptides in the regulation of axonal transport in sensory neurons. Cells were isolated from adult mouse dorsal root ganglia and cultured in F-12 medium containing fetal bovine serum for 48 h until their neurites were grown. These isolated and cultured DRG cells were mostly (>98%) small (diameter <25 microm) and medium (diameter, 25-40 microm) in size, and were immunoreactive for substance P and CGRP (85.9 and 66. 0% of total cells, respectively). Video-enhanced microscopy was applied to observe particles transported within neurites. Application of substance P (100 nM) decreased the number of particles transported in both anterograde and retrograde directions in each of DRG neurons tested (n=5). The instantaneous velocities of individual particles transported in anterograde and retrograde directions were also reduced by substance P. In contrast, alpha-CGRP (100 nM) increased the number of particles transported in both directions in each of DRG neurons tested (n=5), and also increased the instantaneous velocities of particles transported bidirectionally. Application of beta-CGRP (100-1000 nM) did not elicit any effect on axonal transport. Therefore, axonal transport in sensory neurons seems to be modulated by substance P and alpha-CGRP, both of which can be derived from its own and adjacent sensory neurons.

Prostaglandin E(2) enhances axonal transport and neuritogenesis in cultured mouse dorsal root ganglion neurons.

The effects of prostaglandin E(2) on axonal transport in cultured mouse dorsal root ganglion neurons were investigated by analysing the number of axonally transported particles under video-enhanced microscopy. Application of prostaglandin E(2) increased the number of particles transported in anterograde and retrograde directions. The EP(2) prostaglandin receptor agonist butaprost mimicked the effect of prostaglandin E(2), but the EP(1)/EP(3) prostaglandin receptor agonist 17-phenyl trinor prostaglandin E(2) and the EP(3) prostaglandin receptor agonist M&B 28767 had no effect. The membrane-permeable cyclic AMP analogue dibutyryl cyclic AMP and the adenylate cyclase activator forskolin mimicked the effect of prostaglandin E(2). The protein kinase A inhibitor H-89 reversibly reduced the number of particles in both anterograde and retrograde directions. The effects of prostaglandin E(2) and dibutyryl cyclic AMP were blocked by H-89. Taken together with previous biochemical studies showing that prostaglandin E(2) increases cyclic AMP levels, the present results suggest that prostaglandin E(2) enhances axonal transport via the EP(2) receptor and cyclic AMP-dependent protein kinase A pathway. We further investigated the role of prostaglandin E(2) in neurite growth. Prostaglandin E(2) increased both the number of cells exhibiting neurites and the neurite growth rate, operating by a similar mechanism to stimulation of axonal transport. Prostaglandin E(2) may modulate axonal transport to supply materials for morphogenesis as well as other functions in sensory neurons.

Neurotoxicity of intrathecally administered tetracaine commences at the posterior roots near entry into the spinal cord.

BACKGROUND AND OBJECTIVES: Neurotoxicity of intrathecally administered local anesthetics is generating increased interest. This study was designed to examine the histopathologic effects of intrathecally administered tetracaine. METHODS: Sixty Wistar rats randomly received either 20%, 10%, 5%, 3%, 1%, 0.5%, or 0% tetracaine dissolved in 10% glucose solution or no solution via a chronically implanted intrathecal catheter. The spinal cord at L1, posterior and anterior roots and cauda equina were excised 5 days later, sectioned, processed, and prepared for light and electron microscopic examinations. RESULTS: Rats treated with tetracaine at 10% or 20% developed lesions in the posterior white matter and posterior roots. Rats injected with 3% or 5% tetracaine developed lesions, which began in the posterior roots close to the spinal cord and extended to the posterior white matter. The lesions were characterized by axonal degeneration. Injections of < or =1% of tetracaine did not cause any pathological changes. CONCLUSIONS: Our results suggest that the initial target of intrathecal tetracaine neurotoxicity may be the posterior roots at their entry into the spinal cord, where the axons are devoid of myelin sheath and thus representing a sensitive area for neurotoxic change.

Effect of epidural epinephrine infusion with bupivacaine on labor pain and mother-fetus outcome in humans.

BACKGROUND AND OBJECTIVES: Epinephrine is used with local anesthetics to prolong the duration of epidural analgesia and decrease the peak plasma concentrations of local anesthetics. In the practice of obstetric anesthesia, the utero-placental and fetal effects of epinephrine are controversial issues. We designed a prospective, randomized, and double-blind study to examine the effects of epinephrine infusion on the quality of analgesia and uterine or umbilical blood flows with Doppler ultrasound, as well as the duration of the first or the second stage of labor, and fetal outcome. METHODS: Twenty-eight parturients received continuous epidural bupivacaine 0.25% (4 mL/h) combined either with epinephrine (20 microg/h) (n = 13) or without epinephrine (n = 15) for analgesia during labor. If patients requested additional analgesia, an additional bolus of 1% or 1.5% lidocaine (6 to 10 mL) was administered. RESULTS: The total amount of additional lidocaine was greater in the plain bupivacaine group (130 [0, 280] mg; median [25th, 75th percentile] with P < .05) than in the epinephrine group (0 [0, 60] mg). Epinephrine infusion did not alter the resistance of the uterine and umbilical arteries as measured by resistance index. The duration of the first or second stages of labor did not significantly differ in the 2 groups. Epinephrine infusion did not change the fetal heart rate or the blood gas data in the umbilical artery. CONCLUSIONS: A low-dose epidural infusion of epinephrine decreased anesthetic requirements.

[Intrathecal 2% tetracaine causes mild histological lesions in the spinal cord without detectable sensory deficits on paw stimulation test in rats].

The purpose of this study is to determine if intrathecal 2% tetracaine (TC) causes histological changes by its neurotoxicity, and to examine the relationship between the lesions and neurological functions. Twenty-two rats received either 2% TC or 0% TC dissolved in 10% glucose, via an intrathecal catheter terminated at T 13 level. Neurological deficits were evaluated by rat's behavior and paw stimulation test (UCSF). Five days after drug administration, the L 1 spinal cord with the anterior and posterior roots and cauda equina were excised for light and electron microscopy. Four rats out of 8 in 2% TC group showed mild pathological changes induced by neurotoxicity mainly in the posterior roots and slightly in the posterior column. However, there were no significant differences in sensory and behavioral function between the rats who had received 2% TC with lesion and the others with no lesion. As many rootlets enter one segment of the spinal cord, mild and restricted lesions may be difficult to detect by sensory tests. These findings may explain the fact that the patients with transient neurologic symptoms (TNS) are normal by neurological tests.

Changes in left ventricular end-diastolic area, end-systolic wall stress, and fractional area change during anesthetic induction with propofol or thiamylal.

PURPOSE: To elucidate the mechanisms of the more profound hypotensive effects of propofol relative to thiamylal, we monitored changes in left ventricular (LV) preload, afterload, and contractility during the course of anesthetic induction with propofol and thiamylal. METHODS: Thirty-two patients (ASA I) were randomly assigned into two groups and injected with propofol (2 mg.kg(-1)) or thiamylal (4 mg.kg(-1)) as anesthetic induction agents. Transthoracic echocardiography (TTE) was used to assess LV performance before and during induction by the two anesthetics. The LV end-diastolic area (EDA) and LV end-systolic wall stress (ESWS) were used as indices of LV preload and LV afterload, respectively, while LV contractility was assessed by the fractional area change (FAC). RESULTS: Both propofol and thiamylal significantly reduced EDA and ESWS without significant change in FAC. Propofol-induced reductions in EDA and ESWS were significantly greater than those of thiamylal. CONCLUSION: The more profound hypotension observed during induction of anesthesia with propofol is due to the greater decrease in preload and afterload than with thiamylal, but not to a decrease in LV contractility.

Saline volume and local anesthetic concentration modify the spread of epidural anesthesia.

PURPOSE: To examine the effects of the volume of saline and the concentration of local anesthetic on the quality of anesthetic level. METHODS: One hundred and fifty two patients received thoracic epidural anesthesia were allocated into two groups; mepivacaine 1% (75 patients) and 1.5% (77 patients). Each group was randomly divided into three subgroups depending on epidural saline volumes of 1 ml, 5 ml, or 10 ml. Fifteen minutes after the injection of 10 ml mepivacaine, the dermatome levels of hypesthesia to cold and pinprick were determined by an individual blinded to the saline volume. RESULTS: The number of spinal segments with hypesthesia to cold in the three subgroups in the mepivacaine 1% group were 12.5 [6-20], 13 [8.5-20.5] and 12.5 [6.5-22], respectively (median [range]). The segments in the mepivacaine 1.5% group were 12 [7-18.5], 14 [8.5-19]* and 15 [6-23]*, respectively (*P < 0.05 vs 1-ml group). The number of spinal segments with hypesthesia for pinprick in the three subgroups in the 1% mepivacaine group were 10.5 [2-22], 10.5 [4-17] and 11 [4-19], respectively. The segments in the mepivacaine 1.5% group were 12 [7.5-16], 12 [7.5-17] and 11.5 [5-22.5], respectively. Saline volume did not alter the anesthetic level of the mepivacaine 1%, although it did affect the anesthetic spread of the mepivacaine 1.5%. In both groups, a differential nerve block was elicited in the 5 ml and 10 ml saline subgroups. CONCLUSION: When a large volume of saline is administered prior to local anesthetic, more differential blockade and a greater extent of anesthesia may be elicited.