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Biomedical subjects

T Miyata

Publications and source records attributed to T Miyata.

At least 127 records · Page 7Linked to original sources
PubMed2000

Advanced glycation and lipidoxidation of the peritoneal membrane: respective roles of serum and peritoneal fluid reactive carbonyl compounds.

BACKGROUND: Advanced glycation of proteins has been incriminated in the progressive alteration of the peritoneal membrane during chronic peritoneal dialysis (PD). Advanced glycation end products (AGEs) result from a modification of proteins by reactive carbonyl compounds (RCOs). RCOs resulting from glucose breakdown are present in commercial PD fluid. They also accumulate in uremic plasma. The present study was undertaken to evaluate the respective contribution of these two sources of RCOs in the genesis of peritoneal AGEs. METHODS: Three major RCOs formed during heat sterilization of PD fluid, that is, glyoxal, methylglyoxal, and 3-deoxyglucosone, and total RCOs were measured in commercial PD fluid and in PD effluent. The generation of pentosidine, used as a surrogate marker for AGEs, during one-week incubations of PD fluid and effluent samples fortified with bovine serum albumin (BSA) was measured by high-performance liquid chromatography. Peritoneal samples were stained with antibodies specific for two AGEs derived from carbohydrate-dependent RCOs, Nepsilon-(carboxymethyl)lysine (CML) and pentosidine, or for two advanced lipoxidation end products (ALEs) derived from lipid-dependent RCOs, malondialdehyde (MDA)-lysine and 4-hydroxynonenal (HNE)-protein adduct. RESULTS: Glyoxal, methylglyoxal, and 3-deoxyglucosone were identified in commercial PD fluid. Their levels in PD effluents decreased with dwell time probably by diffusion into blood circulation. In contrast, the levels of total RCOs were initially low in commercial PD fluid, increased in PD effluent with dwell time probably by diffusion from circulation into the peritoneal cavity, and after 12 hours, reached values observed in uremic serum. The relevance of the rise in total RCOs for AGE formation is demonstrated by a parallel increase in the generation of pentosidine during incubations of PD effluents. In contrast with RCOs present in glucose-rich PD fluid, RCOs diffusing from uremic circulation originate from both carbohydrates and lipids. Their role in the modification of peritoneal proteins is demonstrated by the immunohistochemical study of peritoneal tissue. Two AGEs and two ALEs increase in parallel in the mesothelial layers and in vascular wall of small arteries in the peritoneum. CONCLUSIONS: Protein modification of the peritoneum is determined not only by RCOs originating in PD fluid, but also by RCOs originating from the uremic circulation. The present data might be relevant to current attempts to improve PD fluid toxicity by lowering its glucose content.

Adult↗
PubMed2000

Effect of dwell time on carbonyl stress using icodextrin and amino acid peritoneal dialysis fluids.

BACKGROUND: Deterioration of the peritoneal membrane limits the technical survival of peritoneal dialysis (PD). Advanced glycation of the membrane has been incriminated in this evolution. Advanced glycation end products (AGEs) develop under the influence of glucose and of its degradation products, mainly reactive carbonyl compounds (RCOs) such as glyoxal (GO), methylglyoxal (MGO), and 3-deoxyglucosone (3-DG). The present study was undertaken to evaluate the impact of recently developed glucose-free PD fluids on AGE generation. METHODS: Recently developed glucose-free PD fluids containing either icodextrin or amino acids were investigated. GO, MGO, and 3-DG [high-performance liquid chromatography (HPLC)] and total RCOs (spectrophotometry) were measured in fresh solutions and in effluents after various dwell duration. The AGE formation potential of PD fluids and effluents was assessed by incubation at 37 degrees C, for one week, with bovine serum albumin and by the eventual measurement of pentosidine (HPLC) and Nepsilon-carboxymethyllysine (CML; gas chromatography/mass spectrometry). RESULTS: GO, MGO, and 3-DG (P < 0. 001) as well as total RCOs levels (P < 0.01) were significantly lower in icodextrin and amino acid PD fluid than in commercial, heat-sterilized, 1.36% glucose PD fluid. Pentosidine and CML generation were also significantly lower (P < 0.001) in icodextrin and amino acid PD fluid than in conventional 1.36% glucose PD fluid. The levels of total RCOs, however, increased in icodextrin and amino acid PD fluid effluents with dwell time. AGE formation potential rose accordingly, as demonstrated by a parallel increase in the generation of pentosidine and CML during incubation of PD effluents. CONCLUSION: The present data demonstrate lower RCO contents and AGE formation potential in fresh icodextrin and amino acid PD fluids than in fresh heat-sterilized glucose PD fluids. However, this difference decreases progressively during dwell time, mainly as a result of the influx of total RCOs.

Aged↗
PubMed2000

Relevance of oxidative and carbonyl stress to long-term uremic complications.

Oxidative stress is a disturbance of balance between oxidants and antioxidant species. The existence of an increased oxidative stress in chronic renal failure is supported by evidence of increased lipid, carbohydrate, and protein oxidation products in plasma and cell membrane. Recent studies have implicated the oxidative stress in the nonenzymatic biochemistry leading to irreversible protein modifications. Reactive oxygen species may directly alter proteins with the eventual formation of oxidized amino acids. Alternatively, reactive carbonyl compounds formed by the oxidation of carbohydrates and lipids may indirectly lead to advanced glycation or lipoxidation of proteins. Chronic uremia is associated with increased modification of protein caused by reactive carbonyl compounds derived from both carbohydrates and lipids. Increased carbonyl modification of proteins subsequently results in the rise of plasma and tissue contents of advanced glycation end products and advanced lipoxidation end products, in which the deleterious biological effects have been revealed. This article focuses on the irreversible nonenzymatic modification of proteins, which might, at least in part, contribute to the development of complications associated with chronic renal failure and long-term dialysis, such as atherosclerosis and dialysis-related amyloidosis.

Amyloidosis↗
PubMed2000

Ten years' experience of aortic aneurysm associated with systemic lupus erythematosus.

BACKGROUND: aortic aneurysm is a rare but life-threatening cardiovascular complication in patients with systemic lupus erythematosus (SLE). The purpose of this study was to clarify the characteristic clinical features and the pathological mechanism of aneurysmal formation in these patients. METHODS: among 429 patients operated on for abdominal aortic aneurysm (AAA) during the past 10 years, five cases with SLE were treated surgically. Their clinical data were reviewed, and the resected aneurysmal wall of the five patients was also examined histologically. RESULTS: the mean age of the patients with SLE was 55 years, which was statistically younger than that of the other patients (mean 77 years, s.d. 7.9, p <0.05). They had received long-term corticosteroid therapy for the treatment of SLE for a mean of 23 years. Histologically, destruction of the medial elastic lamina was characteristic. Four patients had no complications in the postoperative follow-up period (mean 4 years), while the remaining patient died of rupture of a dissecting aneurysm two years after operation. CONCLUSION: prolonged steroid therapy may play a major role in accelerating atherosclerosis, which can result in aortic aneurysmal enlargement, possibly together with primary aortic wall involvement and/or vasculitic damage in patients with SLE.

Adrenal Cortex Hormones↗
PubMed2000

Studies on congenital protein C deficiency in Japanese: prevalence, genetic analysis, and relevance to the onset of arterial occlusive diseases.

Hereditary protein C deficiency is associated with a predisposition to venous thrombosis. We identified 43 patients with protein C deficiency by screening approximately 26,800 patients admitted to the National Cardiovascular Center Hospital. The observed prevalence of protein C deficiency was 1 per 620. We performed genetic analyses of 57 Japanese families with protein C deficiency. Combined with the results of the other studies in 10 families, the 67 Japanese families with protein C deficiency have been examined and 39 different gene defects have been identified. Some changes were solely identified in Japanese subjects, whereas others showed no such ethnic bias. The recurrent defects of Phe139Val, Arg169Trp, Val297Met, and Met364Ile substitutions and a G8857 deletion were found in 33 Japanese families, accounting for 49% of Japanese families with protein C deficiency, Finally, we examined the relevance of protein C deficiency to the onset of arterial occlusive diseases. In the examination of whether protein C deficiency hastens arterial occlusion, we found a significant difference (p = 0.02) in the age at onset of acute myocardial infarction between the patients with protein C deficiency (n = 10: 49.4 +/- 14.8 years) and a group of patients with normal protein C levels (n = 42: 60.5 +/- 10.6 years). At the onset of atherothrombotic cerebral infarction, the patients with protein C deficiency were significantly (p = 0.022) younger (n = 11:57.4 +/- 12.8 years) than those with normal protein C levels (n = 48: 64.6 +/- 10.1 years). Thus, we conclude that congenital protein C deficiency hastens the onset of arterial occlusive diseases, especially acute myocardial infarction, in Japanese subjects.

Age of Onset↗
PubMed2000

Double-catheter method to prevent dislodgement during percutaneous transhepatic cholangioscopy.

BACKGROUND: We evaluated the utility of the double-catheter method to establish the track for percutaneous transhepatic cholangioscopy (PTCS). METHODS: Dilatation of the percutaneous transhepatic track to 16F for PTCS was attempted in 105 patients. The results were prospectively analyzed. Using the single-catheter method (n = 22), a 16F PTCS catheter was replaced without the inner catheter. Using the double-catheter method (n = 83), a 7F catheter with a balloon tip was inserted through a 16F PTCS catheter. The balloon was located distal to the major duodenal papilla. The double-catheter method was further subclassified as follows: Method 2A (n = 62), the tip of the outer catheter (16F) was not advanced through biliary stenoses; Method 2B (n = 21), the catheter was advanced through biliary stenoses. RESULTS: In the patients treated by the double-catheter method, dislodgement of the catheter did not occur, whereas the single-catheter became dislodged in 18% (p < 0.0005). The morbidity of method 2A (0%) was less than that of method 2B (14%) (p < 0.005). CONCLUSION: The double-catheter method prevents dislodgement of the PTCS catheter. The outer catheter should not be advanced to the biliary stenosis.

Adult↗
PubMed2000

Access for percutaneous transhepatic cholangioscopy in patients with nondilated bile ducts using nasobiliary catheter cholangiography and oblique fluoroscopy.

BACKGROUND: Percutaneous transhepatic biliary drainage is required for percutaneous transhepatic cholangioscopy. However, puncture of nondilated bile ducts under ultrasonographic guidance is difficult. METHODS: In 10 patients with no ultrasonographic evidence of intrahepatic bile duct dilatation, percutaneous transhepatic biliary drainage was performed under fluoroscopic guidance using cholangiography obtained via a nasobiliary drainage catheter. Direct puncture was performed by means of a left ventral approach using oblique C-arm fluoroscopy. RESULTS: Bile duct puncture was successful in all patients. There were no procedure-related complications. Subsequent cholangioscopy was successful in all patients. CONCLUSIONS: Direct puncture using nasobiliary drainage cholangiography and oblique fluoroscopy is a useful method when cholangioscopy is necessary in patients with nondilated bile ducts.

Adult↗
PubMed2000

In vivo retention of endothelial cells adenovirally transduced with tissue-type plasminogen activator and seeded onto expanded polytetrafluoroethylene.

PURPOSE: Seeding a prosthetic graft with genetically engineered vascular endothelial cells (ECs) has the potential to enhance the graft's antithrombotic properties. However, it has been reported that ECs transduced with tissue-type plasminogen activator (tPA) have very low levels of retention on grafts, probably because of increased proteolytic activity. We examined the retention of human tPA (htPA)-transduced ECs after the cells were seeded onto expanded polytetrafluoroethylene (ePTFE) grafts and implanted into dogs. We also examined the function of secreted htPA in this model. METHODS AND RESULTS: Canine jugular venous ECs were transduced with adenoviral vectors encoding htPA (Adex1CAhtPA) and beta-galactosidase (Adex1CALacZ). There was a positive relationship between the percentage of X-gal ECs staining and the multiplicity of infection (MOI) of Adex1CALacZ. The level of htPA production in vitro increased with the increasing MOI of Adex1CAhtPA, but decreased gradually 4 days after infection. ECs coinfected with Adex1CAhtPA and Adex1CALacZ (htPAEC) or ECs infected with Adex1CALacZ alone (LacZEC) were seeded onto ePTFE grafts at densities equivalent to confluence to visualize retained ECs in an in vivo flow study. The grafts were implanted into canine carotid arteries and harvested after 5 hours of exposure to blood flow. The harvested grafts showed patchy defects in ECs, most of which were covered with mural thrombi. There was no significant difference in retention between htPAEC (29.3% +/- 8.7%) and LacZEC (19.5% +/- 3. 6%). There was a significant negative correlation between the in vivo EC retention on the grafts and the in vitro cellular passage level of ECs (P =.041; r = -.40). htPAEC produced 210.3 +/- 22.2 ng htPA antigen/10(6) cells per 6 hours in vitro and continued to secrete htPA on the harvested graft. CONCLUSIONS: We demonstrated that a large amount of functional htPA was produced by adenovirally modified canine ECs. The results of the in vivo study may suggest that overexpression of tPA has little effect on the short-term retention of early passage ECs seeded onto ePTFE grafts.

Adenoviridae↗
PubMed2000

'Carbonyl stress' and dialysis-related amyloidosis.

Advanced glycation end products (AGEs) are formed by nonenzymatic glycation and oxidation (glycoxidation) reactions. As AGE formation is related to hyperglycaemia, they have been implicated in the pathogenesis of diabetic complications. They also increase in normoglycaemic uraemic patients: AGEs, such as pentosidine and carboxymethyllysine (CML), are elevated in both the plasma proteins and skin collagen of uraemic patients, being several times greater than in normal subjects and nonuraemic diabetic patients. However, AGE concentrations do not differ between diabetics and non-diabetics in uraemia. AGE accumulation in uraemia, therefore, cannot be attributed to hyperglycaemia, or simply to the decreased removal by glomerular filtration of AGE-modified proteins as over 90% of plasma pentosidine and CML are linked to albumin. Recently, evidence has suggested that, in uraemia, the increased carbonyl compounds, derived from both carbohydrates and lipids, modify proteins both by the glycoxidation reaction (leading to augmented AGE production) and also by the lipoxidation reaction (leading to the augmentation of the advanced lipoxidation end product, ALE, production). Thus, uraemia might be a state of carbonyl overload with potentially damaging proteins ('carbonyl stress'). Carbonyl stress in uraemia appears to be relevant to long-term complications associated with chronic renal failure and dialysis, such as dialysis-related amyloidosis. Immunohistochemical studies, with specific antibodies to AGEs and ALEs, identified carbonyl stress in long-lived beta2-microglobulin amyloid deposits. Furthermore, proteins modified with carbonyl stress exhibit several biological activities through interactions with several types of cell, e.g. monocytes/macrophages, synovial cells and osteoclasts/osteoblasts, which might partially account for dialysis arthropathies.

Amyloidosis↗
PubMed2000

Nitric oxide inhibits the formation of advanced glycation end products.

BACKGROUND: Advanced glycation end products (AGEs) are elevated in renal failure and have been implicated in the pathogenesis of several uremic complications. Their formation is closely associated with oxidative stress. The recent observation that nitric oxide (NO) has an antioxidant effect led us to examine the possible role of NO in the generation of AGEs. METHODS: We examined the effect of NO donors, 2, 2'-(hydroxynitrosohydrazono)bis-ethanamine (NOC18) and S-nitroso-N-acetyl-DL-penicillamine (SNAP), on the in vitro formation of pentosidine, which was used as a surrogate marker for AGEs. Bovine serum albumin was incubated under air at 37 degrees C in a medium containing either several AGE precursors or uremic plasma. To elucidate further the mechanism of the NO effect on AGE formation, we examined the generation of free radicals and carbonyls in pentose-driven pentosidine formation. RESULTS: NO donors significantly inhibit the formation of pentosidine in a dose-dependent manner. The effect is abolished by the addition of a NO scavenging agent, 2-(4-carboxyphenyl)-4,4,5, 5-tetramethylimidazoline-1-oxyl 3-oxide (carboxy-PTIO). The inhibitory effect results from NO but not from the NO donor molecule. It is best explained by the ability of NO to scavenge carbon-centered radicals, hydroxyl radical, and carbonyl compounds. CONCLUSIONS: NO inhibits pentosidine formation by scavenging free radicals and by inhibiting carbonyl compound formation. NO might be implicated in the atherogenic and inflammatory effects of AGEs: Reduced NO production and increased oxidative stress associated with atherosclerotic lesions may accelerate AGE formation and, thus, exacerbate endothelial dysfunction and accelerate the development of atherosclerosis in uremia.

Adult↗
PubMed2000

Musashi1: an evolutionally conserved marker for CNS progenitor cells including neural stem cells.

In situ detection of neural progenitor cells including stem-like cells is essential for studying the basic mechanisms of the generation of cellular diversity in the CNS, upon which therapeutic treatments for CNS injuries, degenerative diseases, and brain tumors may be based. We have generated rat monoclonal antibodies (Mab 14H1 and 14B8) that recognize an RNA-binding protein Musashi1, but not a Musashi1-related protein, Musashi2. The amino acid sequences at the epitope sites of these anti-Musashi1 Mabs are remarkably conserved among the human, mouse, and Xenopus proteins. Spatiotemporal patterns of Musashi1 immunoreactivity in the developing and/or adult CNS tissues of frogs, birds, rodents, and humans indicated that our anti-Musashi1 Mabs reacted with undifferentiated, proliferative cells in the CNS of all the vertebrates tested. Double or triple immunostaining of embryonic mouse brain cells in monolayer cultures demonstrated strong Musashi1 expression in Nestin(+)/RC2(+) cells. The relative number of Musashi1(+)/Nestin(+)/RC2(+) cells increased fivefold when embryonic forebrain cells were cultured to form 'neurospheres' in which stem-like cells are known to be enriched through their self-renewing mode of growth. Nestin(+)/RC2(-) cells, which included Talpha1-GFP(+) neuronal progenitor cells and GLAST(+) astroglial precursor cells, were also Musashi1(+), as were GFAP(+) astrocytes. Young neurons showed a trace of Musashi1 expression. Cells committed to the oligodendroglial lineage were Musashi(-). Musashi1 was localized to the perikarya of CNS stem-like cells and non-oligodendroglial progenitor cells without shifting to cell processes or endfeet, and is therefore advantageous for identifying each cell and counting cells in situ.

Amino Acid Sequence↗
PubMed2000

Induction of apoptosis by glyoxal in human embryonic lung epithelial cell line L132.

Oxidative stress has been suggested to play a central role in the pathogenesis of lung fibrosis and lung epithelial cell apoptosis is considered to be a key event during fibrogenesis. Studies from various laboratories have indicated that metabolic conditions may initiate oxidative stress, thereby contributing to epithelial cell death. This study was designed to test the hypothesis that glyoxal, an intermediate product in the glycation reaction leading to advanced glycation end products (AGEs), may induce lung epithelial cell apoptosis. We investigated the in vitro effects of glyoxal on fetal human lung epithelial L132 cells. Immunocytochemical analysis of paraffin-embedded cells and fluorescence-activated cell sorter analysis revealed a dose-dependent accumulation of the glycoxidation product (epsilon)N-carboxymethyllysine (CML) in all compartments of the cell. It has been shown that CML modification of proteins may serve as an indicator for oxidative stress. To examine the role of apoptosis in epithelial lung cells we investigated glyoxal-dependent changes in pro- and antiapoptotic mediators bax and activated caspase-3, and galectin-3 and bcl-2, respectively. Increasing concentrations of glyoxal (50 to 400 microM) induced an increase in the number of apoptotic cells. The apoptotic changes were confirmed by transmission electron microscopy. Immunocytochemical analysis of treated cells revealed the presence of other AGEs such as pentosidine as well as products of lipid peroxidation.

Apoptosis↗
PubMed2000

4-hydroxynonenal induces a cellular redox status-related activation of the caspase cascade for apoptotic cell death.

4-Hydroxynonenal (HNE), a diffusible product of lipid peroxidation, has been suggested to be a key mediator of oxidative stress-induced cell death. In this study, we partially characterized the mechanism of HNE-mediated cytotoxicity. Incubation of human T lymphoma Jurkat cells with 20-50 microM HNE led to cell death accompanied by DNA fragmentation. Western blot analysis showed that HNE-treatment induced time- and dose-dependent activation of caspase-8, caspase-9 and caspase-3. HNE-induced caspase-3 processing was confirmed by a flow cytometric demonstration of increased catalytic activity on the substrate peptide. HNE treatment also led to remarkable cleavage of poly(ADP-ribose) polymerase (PARP), which was prevented by pretreatment of cells with DEVD-FMK as a caspase-3 inhibitor. The HNE-mediated activation of caspases, cleavage of PARP and DNA fragmentation were blocked by antioxidants cysteine, N-acety-L-cysteine and dithiothreitol, but not by two other HNE-reactive amino acids lysine and histidine, or by cystine, the oxidized form of cysteine. HNE rapidly decreased levels of intracellular reduced glutathione (GSH) and its oxidized form GSSG, and these were also attenuated by the reductants. Coincubation of Jurkat cells with a blocking anti-Fas antibody prevented Fas-induced but not HNE-induced activation of caspase-3. HNE also activated caspase-3 in K562 cells that do not express functional Fas. Our results thereby demonstrate that HNE triggers oxidative stress-linked apoptotic cell death through activation of the caspase cascade. The results also suggest a possible mechanism involving a direct scavenge of intracellular GSH by HNE.

Aldehydes↗
PubMed2000

[Effects of fudosteine, a new cysteine derivative, on airway secretion in rabbits and rats].

We examined the effects of fudosteine [(-)-(R)-2-amino-3-(3-hydroxypropylthio) propionic acid], a new cysteine derivative, on airway secretion in rabbits and rats. Indirect measurement of airway secretion in rabbits, which was expressed by the amount of dye excreted into the respiratory tract, was carried out according to the Sakuno's method, with some modifications. Fudosteine (500 mg/kg, p.o.) significantly increased the amount of dye excreted into the respiratory tract. As a direct method of measurement of airway secretion, the modified Perry and Boyd's method was used to collect respiratory tract fluid (RTF) in rabbits. Fudosteine (500 mg/kg, p.o.) significantly augmented the output volume of RTF, but there was no difference from the control in protein and phosphatidylcholine (PC) contents into RTF. On the other hand, fudosteine increased chloride ion concentration in broncho-alveolar lavage of rats. Fudosteine did not stimulate PC secretion in a primary culture of rat type II pneumocytes, and it did not have a mucolytic effect against gastric mucin in vitro. From the results described above, it was concluded that fudosteine may be a new cysteine derivative which offers a serous secretion.

Animals↗
PubMed2000

[Congenital thrombophilia caused by protein C deficiency].

To clarify the prevalence of protein C deficiency in patients with cardiovascular problems, we identified 54 patients with protein C deficiency by screening approximately 26,800 patients. The observed prevalence of protein C deficiency was 1 in 500. From the results of genetic analysis of 67 Japanese families with protein C deficiency, the recurrent defects of Phe139Val, Arg169Trp, Val297Met, Met364Ile substitutions and a G8857 deletion were accounting 49% of Japanese families with protein C deficiency. The defects including Phe139Val and Met364Ile substitutions and a G8857 deletion were only found in Japanese subjects and seemed to be a founder effect. Protein C deficiency is associated with a predisposition to venous thrombosis. It is not clear whether the deficiency is involved in arterial occlusion. We identified 34 patients with protein C deficiency manifested 45 episodes of arterial occlusive disease. We compared the onset age of arterial occlusive disease between patients with protein C deficiency and a group of patients with normal protein C levels. We found the early onset of acute myocardial infarction and atherothrombotic cerebral infarction in patients with protein C deficiency. Thus, our study suggests that congenital protein C deficiency contributes to earlier onset of arterial occlusive diseases in Japanese subjects.

Arterial Occlusive Diseases↗
PubMed2000

Carotid artery reconstruction for Takayasu's arteritis the necessity of all-autogenous-vein graft policy and development of a new operation.

BACKGROUND: We have adopted an all-autogenous-vein-graft policy in carotid reconstruction for Takayasu arteritis, namely an ascendo-right carotid and right subclavian (axillary) arteries bypass using a pantaloon vein graft for patients all of whose arch branches are occluded, and an extra-anatomical bypass from the right subclavian artery for patients whose brachiocephalic artery is the only arch branch that remains patent. This report is to elaborate on these operations and to assess the long-term outcome. METHODS: Six patients were operated on according to this policy; (5 women, 1 man, age range: 14 to 59 years (mean: 30). The indications for surgery were severe cerebral ischaemia that significantly interfered with their daily lives. The pantaloon vein graft bypass was performed in four patients, and an extra-anatomical bypass in two. The specific management protocol to prevent the "postbypass hyperperfusion syndrome" and cerebral oedema included a shunt procedure to the internal carotid artery using one limb of the pantaloon vein graft, induced hypotension just before the completion of the carotid reconstruction and the administration of a glycerine-fructose solution. RESULTS: Cerebral ischaemic symptoms disappeared in all patients. All but one, who died of a ruptured thoraco-abdominal aneurysm on the 35th postoperative month, are living a normal life with a patent graft. No suture line complications have as yet been encountered (follow-up: 10 to 205 months, mean: 126 months). CONCLUSIONS: Carotid vein bypass for Takayasu arteritis, particularly, the pantaloon vein graft bypass is recommended for those of whom all aortic arch branches are occluded, resulting in severe brain ischaemia. Perioperative blood pressure control is important for prevention of the hyperperfusion syndrome.

Adolescent↗