Orthotopic, but reversed implantation of the liver allograft in situs inversus totalis-a simple new approach to a difficult problem.

Situs inversus totalis is a rare congenital anomaly in which the heart and abdominal organs are oriented in a mirror image of normal. It provides a unique challenge as there is no established technique for liver transplantation in these patients. Employing two major alterations from our standard technique, a liver was transplanted in the left subphrenic space of a patient with situs inversus totalis. First, the liver was flipped 180 degrees from right to left (facing backward). Second, a reversed cavaplasty (anterior, not posterior, donor suprahepatic caval incision) was performed. Otherwise, it was standard, with end-to-end anastomoses of the portal vein, hepatic artery and bile duct. Three years after the entirely uneventful transplant, the recipient continues to enjoy the benefits of a normally functioning liver. The described technique prevented torsion, kinking and tension on the anastomosed structures by allowing the liver to sit naturally in an anatomical position in the left hepatic fossa. As it required no special measurements or maneuvers, the technique was easy to execute and required no donor liver size restrictions. This novel technique, with a reversed cavaplasty and a 180 degrees right-to-left flip of the liver into a left-sided hepatic fossa, may be ideal for situs inversus totalis.

Ultrasound guidance compared with electrical neurostimulation for peripheral nerve block: a systematic review and meta-analysis of randomized controlled trials.

BACKGROUND: Despite the growing interest in the use of ultrasound (US) imaging to guide performance of regional anaesthetic procedures such as peripheral nerve blocks, controversy still exists as to whether US is superior to previously developed nerve localization techniques such as the use of a peripheral nerve stimulator (PNS). We sought to clarify this issue by performing a systematic review and meta-analysis of all randomized controlled trials that have compared these two methods of nerve localization. METHODS: We searched Ovid MEDLINE, the Cochrane Central Register of Controlled Trials, and Google Scholar databases and also the reference lists of relevant publications for eligible studies. A total of 13 studies met our criteria and were included for analysis. Studies were rated for methodological quality by two reviewers. Data from these studies were abstracted and synthesized using a meta-analysis. RESULTS: Blocks performed using US guidance were more likely to be successful [risk ratio (RR) for block failure 0.41, 95% confidence interval (CI) 0.26-0.66, P<0.001], took less time to perform (mean 1 min less to perform with US, 95% CI 0.4-1.7 min, P=0.003), had faster onset (29% shorter onset time, 95% CI 45-12%, P=0.001), and had longer duration (mean difference 25% longer, 95% CI 12-38%, P<0.001) than those performed with PNS guidance. US guidance also decreased the risk of vascular puncture during block performance (RR 0.16, 95% CI 0.05-0.47, P=0.001). CONCLUSIONS: US improves efficacy of peripheral nerve block compared with techniques that utilize PNS for nerve localization. Larger studies are needed to determine whether or not the use of US can decrease the number of complications such as nerve injury or systemic local anaesthetic toxicity.

Amrinone for refractory cardiogenic shock following chloroquine poisoning.

Cardiac arrhythmias and circulatory collapse account for the high mortality reported after severe chloroquine poisoning. We have recently observed a 17-year-old man who ingested an 8 g chloroquine overdose. Cardiac arrest occurred within 1 h. Cardiogenic shock was refractory to epinephrine, dopamine and molar sodium lactate. Amrinone, a bipyridine analog, was then successfully used to improve haemodynamic conditions.

Halothane alters electrical activity and calcium dynamics in cultured mouse cortical, spinal cord, and dorsal root ganglion neurons.

Halothane inhibits neural plasma membrane Ca(2+)-ATPase, a pump that ejects Ca2+ from the cell after influx through voltage- or ligand-activated channels. Intracellular microelectrode recordings in mouse embryonic cortical and spinal cord neurons showed that halothane and eosin, a pump inhibitor, prolonged repolarization associated with spontaneous bursts of depolarization. These agents also prolonged the repolarization phases of electrically induced action potentials and of capsaicin-mediated Ca(2+)-dependent depolarization in mouse adult dorsal root ganglion neurons. In keeping with these findings, confocal microfluorimetry showed that halothane delayed clearance of intracellular Ca2+ accumulated by N-methyl-D-aspartate stimulation of single neurons.

Nitrous oxide and xenon enhance phospholipid-N-methylation in rat brain synaptic plasma membranes.

Halothane and isoflurane increase the rate of phospholipid methylation (PLM) in rat brain synaptosomal membranes, a process linked to the coupling of neuronal excitation to neurotransmitter release. In contrast, synaptic plasma membrane (SPM) Ca2+ ATPase (PMCA) pumping is reduced by exposure to halothane, isoflurane, xenon and nitrous oxide (N2O). To examine further the relationship between PLM, PMCA and anesthetic action, we investigated the effect of clinically relevant concentrations of two less potent anesthetic gases, N2O and xenon, on PLM in SPM. Biochemical assays were performed on SPM exposed to 1.3 MAC of N2O (2 atm), 1.3 MAC of xenon (1.23 atm) or an equivalent pressure of helium for control. N2O or xenon exposure increased PLM to 115% or 113%, respectively, of helium control (p < 0.02). Similar exposures to N2O or xenon depressed PMCA activity to 78% and 85% of control (p < 0.05). Observations that PLM and PMCA are both altered by a wide variety of inhalation anesthetic agents at clinically relevant partial pressures lend support to a possible involvement and interaction of these processes in anesthetic action.

Diminished brain synaptic plasma membrane Ca(2+)-ATPase activity in spontaneously hypertensive rats: association with reduced anesthetic requirements.

We have recently reported that plasma membrane Ca(2+)-ATPase (PMCA) pumping activity in rat brain synaptic plasma membranes (SPM) was reduced by in vitro or prior in vivo exposure to inhalation anesthetics (IA). In addition, rats with streptozocin-induced diabetes were found to have diminished brain synaptic PMCA pumping and a decrease in the partial pressures of several IA required to prevent movement in response to stimulation, defined as the minimum effective dose or MED. Diminished PMCA activity in erythrocytes of spontaneously hypertensive rats (SHR) has been noted. Because PMCA is ubiquitous, it seemed possible that PMCA pumping might be decreased in the brain of SHR and perhaps associated with decreased IA requirement. Eighteen SHR and 18 control, normotensive Wistar-Kyoto rats (WKY) were studied. PMCA activity was assessed by measurement of Ca2+ uptake into synaptic plasma membrane vesicles prepared from cerebrum and diencephalon-mesencephalon (D-M) in WKY and SHR. Ca2+ pumping was significantly less in SHR than in WKY, 85% of control in the cerebrum and 90% in the D-M (p < 0.01). The MEDs for halothane, isoflurane and desflurane were also lower in SHR than in WKY, 91%, 90% and 89%, respectively, of control (p < 0.05). Thus, an animal model of primary hypertension (SHR) manifested diminished brain synaptic PMCA activity and reduced MED for several volatile anesthetics. These findings provide further evidence for a role for PMCA in anesthetic action.

Lack of effect of flurothyl, a non-anesthetic fluorinated ether, on rat brain synaptic plasma membrane calcium-ATPase.

Plasma membrane Ca2+-ATPase (PMCA), a regulator of intracellular calcium, is inhibited by volatile anesthetics and by xenon and nitrous oxide. Response of a cellular system to anesthetics, particularly to volatile agents, raises the question of non-specific, even toxic, side effects unrelated to anesthetic action. Compounds with chemical and physical properties similar to halogenated anesthetics, but which lack anesthetic effect, have been used to address this question. We have compared the effects of halothane and flurothyl, a non-anesthetic fluorinated ether, on PMCA Ca2+ transport across isolated brain synaptic plasma membranes (SPM). Flurothyl, at concentrations predicted by the Meyer-Overton curve to range from 0.4 to 2.6 MAC (minimum alveolar concentration), had no significant on PMCA activity. In contrast halothane, 1.3 MAC, reduced Ca2+ transport 30 to 40%. These findings provide further evidence for a specific effect of inhalation anesthetics on neuronal plasma membrane Ca2+-ATPase.

Inhibition of plasma membrane Ca(2+)-ATPase pump activity in cultured C6 glioma cells by halothane and xenon.

We have compared the effect of two inhalational anesthetics, halothane and xenon, on Ca(2+)-ATPase (PMCA) pumping activity in plasma membrane vesicles prepared from cultured rat C6 glioma cells. Halothane, at concentrations ranging from 0.5 to 1.75 vol% (equivalent to 0.5 to 1.6 MAC), significantly inhibited Ca2+ uptake (transport) by plasma membrane vesicles in a dose-related fashion. Xenon, at partial pressures ranging from 0.5 to 1.5 atm (equivalent to 0.5 to 1.6 MAC), similarly inhibited PMCA pumping activity. Additive effects on suppression of PMCA pump activity were observed when C6 cell plasma membrane vesicles were exposed to increasing partial pressures of xenon in the presence of halothane (1 vol%). Halothane also inhibited PMCA pumping in cells from two other lines of neural origin, B104 (rat neuroblastoma) and PC12 (rat pheochromocytoma). Studies described in this report support the thesis that PMCA in cells of neural origin is inhibited by quite different inhalational anesthetics at clinically relevant concentrations.

Diminished brain synaptic plasma membrane Ca(2+)-ATPase activity in rats with streptozocin-induced diabetes: association with reduced anesthetic requirements.

Recent evidence suggests that chronic hyperglycemia may inhibit plasma membrane Ca(2+)-ATPase (PMCA) in cells from several tissues. Inhalational anesthetics (IA) can inhibit brain synaptic PMCA activity. We proposed that diabetic rats may manifest chronic inhibition of brain synaptic PMCA and thus provide a model for testing the hypothesis that synaptic PMCA plays a key role in IA pharmacodynamics. Ca2+ pumping activity of PMCA was measured in cerebral synaptic plasma membrane (SPM) vesicles prepared from rats with streptozocin (STZ)-induced diabetes and from control, normoglycemic rats. Dose requirements for halothane and xenon were estimated in treated and untreated rats. Brain PMCA activity in hyperglycemic rats was depressed by about 8.4%, compared to controls. In vitro glycation also caused a significant decrease in PMCA pumping activity. Halothane requirement for STZ-hyperglycemic rats was dramatically reduced to about 65% of control. Xenon requirement was also significantly reduced, to 88% of control. Correlation of IA dose with percent glycated hemoglobin for each rat revealed a strong association between reduced requirements for halothane or xenon and increased protein glycation. These results indicate that inhibition of brain synaptic PMCA in chronically hyperglycemic rats is associated with a significant reduction in IA requirement.

Reduced anesthetic requirements in aged rats: association with altered brain synaptic plasma membrane Ca(2+)-ATPase pump and phospholipid methyltransferase I activities.

Aging is associated with a decrease in anesthetic requirements. Animal models of aging manifest alteration of brain Ca2+ homeostasis and increased methyltransferase I (PLMTI) activity. In this study we evaluated concurrently anesthetic requirements and brain plasma membrane Ca(2+)-ATPase (PMCA) and PLMTI activities in young and aged rats. Halothane, desflurane, isoflurane and xenon MEDs (lowest partial pressures that suppress a pain response) were measured in 2 and 25 month old, male Fisher-344 rats. Halothane MED was also measured in 2 and 30 month old F344/BNF1 rats, a strain that undergoes aging with less debilitation. PMCA pumping and PLMTI activities were measured in synaptic plasma membranes (SPM) prepared from the cortex and diencephalon-mesencephalon (DM). For aged Fisher-344 rats, MEDs for halothane, desflurane, isoflurane and xenon were reduced to 81%, 82%, 67% and 86%, respectively, of young controls; PMCA activity was diminished to 91% in cortical SPM and 82% in DM SPM; and cortical and DM PLMTI activities were increased to 131% and 114% of young control. For F344/BNF1 rats, MED for halothane was reduced to 87%, PMCA activity was diminished to 90% in cortical SPM and 72% DM SPM, and PLMTI activity was increased to 133% in cortical SPM and 112% in DM SPM. The strong association between age and reduced anesthetic requirements for inhalational agents on the one hand and altered PMCA and PLMTI activity on the other lends support to the underlying hypothesis that PMCA and PLMTI may be involved in the production of the anesthetic state.

Reduced anesthetic requirements, diminished brain plasma membrane Ca(2+)-ATPase pumping, and enhanced brain synaptic plasma membrane phospholipid methylation in diabetic rats: effects of insulin.

We have recently reported that streptozocin (STZ)-induced diabetes in rats was associated with i) reduced Ca2+ pumping by rat brain synaptic plasma membrane Ca(2+)-ATPase (PMCA) and ii) a substantial reduction in the partial pressures of halothane and xenon required to prevent movement in response to stimulation (minimum effective dose or MED). MED for both agents correlated well with the degree of hemoglobin glycation and with PMCA activity. We now report that MEDs for isoflurane, enflurane, and desflurane were also substantially reduced in STZ-diabetic rats, compared with placebo-injected controls. In addition, we examined the effect of insulin treatment, begun 2 weeks after induction of diabetes and continued for 3 more weeks, on isoflurane MED and on brain synaptic PMCA and phospholipid-N-methyltransferase I (PLMT I), another enzyme altered by inhalation anesthetics (IA). Partial treatment of diabetes, as indicated by decreased glycated hemoglobin (GHb) compared to untreated diabetic rats, was associated with an isoflurane MED of 1.05 vol%, intermediate between a control mean of 1.57 vol% and an untreated diabetic mean of 0.82 vol% (p < 0.01), with a trend toward normalization of both PMCA and PLMT I activity. We also examined isoflurane MED and PMCA activity in the cerebrum and diencephalon-mesencephalon (D-M) of control and diabetic rats 2 and 12 weeks after induction of diabetes. Isoflurane MED was substantially reduced in diabetic rats from both treatment periods. Cerebral and D-M PMCA activities were each reduced to about 90% of control values 2 weeks after STZ induction. At 12 weeks, cerebral PMCA pumping in SPM from diabetic rats did not differ from control values, but PMCA pumping in SPM from the D-M was reduced to about 85% of control levels. Good correlation (r = 0.89, p < 0.01) was found between isoflurane MED and GHb in all treatment groups. These findings provide further evidence for an important role for PMCA in IA action. They also suggest that anesthetic effects on the calcium pump at specific anatomic sites may be of major importance in producing anesthesia.

Increased anesthetic requirements for isoflurane, halothane, enflurane and desflurane in obese Zucker rats are associated with insulin-induced stimulation of plasma membrane Ca(2+)-ATPase.

A wide spectrum of structurally disparate inhalational anesthetics reduce brain synaptic plasma membrane Ca(2+)-ATPase (PMCA) activity, whereas phospholipid methyltransferase I (PLMTI) is enhanced by anesthetics. Several rat models with incidental or disease-induced reduction of PMCA and enhancement of PLMTI activities manifest increased sensitivity to inhalational anesthetics. Because insulin is known to stimulate PMCA, anesthetic requirements in hyperinsulinemic obese Zucker rats (fa/fa) and in normoinsulinemic lean Zucker heterozygotes (fa/+) were examined, and brain synaptic PMCA and PLMTI activities were determined in both genotypes. Significantly higher partial pressures of halothane, enflurane, isoflurane, and desflurane were required to inhibit the pain response in obese rats compared to lean Zucker rats. Dose dependent stimulation of PMCA pumping was observed in synaptic membranes from both types, but insulin concentrations in extracts of diencephalon-mesencephalon, cerebellum, and medulla (but not cortex) were higher in obese than in lean Zucker rats. Microdialysis of three subcortical regions showed marked increases in insulin levels with halothane exposure in obese rats, compared to lean controls. These observations in an anesthetic resistant rat model lend further support to the hypothesis that the calcium pump plays a functional role in production of the anesthetic state.

Construction of an Infant Neurological International Battery (Infanib) for the assessment of neurological integrity in infancy.

In this article, we describe the construction of an instrument for the assessment of the neurological integrity of infants. In a follow-up program for infants from the neonatal intensive care unit, 365 evaluations of 308 infants were made by using a 32-item battery with items from four methods. Factor analyses were used for data analyses, which yielded a 20-item instrument with five factors. We named the instrument the Infant Neurological International Battery (Infanib). The Infanib has sufficient reliability for clinical and research purposes. We have formed scoring sheets, which permit clinical use of the instrument. Cut points are recommended for the separation of infants with normal, transiently abnormal, and abnormal neurologic development. The quantified scoring system enables comparison of infants on item scores, subscores (factor scores), and total scores. It also permits entry of these scores in the computer so that more complex descriptions are possible of the relationship of the neurological assessment of infants both to earlier (eg, birth) and later variables (eg, cerebral palsy, cognitive function, and school performance).

Age changes on tests of fluid and crystallized ability for women and men on the Kaufman Adolescent and Adult Intelligence Test (KAIT) at ages 17-94 years.

Within a norm sample of 1,500 men and women, 17-94 years of age (13 age groupings), using Multivariate Analysis of Variance and Covariance, it was found that four measures designed to indicate fluid reasoning (Gf) and the composite measure of Gf declined steadily over the entire adulthood period, the decline accelerating during the period beginning at about age 55 years. Also, four measures of crystallized knowledge (Gc) and the composite measure of Gc increased through the 20s, neither increased nor decreased through mid-adulthood until about age 60 years, and declined thereafter. For the composite measures of Gf and Gc, there were no main effects or interaction effects associated with Gender. When educational attainment was covaried, small but statistically significant Gender main effects were found for four of the subtest measures of Gf and Gc; significant Gender x Age interaction effects were found for two subtests. Interpreted within Gf-Gc theory, the results replicate and extend evidence of the adulthood development of cognitive capabilities.

Phonetically inaccurate spelling among learning-disabled, head-injured, and nondisabled young adults.

We applied the Boder and Jarrico (1982, The Boder Test of Reading-Spelling Patterns, New York: Grune & Stratton) criteria to the WRAT spelling list and examined the phonetically inaccurate spelling error patterns of learning-disabled (LD), head-injured (HI), and nondisabled young adults. Phonetically inaccurate (PI) errors were reliably rated (interrater r = .94) and were correlated significantly more strongly with dysphasic errors (r = .33) than with dyscopia (r = .16). ANOVA showed that LD and HI, which did not differ, made significantly more PI errors than both nondisabled and HI. These results indicate that PI errors reflect an underlying language disorder. The results also suggest that PI errors are more frequent in brain-related disorders. Finally, when group differences in cognitive ability are statistically controlled, PI errors are more common only among LD persons.

A differential assessment model for alcoholism. The scales of the Alcohol Use Inventory.

The development and use of the Alcohol Use Inventory are discussed. The scales of the Inventory allow the measurement of multiple manifestations of alcohol problems.

Failure of short-term luminal IGF-I to protect against atrophy in a model of fetal esophageal atresia.

Short-term luminal infusion in utero (3 days) of insulin-like growth factor I (IGF-I) failed to protect the fetal small intestine against atrophy induced by ablation of swallowing. Human recombinant IGF-1 (or vehicle) was infused into the duodenum of fetal sheep at 125 days' gestation for 3 days (day 1, 0.025 mg; day 2, 0.25 mg: day 3, 2.5 mg). Fetal swallowing was prevented by esophageal ligation, and a carotid catheter was implanted for blood sampling. There were no changes in body growth of in major organ growth. Small intestinal (SI) weight (corrected for body weight) was significantly lower for IGF-I treated fetuses. Villus height decreased significantly in proximal regions. Villus enterocyte cellularity was reduced significantly in the proximal regions. The percentage of crypt cells labeled with a 4-hour pulse of tritiated thymidine (as assessed by autoradiography) decreased significantly in the proximal SI only, from 16.14% (1.06% SEM) to 13.28% (1.05% SEM) (P < .05). Plasma levels of IGF-1 increased in the treated fetuses by an average of 76%. IGF-1 immunoreactivity was detected in the apical endocytic complex of enterocytes from proximal SI. This study shows that wasting of fetal intestinal tissues in the absence of enteral input cannot be prevented by IGF-1 delivered luminally.

Polyuria during Guillain-Barré syndrome.

Severe Guillain-Barré syndrome (GBS) usually results in life-threatening autonomic disturbances requiring a close monitoring of the patient in an Intensive Care Unit. Besides dangerous cardiac manifestations, neuroendocrine changes are also reported and could induce electrolytes and fluid balance impairments. Polyuria has been observed in a severe case of GBS occurring in a 16-year-old boy. Consecutive blood samples were obtained for renin, aldosterone, antidiuretic hormone and atrial natriuretic factor measurements. Polyuria in GBS is multifactorial and would be partly due to a dysregulation of osmoreceptors.

Disturbed sleep and worries among learning disabled adolescents.

This study tested the clinical assumption that sleep problems reflect underlying emotional concerns. The hypothesis that worry-correlates of disturbed sleep for learning disabled adolescents would be related to their disability was borne out by findings of sleep problems associated with concerns about intellectual and academic adequacy. Other significant correlates suggested the effect of social anxiety which may be age-appropriate.