Splenic artery steal syndrome in living donor liver transplantation: a case report.

Splenic artery steal syndrome (SASS) has only recently been recognized as a potential threat to transplanted livers. We report a case of SASS with progressive liver dysfunction that developed after living donor right lobe liver transplantation. SASS suspected by serial pre- and postoperative computed tomographic (CT) scans was diagnosed by celiac trunk angiography. It was successfully salvaged by splenic artery embolization. In this case, serial examinations of CT scans were useful to diagnose SASS. This case showed that portal hyperperfusion injury is a cause of liver graft dysfunction in SASS. The splenic artery embolization technique is a safe procedure that can be applied to treat such injury.

A study on thapsigargin-induced calcium ion and cation influx pathways in vascular endothelial cells.

To investigate Ca2+/cation entry pathway in vascular endothelial cells, we examined the effects of thapsigargin on [Ca2+]i and Mn2+ entry in cultured porcine aortic endothelial cells. Thapsigargin inhibits the activity of endoplasmic reticulum (ER, intracellular Ca2+ pool) Ca(2+)-ATPase, and stimulates Ca2+ entry from extracellular space by depleting intracellular Ca2+ pool. Cultured endothelial cells were loaded with fura-2/AM, and [Ca2+]i was measured by the ratios of fluorescence at 340/380 nm excitation, and Mn2+ entry was observed by the quenching of fluorescence at 360 nm excitation. Thapsigargin elevated [Ca2+]i in a time- and dose-dependent manner. The increase in [Ca2+]i caused by thapsigargin was lowered in Ca(2+)-free solution containing 3 mM EGTA. Verapamil (10(-5) M) and equimolar replacement of extracellular NaCl by LiCl had no effects on the maximum elevation of [Ca2+]i by thapsigargin. The increase in [Ca2+]i by thapsigargin was significantly inhibited by either NiCl2 (10(-3) M) or membrane depolarization using 50 mM KCl. Thapsigargin stimulated Mn2+ entry concomitantly with the increase in [Ca2+]i. Mn2+ entry was augmented in Ca(2+)-free solution. These results suggested that (1) the increase in [Ca2+]i by thapsigargin consisted of both Ca2+ release from ER and Ca2+ entry from extracellular space, and (2) thapsigargin also stimulated Mn2+ entry, which was interfered with in the presence of extracellular Ca2+.

Effects of thyroid hormone on the sorbitol pathway in streptozotocin-induced diabetic rats.

Sorbitol accumulation plays an important role in diabetic complications involving the kidney, nerves, retina, lens and cardiac muscle. To investigate the influence of thyroid hormone on the sorbitol pathway, we studied the effects of thyroid hormone on polyol metabolism in normal and diabetic rats. Rats were divided into three groups: controls, streptozotocin (STZ)-induced diabetic euthyroid rats (DM) and STZ-induced diabetic hyperthyroid (thyroxine-injected) rats (DM+HT). The sorbitol (Sor) concentrations in the kidney, liver and sciatic nerve (2.53+/-0.74, 0.97+/-0.16 and 24.0+/-5.1 nmol/mg protein, respectively) of the DM rats were significantly higher than those (1.48+/-0.31, 0.58+/-0.13 and 3. 1+/-0.6 nmol/mg protein) of the control rats. The Sor concentrations in the kidney and sciatic nerve of the DM+HT rats (1.26+/-0.29 and 9. 40+/-1.2 nmol/mg protein) were significantly lower than those in the DM rats. These values were reduced in the liver, unchanged in the kidney, and increased in the sciatic nerve from the hyperthyroid rats without diabetes. Thyroid hormone reduced the aldose reductase (AR) activities in the kidney, liver and sciatic nerve of the DM rats, and similarly reduced AR in the kidney and liver, but not in the sciatic nerve, of the non-diabetic rats. The sorbitol dehydrogenase (SDH) activities were decreased by thyroid hormone in the kidney and liver but not the sciatic nerve of DM rats. In the non-diabetic rats, this enzyme activity was decreased in liver, but not in kidney or sciatic nerve. A positive correlation between the Sor concentration and AR activity was observed in the kidney and liver but not in the sciatic nerve from control, DM and DM+HT rats. A negative correlation was observed between the Sor concentration and SDH activities in the same organs. These data suggest that thyroid hormone affects the sorbitol pathway, but the detailed mechanism whereby this hormone reduces the sorbitol content (especially in diabetic rats) remains to be clarified.

Lipid peroxidation levels in rat cardiac muscle are affected by age and thyroid status.

Free radicals, hydroxyperoxides and H(2)O(2) are all known to damage cell components. This study was designed to compare the concentrations of hydroxyperoxide and free radical scavengers in the cardiac muscles of old rats in the hyper- or hypothyroid condition, to determine whether rates of peroxidation would differ with age, thyroid status, or both. Rats were rendered hyper- or hypothyroid by administration of l-thyroxine or methimazole for 4 weeks. Among the old rats, the lipid peroxide (LPO) concentrations, measured as thiobarbituric acid (TBA) reactants, were significantly greater in the hyperthyroid than in the euthyroid state and the LPO concentrations measured as TBA+Fe(3+) reactants, which may be precursors of LPO, were significantly greater in the hyperthyroid state, whereas in young rats, the LPO concentrations measured by TBA or TBA+Fe(3+) methods did not differ significantly in the hyperthyroid state. In the euthyroid state, the concentration of LPO measured as TBA+Fe(3+) reactants was significantly reduced with age. Xanthine oxidase (XOD) activity also was markedly increased with age, being more pronounced in the hyperthyroid than in the euthyroid state. The Mn and Cu/Zn superoxide dismutase activities were greater in the hyperthyroid than in the euthyroid state. Glutathione peroxidase activity decreased with age in the euthyroid and, particularly, in the hyperthyroid state. Catalase activity was not affected in the old rats. Concentrations of alpha-tocopherol in the old rats were high in the hyperthyroid state and low in the hypothyroid state, whereas the levels of beta- and gamma-tocopherols in these rats were unchanged in both conditions as compared with the euthyroid state findings. Data suggest that the site of free radical generation differs in older rats, with additional shifts in the location of intracellular lipid peroxidation being noted during hyperthyroidism. Thus, as rats age, the reduction of the free radical scavenger system and the increase in LPO and XOD activities might induce myocardial dysfunction.

Glucose transporter 2 concentrations in hyper- and hypothyroid rat livers.

The deterioration of glucose metabolism frequently observed in hyperthyroidism may be due in part to increased gluconeogenesis in the liver and glucose efflux through hepatocyte plasma membranes. Glucose transporter 2 (GLUT 2), a facilitative glucose transporter localized to the liver and pancreas, may play a role in this distorted glucose metabolism. We examined changes in the levels of GLUT 2 in livers from rats with l-thyroxine-induced hyperthyroidism or methimazole-induced hypothyroidism by using Western blotting to detect GLUT 2. An oral glucose tolerance test revealed an oxyhyperglycemic curve (impaired glucose tolerance) in hyperthyroid rats (n=7) and a flattened curve in hypothyroid rats (n=7). GLUT 2 levels in hepatocyte plasma membranes were significantly increased in hyperthyroid rats and were not decreased in hypothyroid rats compared with euthyroid rats. The same results were obtained with a densitometric assay. These findings suggest that changes in the liver GLUT 2 concentration may contribute to abnormal glucose metabolism in thyroid disorders.

Polymorphisms of the insulin gene among Japanese subjects.

We have sequenced the insulin gene in 72 unrelated Japanese subjects (52 with type 2 diabetes mellitus and 20 with normal glucose tolerance). We identified 6 mutations and all were found at a low frequency (1% to 4%). Three mutations were new. These included a C-to-G substitution in the promoter region, a G-to-A substitution in codon-2 resulting in an Ala-to-Thr replacement in amino acid -2 of the signal peptide, and a G-to-A substitution in intron 2. We have no evidence that any of the mutations that we found are the cause of diabetes. Thus, mutations in the insulin gene do not appear to be an important genetic factor contributing to the development of diabetes in this population.

Tricuspid valve closure for neonatal Ebstein's anomaly.

A respirator-dependent 11-day-old boy with Ebstein's anomaly is presented. His cardiac anomaly with progressive cardiomegaly was first noticed at 24 weeks' gestation on fetal echocardiography. After birth, he required mechanical ventilation because of massive tricuspid regurgitation and restricted pulmonary blood flow. The operation of tricuspid valve patch closure, resection of right atrial wall, and central shunt successfully weaned him from the respirator on postoperative day 13. Cavopulmonary anastomosis was performed without problem when the patient was 8 months of age.

The therapeutic effect of lipo PGE1 on diabetic neuropathy-changes in endothelin and various angiopathic factors.

A high blood concentration of endothelin (ET)-1 may participate in the onset and progress of diabetic microangiopathy, resulting in neuropathy. We examined the therapeutic effects of prostaglandin E1 (PGE1), which possesses both a peripheral vasodilating action and inhibition of platelet aggregation, on diabetic microangiopathy. Increases in both skin temperature and peripheral never conduction velocity in diabetic patients were recorded four weeks after Lipo PGE1 administration. A quantitative decrease in urinary albumin concentration was also observed, suggesting its efficacy of action was on diabetic nephropathy. Lipo PGE1 administration reduced the elevated circulating plasma ET-1 levels in the diabetic patients. As an increase in ET-1 concentrations is thought to correlate with the onset and progress of diabetic microangiopathy, the reduction of plasma ET-1 concentration by Lipo PGE1 administration may be one reason for the improvement in diabetic neuropathy and nephropathy.

Effects of thyroid hormone on catecholamine and its metabolite concentrations in rat cardiac muscle and cerebral cortex.

Clinical and experimental data suggest that thyroid hormone affects the actions of catecholamine (CA). However, the serum or tissue levels of CA during thyroid disorders have not been well defined. Accordingly, we investigated the levels of CA and their metabolites in the cardiac muscle, the cerebral cortex, and the plasma of rats with hyperthyroidism and hypothyroidism versus euthyroid animals. The Neurochem analyzer system (ESA, Inc., Bedford, MA) was used in such determinations. The cardiac muscles of hyperthyroid rats exhibited a 16% decrease in the levels of 1-dopa, 3-methoxytyramine (3-MT) and homovanillic acid (HVA) as compared with those in euthyroid rats. The levels of norepinephrine (NE) in cardiac muscle of these rats increased significantly (5.2-fold) relative to the levels in euthyroid rats. NE was undetectable in the cardiac muscles of the hypothyroid rats. Epinephrine (E) and dopamine (DA) were not detected in the cardiac muscles of the rats with either thyroid disorder. Levels of E and 3,4-dihydroxymandelic acid (DOPEG) were detected only in the cerebral cortex of hyperthyroid rats. The cerebral cortex levels of 3-methyoxytyramine (3-MT), 3,4-dihydroxyphenylacetic acid (DOPAC), metanephrine (MN), and homovanillic acid (HVA) were all significantly increased in the hyperthyroid versus the euthyroid rats. The cerebral cortex levels of DA, NE, normetanephrine (NMN), and VMA in the hyperthyroid rats all showed a significant decrease. Levels of NE, NMN, and DOPAC in the cerebral cortex increased significantly in the hypothyroid rats. The level of VMA was undetectable in cerebral cortex of such animals. Data from studies on cardiac muscle and cerebral cortex indicate that the changes in CA and CA metabolites are responsible in part for the cardiovascular and the central nervous system symptoms observed in hyperthyroidism and hypothyroidism.

Effects of mean and swing pressures on piston-type high-frequency oscillatory ventilation in rabbits with and without acute lung injury.

To determine whether low mean airway pressure (MAP) and/or stroke volume (SV) settings cause lung injury during piston-type high-frequency oscillatory ventilation (HFOV), we investigated the influence of various combinations of MAP and SV on the amplitude of the pressure swing at four different sites in the normal lung of rabbits. We also examined the effects of these factors on progression of lung injury in lavaged surfactant-deficient lungs. We measured changes in the mean pressure (MP) and swing pressure (SP) during HFOV at MAPs ranging between 5-30 cm H2O in combination with SVs ranging from 5-30 mL in 13 rabbits at four different sites: 1) the proximal airway, 2) the distal end of the endotracheal tube, 3) the bronchi, and 4) the pleural space. Lung lavage was performed in 8 rabbits and differences in MP and SP between normal and surfactant-deficient rabbits were investigated. In the remaining 5 rabbits, lungs were lavaged and subjected to two trials of sustained inflation to 30 cm H2O for 15 s to reverse atelectasis, and the resulting SP was measured. In normal lungs, SP increased at the bronchial and pleural sites as MAP was increased. Alterations in SV did not affect MP in normal or lavaged lungs. In the lavages, surfactant-deficient lungs at MAPs < or = 15 cm H2O, there were significant increases in SP at the distal end of the endotracheal tube and the bronchial sites. SP decreased to the prelavaged level following sustained inflation to 30 cm H2O for 15 s. We conclude that low MAP settings are insufficient to open alveoli in the low-compliance lung and allow for development of atelectasis rather than air trapping. SP was markedly increased in the presence of atelectasis, possibly leading to excessive expansion of the airway. In the clinical setting, such overexpansion of the distal airways may contribute to lung injury. Our findings suggest that physicians should use caution in reducing MAP during piston-type HFOV until lung compliance has normalized, especially in infants with respiratory distress syndrome.

Changes in superoxide dismutase activities and concentrations and myeloperoxidase activities in leukocytes from patients with diabetes mellitus.

To investigate whether the two free-radical scavengers, Cu, Zn- and Mn-superoxide dismutase (SOD), are changed in leukocytes of diabetic patients, and the alteration of these enzymes correlates with the diabetic state, we measured the activity and concentration of these enzymes in leukocytes from diabetic patients. Both Cu, Zn-SOD and Mn-SOD activities in neutrophils and lymphocytes were significantly lower in patients with non-insulin-dependent diabetes mellitus than in healthy controls. The concentrations of these enzymes in leukocytes from diabetic patients, however, did not differ from those in controls. Cu, Zn-SOD and Mn-SOD activities in neutrophils inversely correlated with HbA(1c) concentrations. Myeloperoxidase activity in leukocytes was significantly reduced in NIDDM patients. These findings suggest that changes in these enzymes may affect the susceptibility to infection and immunocompetence of patients with diabetes.

Two cases of protruding atherosclerotic plaque with mobile projections in the aortic arch.

We recently studied two patients with cerebral embolism, in whom transesophageal echocardiography revealed protruding atherosclerotic plaques with freely mobile projections in the aortic arch. Ultrasonic imaging showed that the carotid artery was normal, and transthoracic and transesophageal echocardiography did not reveal a cardiac embolic source in either case. In one patient, we observed that an atherosclerotic plaque became ulcerated and developed mobile projections over the course of a year. More consideration should be given to the thoracic aorta as a source of embolism in patients with unexplained stroke.

A three-dimensional laminated paper model of the scaphoid from computed tomography.

PURPOSE: To describe a method of producing a life-sized three-dimensional (3D) solid model of a scaphoid bone by combining multidetector-row computed tomography (MDCT) volume data and rapid prototyping technique using thin paper as material, and to evaluate the dimensional accuracy of the experimental model. MATERIAL AND METHODS: We experimentally produced life-sized 3D solid models of 14 cadavers' scaphoid bones using high-resolution MDCT volume data, and evaluated the dimensional accuracy of the 3D solid models. RESULTS: The 3D solid model was almost perfectly produced in both size and shape (length, height, width, dorsal cortical angle, and landmarks of the scaphoid bone) compared to the real cadaver's scaphoid bone. In addition to accuracy, the cost and time for creating the model might be reasonable. CONCLUSION: This technique may be useful in assisting repair of scaphoid bone fracture.

Endovascular therapy for massive haemothorax caused by ruptured extracranial vertebral artery aneurysm with neurofibromatosis Type 1.

Extracranial vertebral artery aneurysm is uncommon, and the common cause is penetrating trauma. Rupture of extracranial vertebral artery aneurysm into the thoracic cavity is extremely rare and fatal due to haemorrhagic shock by massive haemothorax. We report an intrathoracic rupture of the extracranial vertebral artery aneurysm with neurofibromatosis Type 1, successfully treated by coil and liquid embolisation.

Endovascular therapy for abdominal pseudoaneurysms: analysis from technical and clinical aspects.

PURPOSE: To clarify the factors of outcomes by endovascular therapy for abdominal pseudoaneurysm (PSA) from both technical and clinical aspects. MATERIAL AND METHODS: Sixteen patients with PSAs underwent embolization. Embolic methods were classified into two groups: proximal and distal embolization (PDE) and proximal embolization alone (PE). The patients were classified into four groups by shock index. Pre-embolization hemoglobin (Hb) level and decrease in Hb level were evaluated. Outcomes were classified into two groups: successful recovery and failure despite successful PSA embolization. RESULTS: There were no statistical differences in success, recurrence, and complication rate, and outcomes between the two embolic methods. There was a statistically significant correlation between the grades of shock indices and outcomes (P<0.05). There was no statistical difference between the Hb levels and outcomes. CONCLUSION: Outcomes were not dependent on the embolic methods. Shock index reflecting clinical status may be a simple predictor of outcome. PSA should therefore be treated by optimal embolic methods as quickly as possible to avoid rupture.