Biomedical subjects

T Namba

Publications and source records attributed to T Namba.

At least 19 recordsLinked to original sources

PubMed2001

Reversible inhibition of hypoxia-inducible factor 1 activation by exposure of hypoxic cells to the volatile anesthetic halothane.

Volatile anesthetics modulate a variety of physiological and pathophysiological responses including hypoxic responses. Hypoxia-inducible factor 1 (HIF-1) is a transcription factor that mediates cellular and systemic homeostatic responses to reduced O(2) availability in mammals, including erythropoiesis, angiogenesis, and glycolysis. We demonstrate for the first time that the volatile anesthetic halothane blocks HIF-1 activity and downstream target gene expressions induced by hypoxia in the human hepatoma-derived cell line, Hep3B. Halothane reversibly blocks hypoxia-induced HIF-1alpha protein accumulation and transcriptional activity at clinically relevant doses.

Anaerobiosis↗

PubMed2001

Breakthrough waves during ventricular fibrillation depend on the degree of rotational anisotropy and the boundary conditions: a simulation study.

INTRODUCTION: The left ventricle (LV) and right ventricle (RV) are characterized by specific fiber orientation known as "rotational anisotropy." However, it remains unclear whether the LV and RV are different with regard to the effect of rotational anisotropy on the dynamics of scroll waves during ventricular fibrillation (VF). To resolve this issue, we used a computation-based model to study scroll wave behavior. METHODS AND RESULTS: We composed an environment of simulated three-dimensional ventricular wall slabs, with optional ratios of fiber rotation to wall thickness (0 degrees, 6 degrees, and 12 degrees/mm thickness; LV 10 mm, RV 5 mm), using Luo-Rudy phase I equations. When rotational anisotropy was not incorporated into the LV wall slab (theta endo to approximately theta epi = 0 degrees), most scroll waves rotated around the filaments perpendicular to the tissue surface, with only a few accompanying breakthrough waves. In a twisted LV model (theta endo to approximately theta epi = 60 degrees and 120 degrees), the scroll waves were demonstrated as multiple wavelets scattered spatiotemporally, frequently accompanied by breakthrough waves that were promoted by rotational anisotropy. In a twisted RV model (theta endo to approximately theta epi = 30 degrees and 60 degrees), single scroll waves and/or figure-of-eight reentrant waves appeared, with comparatively few breakthrough waves, regardless of the degree of fiber twist. CONCLUSION: The proportion of electrical effects of rotational anisotropy and tissue boundaries plays an important role in the genesis of breakthrough waves during VF, and the difference in wave propagating patterns and frequency spectrum of the ventricles may arise, in part, from the number of breakthrough waves promoted by rotational anisotropy.

Anisotropy↗

PubMed2001

Electroporation in a model of cardiac defibrillation.

INTRODUCTION: It is known that high-strength shock disrupts the lipid matrix of the myocardial cell membrane and forms reversible aqueous pores across the membrane. This process is known as "electroporation." However, it remains unclear whether electroporation contributes to the mechanism of ventricular defibrillation. The aim of this computer simulation study was to examine the possible role of electroporation in the success of defibrillation shock. METHODS AND RESULTS: Using a modified Luo-Rudy-1 model, we simulated two-dimensional myocardial tissue with a homogeneous bidomain nature and unequal anisotropy ratios. Spiral waves were induced by the S1-S2 method. Next, monophasic defibrillation shocks were delivered externally via two line electrodes. For nonelectroporating tissue, termination of ongoing fibrillation succeeded; however, new spiral waves were initiated, even with high-strength shock (24 V/cm). For electroporating tissue, high-strength shock (24 V/cm) was sufficient to extinguish ongoing fibrillation and did not initiate any new spiral waves. Weak shock (16 to 20 V/cm) also extinguished ongoing fibrillation; however, in contrast to the high-strength shock, new spiral waves were initiated. Success in defibrillation depended on the occurrence of electroporation-mediated anodal-break excitation from the physical anode and the virtual anode. Some excitation wavefronts following electrical shock used a deexcited area with recovered excitability as a pass-through point; therefore, electroporation-mediated anodal-break excitation is necessary to block out the pass-through point, resulting in successful defibrillation. CONCLUSION: The electroporation-mediated anodal-break excitation mechanism may play an important role in electrical defibrillation.

Action Potentials↗

PubMed2001

Biological characterization of eugeniin as an anti-herpes simplex virus type 1 compound in vitro and in vivo.

Eugeniin exhibits antiviral activity against acyclovir and phosphonoacetic acid (PAA)-resistant herpes simplex virus type 1 (HSV-1) as well as the wild-type HSV-1 in vitro. In this study, we characterized the biological activity of eugeniin in cutaneously HSV-1-infected mice and its interaction with HSV-1 DNA polymerase. The oral and intraperitoneal administrations of eugeniin at 0.3 mg/kg showed similar therapeutic efficacy in retarding the development of skin lesions of HSV-1-infected mice. The two routes of administration at 6 or 50 mg/kg significantly prolonged the mean survival times and/or reduced mortality without toxicity. The oral administration of eugeniin at 50 mg/kg reduced virus yields in the skin and brain of infected mice. Thus, the therapeutic efficacy of oral administration at the various doses of eugeniin was similar to that of intraperitoneal administration, suggesting that the oral bioavailability of eugeniin was high with respect to absorption. Furthermore, the anti-HSV-1 activity of eugeniin was characterized by isobolograms analyzing its combined effects with acyclovir or PAA in HSV-1-infected Vero cells. Eugeniin enhanced the anti-HSV-1 activity of acyclovir but was suggested to be antagonistic with PAA. The interaction of eugeniin and PAA on the activity of partially purified HSV-1 DNA polymerase suggested that eugeniin interacted with the polymerase in the vicinity of PAA-binding site. Thus, eugeniin showed different anti-HSV-1 action from acyclovir and PAA and therapeutic anti-HSV-1 activity in mice.

Acyclovir↗

PubMed2001

Atrial blood cyst in an adult with regurgitation of mitral and tricuspid valves.

Blood cysts of the heart are extremely rare in adults and usually involve valves or the left ventricle. Although two cases of blood cysts in the right atrium in adults have been reported, a cyst combined with a disorder of the valves has never been reported. We report a 52-year-old woman with a blood cyst that generated from the right atrial septum. Furthermore, the patient had regurgitation of both the mitral and tricuspid valves and then underwent surgical excision of the blood cyst, mitral valve plasty and tricuspid valve annuloplasty. We believe that it is possible to diagnose blood cysts with echocardiography, CT and magnetic resonance imaging. Echocardiography showed the cyst as a circle without a complete inner free-echo. CT and magnetic resonance imaging showed a mass with a non-enhanced inner structure. Furthermore, the latter showed a cyst that was enhanced by T1- but not T2-weighted images, indicating that the content of the cyst was a persistent substance such as blood. Concerning the generation of blood cysts, we hypothesize that heteroplastic growth arising from primitive pericardial mesothelium causes disorders of valves and blood cysts.

Blood↗

PubMed2000

Inhibition of nitric oxide by phenylethanoids in activated macrophages.

Nitric oxide (NO) is one of the pro-inflammatory molecules. Some phenylethanoids have been previously shown to possess anti-inflammatory effects. Seven phenylethanoids from the stems of Cistanche deserticola, viz. isoacteoside, tubuloside B, acteoside, 2'-O-acetylacteoside, echinacoside, cistanoside A and tubuloside A, were tested for their effect on NO radical generation by activated murine macrophages. At the concentration of 100-200 microM, all the phenylethanoids reduced (6.3-62.3%) nitrite accumulation in lipopolysaccharide (0.1 microgram/ml)-stimulated J774.1 cells. At 200 microM, they inhibited by 32.2-72.4% nitrite accumulation induced by lipopolysaccharide (0.1 microgram/ml)/interferon-gamma (100 U/ml) in mouse peritoneal exudate macrophages. However, these compounds did not affect the expression of inducible nitric oxide (iNOS) mRNA, the iNOS protein level, or the iNOS activity in lipopolysaccharide-stimulated J774.1 cells. Instead, they showed a clear scavenging effect (6.9-43.9%) at the low concentrations of 2-10 microM of about 12 microM nitrite generated from an NO donor, 1-propanamine-3-hydroxy-2-nitroso-1-propylhydrazino (PAPA NONOate). These results indicate that the phenylethanoids have NO radical-scavenging activity, which possibly contributes to their anti-inflammatory effects.

Animals↗

PubMed2000

Inhibition of the human intermediate conductance Ca(2+)-activated K(+) channel, hIK1, by volatile anesthetics.

Ca(2+)-activated K(+) channels (K(Ca)) regulate a wide variety of cellular functions by coupling intracellular Ca(2+) concentration to membrane potential. There are three major groups of K(Ca) classified by their unit conductances: large (BK), intermediate (IK), and small (SK) conductance of channels. BK channel is gated by combined influences of Ca(2+) and voltage, while IK and SK channels are gated solely by Ca(2+). Volatile anesthetics inhibit BK channel activity by interfering with the Ca(2+) gating mechanism. However, the effects of anesthetics on IK and SK channels are unknown. Using cloned IK and SK channels, hIK1 and hSK1-3, respectively, we found that the currents of hIK1 were inhibited rapidly and reversibly by volatile anesthetics, whereas those of SK channels were not affected. The IC(50) values of the volatile anesthetics, halothane, sevoflurane, enflurane, and isoflurane for hIK1 inhibition were 0.69, 0.42, 1.01 and 1.03 mM, respectively, and were in the clinically used concentration range. In contrast to BK channel, halothane inhibition of hIK1 currents was independent of Ca(2+) concentration, suggesting that Ca(2+) gating mechanism is not involved. These results demonstrate that volatile anesthetics, such as halothane, enflurane, isoflurane, and sevoflurane, affect BK, IK, and SK channels in distinct ways.

Anesthetics, Inhalation↗

PubMed2000

Inhibitory effects of an aqueous extract of Apocynum venetum leaves and its constituents on Cu(2+)-induced oxidative modification of low density lipoprotein.

An aqueous extract of Apocynum venetum leaves and its constituents inhibited thiobarbituric acid reactive substances (TBARS) and conjugated-diene formation in the Cu(2+)-induced oxidation of low density lipoprotein (LDL) in vitro. The TBARS formation was most strongly inhibited by chlorogenic acid with an IC(50) value of 1.9 microM, but other constituents were in a range of 2.3-23.3 microM. On the other hand, the lag time in the conjugated-diene formation was dose-dependently prolonged by addition of the aqueous extract. Catechin prolonged the lag time more than 300 min and other constituents such as chlorogenic acid, epicatechin, epigallocatechin, hyperoside and isoquercitrin led to no conjugated-diene formation within 700 min under the experimental conditions.

Cholesterol, LDL↗

PubMed2000

Distribution, metabolism and excretion of butylidenephthalide of Ligustici chuanxiong rhizoma in hairless mouse after dermal application.

The absorption, distribution and excretion of butylidenephthalide after dermal application to hairless mouse have been examined with [8-14C]butylidenephthalide. By the investigation of the whole body autoradiogram and liquid scintillation analysis, it was indicated that the transdermally applied butylidenephthalide quickly permeate into peripheral circulation system without accumulation in the skin and then distribute into lung, liver, bile and kidney. The total radioactivity, however, was decreased due to excretion into urine, and in the case of i.v.-administration, 80% of the administered butylidenephthalide was excreted into urine within 24 h, while only 5% was excreted into feces within 24 h. Then, the metabolite in urine was determined to be a cysteine conjugate by liquid chromatography-mass spectrometry/mass spectrometry (LC-MS/MS) method. Thus, it has been concluded that after dermal application butylidenephthalide quickly permeates through skin into peripheral circulation system; distributes to lung, liver, bile and kidney; and then excreted into urine as a cysteine adduct.

Administration, Cutaneous↗

PubMed2000

Effects of aqueous extracts of Apocynum venetum leaves on spontaneously hypertensive, renal hypertensive and NaCl-fed-hypertensive rats.

Effects of aqueous extracts of Apocynum venetum leaves (Luobuma extracts) on the blood pressure were evaluated in hypertensive animal models, such as spontaneously hypertensive rats (SHR), renal hypertensive rats and NaCl-induced hypertensive rats. In SHR, administration of Luobuma (heat-processed and unprocessed leaves) extracts at a dose of 70 mg/rat per day significantly decreased the systolic blood pressure value, but their decreasing effects were weaker than that of captopril. The urine volume, and the urinary Na(+), K(+) and protein excretions were not significantly different between Luobuma-treated and untreated groups. In 3/4 nephrectomized rats, the Luobuma extracts significantly decreased the systolic blood pressure value, accompanied by significant increases of the urine volume and the urinary Na(+) and K(+) excretions. Furthermore, they decreased the blood urea nitrogen (BUN) level. In NaCl-induced hypertensive rats, the Luobuma extract decreased the systolic blood pressure value. However, it did not change the urinary excretions of Na(+), K(+) and protein. The BUN level was lower than that of control rats, but the serum total cholesterol (TC) level did not changed. From these findings, the Luobuma extracts have an anti-hypertensive effect, possibly due to amelioration of the kidney functions in the three experimental animal models.

Animals↗

PubMed2000

Hepatoprotective effect of Apocynum venetum and its active constituents.

The leaves of Apocynum venetum L. are used as a tea material in north China and Japan. A water extract (500 mg/kg/day, one week administration) of the leaves of A. venetum showed protective effects against carbon tetrachloride (CCl4, 30 microliters/mouse) or D-galactosamine (D-GalN, 700 mg/kg)/lipopolysaccharide (LPS, 20 micrograms/kg)-induced liver injury in mice. Tumor necrosis factor-alpha (TNF-alpha) secreted from LPS-stimulated macrophages is the most crucial mediator in the D-GalN/LPS-induced liver injury model. The extract had no significant inhibition on the increase of serum TNF-alpha (1169 +/- 132 pg/ml vs. 1595 +/- 314 pg/ml of control), but exhibited a complete inhibition at the concentration of 100 micrograms/ml on TNF-alpha (100 ng/ml)-induced cell death in D-GalN (0.5 mM)-sensitized mouse hepatocytes. Further activity-guided fractionation resulted in the isolation of fifteen flavonoids viz. (-)-epicatechin (1), (-)-epigallocatechin (2), isoquercetin (3), hyperin (4), (+)-catechin (5), (+)-gallocatechin (6), kaempferol-6'-O-acetate (7), isoquercetin-6'-O-acetate (8), catechin-[8,7-e]-4 alpha-(3,4-dihydroxpyhenyl)-dihydro-2(3H)-pyranone (9), apocynin B (10), apocynin A (11), cinchonain Ia (12), apocynin C (13), apocynin D (14) and quercetin (15). All the compounds showed inhibitory effects on TNF-alpha-induced cell death with different intensities. The flavonol glycosides 3, 4, 7 and 8 and the phenylpropanoid-substituted flavan-3-ols 11 and 12 showed potent inhibitory effects on TNF-alpha-induced cell death with IC50 values of 37.5, 14.5, 31.2, 55.1, 71.9 and 41.2 microM, respectively. In contrast, the clinically used 5 and its analogues 1, 2 and 6 showed apparent activity only at 80 microM. These flavonoids appeared to be the hepatoprotective principles of the leaves of A. venetum. The hepatoprotective effects exhibited by the extract and its constituents suggest a validation of the leaves as a tea material.

Animals↗

PubMed2000

Genetic heterogeneity of ribosomal RNA gene and matK gene in Panax notoginseng.

Previously, 185 ribosomal RNA gene and matK gene sequences of Chinese herbal medicines, Ginseng Radix, Panacis Japonici Rhizoma and Panacis Quinquefolli Radix were shown to correspond with those of the original plants, Panax ginseng, P. japonicus and P. quinquefolius, respectively, with the species-specific sequences especially for 18S rRNA gene sequences. In P. notoginseng and its derivative, Notoginseng Radix, however, we found two genetic groups with respect to both gene sequences. Five base substitutions were detected on both gene sequences and the homology between two groups was 99.7% for the 18S rRNA gene and 99.6% for the matK gene, respectively. One genetic group was found to have the identical sequences as those of P. ginseng.

Genetic Heterogeneity↗

PubMed2000

Thioredoxin inhibits tumor necrosis factor- or interleukin-1-induced NF-kappaB activation at a level upstream of NF-kappaB-inducing kinase.

Gene induction by tumor necrosis factor-alpha (TNFalpha) or interleukin-1beta (IL-1beta) is mediated in part by activation of the transcription factor nuclear factor kappaB (NF-kappaB), and requires signal adaptor molecules such as TNF receptor-associated factor (TRAFs). The latter interact with the NF-kappaB-inducing kinase (NIK), which is believed to be part of the IkappaB kinase complex. Although the precise mechanism is to be elucidated, it is well-known that antioxidant treatments inhibit the inflammatory cytokine-induced NF-kappaB activation. Thioredoxin (TRX) is a 12-kDa endogenous protein that regulates various cellular functions by modulating the redox state of proteins, overexpression of this molecule inhibits NF-kappaB activation. To elucidate the roles of TRX in the signal transduction of the cytokines, we investigated the effects of TRX on NF-kappaB activation induced by cytokine treatment or by overexpression of the signaling molecules. Our data show that TRX treatment inhibits NF-kappaB-dependent transcription at the level of downstream of TRAFs and upstream of NIK: TRX inhibited TRAF2-, TRAF5-, and TRAF6-induced NF-kappaB activation but does not inhibit NIK-, IKKalpha-, and MEKK-induced activation. In addition, we show that TRX inhibits NF-kappaB activation in a manner different from that for SAPK (stress activated protein kinase) inhibition.

Acetylcysteine↗

PubMed2000

Spatial heterogeneity in refractoriness as a proarrhythmic substrate: theoretical evaluation by numerical simulation.

Spatial heterogeneity in the refractoriness of the ventricular myocardium due to a regionally prolonged refractory period has often been observed in patients with cardiovascular disease as the substrate for functional reentrant tachyarrhythmias. The present study sought to determine how functional reentrant activity could occur due to the spatial heterogeneity, using numerical simulation. Spatial heterogeneity in the refractoriness was introduced into a two-dimensional array by the regionally prolonged refractory period expressed as a square cluster. Double stimulation, conducted from a single source, was introduced into 4 types of matrices, which differed in their level of spatial heterogeneity. A pseudoelectrocardiogram was calculated from these matrices. Spiral waves were initiated in all the matrices except for the lowest heterogeneous matrix. A vulnerable window of the coupling interval, which induced spiral waves, was observed and was wider in proportion to the level of the heterogeneity. A higher level of heterogeneity and more limited range of coupling intervals were required to sustain the spiral waves. Furthermore, in the pseudoelectrocardiogram, sustained spiral waves exhibited a waveform like that in torsades de pointes (TdP) and their transformation into ventricular fibrillation (VF). Spatial heterogeneity in refractoriness due to a regionally prolonged refractory period could be a substrate for functional reentrant tachyarrhythmias, possibly including TdP and VF.

Cardiovascular Diseases↗

PubMed1999

Inhibitory effect of tetrahydroswertianolin on tumor necrosis factor-alpha-dependent hepatic apoptosis in mice.

We investigated the effect of tetrahydroswertianolin (THS), a hepatoprotective agent from Swertia japonica, on tumor necrosis factor-alpha (TNF-alpha)-dependent hepatic apoptosis induced by D-galactosamine (D-GalN) (700 mg/kg, i.p.) and lipopolysaccharide (LPS) (10 microg/kg, i.p.) in mice. Apoptotic symptoms were observed at the initial stage of liver damage. By 5 hr after intoxication, hepatic DNA fragmentation had risen to 2123%, with the value in untreated mice set at 100%, without a significant elevation of serum alanine transaminase (ALT) activity. There was a parallel increase in hepatocytes undergoing chromatin condensation and apoptotic body formation. By 8 hr after intoxication, serum ALT activity had risen to 3707 U/L. Pretreatment with THS (50 mg/kg, p.o.) at 18 and 2 hr before intoxication significantly reduced DNA fragmentation to 821% of that in untreated mice and prevented the emergence of chromatin condensation and apoptotic body formation. A significant and dose-dependent reduction in serum ALT activity at 8 hr also was observed with THS pretreatment. These effects of THS were different from those observed from pretreatment with glycyrrhizin (GCR), which is a clinically used hepatoprotective agent with membrane-stabilizing activity. GCR pretreatment (100 mg/kg, p.o.) did not inhibit hepatic DNA fragmentation (1588% of untreated mice), although this compound significantly protected against serum ALT elevation (1463 U/L). These data suggest that an inhibitory effect on the progression of hepatic apoptosis prior to liver injury may be involved in the hepatoprotective mechanisms of THS, whereas it appears that GCR affects the processes after apoptosis. In a separate experiment, we found that the concentration of serum TNF-alpha rose to 2016 pg/mL at 1 hr after intoxication of mice with D-GalN and LPS, but this increase was suppressed by THS pretreatment (10, 50, or 200 mg/kg, p.o.) to 716, 454, or 406 pg/mL, respectively. Further study with a reverse transcriptase-polymerase chain reaction method showed that THS blocked TNF-alpha production at the transcriptional level. Because TNF-alpha is a critical mediator to elicit apoptosis in this model, the property of suppressing TNF-alpha production may be of prime importance for THS inhibition of hepatic apoptosis.

Analysis of Variance↗

PubMed1999

Chronic colchicine administration attenuates cardiac hypertrophy in spontaneously hypertensive rats.

To determine whether the long-term inhibition of microtubule integrity in vivo by colchicine could attenuate the development of cardiac hypertrophy, we studied five groups of rats: Wistar-Kyoto rats receiving saline for 4 weeks (WKYsaline); WKY receiving colchicine, which depolymerizes microtubules (WKYcolchicine); spontaneously hypertensive rats receiving saline (SHRsaline); SHRs receiving colchicine (SHRcolchicine); and SHRs receiving lumicolchicine, an inactive stereoisomer of colchicine (SHRlumicolchicine). Seven-week-old animals were administered drugs or control substances via alternate day intraperitoneal injection for a period of 4 weeks. Dosage was gradually increased from 0.6 to 1.0 mg/kg to avoid drug toxicity. Depolymerization of myocardial microtubules by the in vivo administration of colchicine into the rats was confirmed by both Western blot analysis and immunofluorescence of tubulin protein in the hearts. Body weight (BW) was lower, while systolic blood pressure was significantly elevated in SHRs vs the WKY rats. No significant difference was found in either of these parameters between the control or treatment groups of each strain. Left ventricular (LV) weight-to-BW ratio was elevated and showed significant increases in the SHRs as compared to WKY animals, indicative of cardiac hypertrophy. When the SHRs were treated with colchicine but not vehicle or lumicolchicine, LV/BW was similar to the WKY. Changes of myocyte cross-sectional area determined using LV mid-free wall specimens were concordant with the LV/BW data. No significant changes were found in collagen volume fraction between groups. Thus the inhibition of microtubule polymerization abolished the progression of cardiac myocyte hypertrophy in SHRs independently of blood pressure.

Animals↗

PubMed1999

The effects of habitat fragmentation on persistence of source-sink metapopulations in systems with predators and prey or apparent competitors.

We consider systems with one predator and one prey, or a common predator and two prey species (apparent competitors) in source and sink habitats. In both models, the predator species is vulnerable to extinction, if productivity in the source is insufficient to rescue demographically deficient sink populations. Conversely, in the model with two prey species, if the source is too rich, one of the prey species may be driven extinct by apparent competition, since the predator can maintain a large population because of the alternative prey. Increasing the rate of predator movement from the source population has opposite effects on prey and predator persistence. High emigration rate exposes the predator population to danger of extinction, reducing the number of individuals that breed and produce offspring in the source habitat. This may promote coexistence of prey by relaxing predation pressure and apparent competition between the two prey species. The number of sinks and spatial arrangement of patches, or connectivity between patches, also influence persistence of the species. More sinks favor the prey and fewer sinks are advantageous to the predator. A linear pattern with the source at one end is profitable for the predator, and a centrifugal pattern in which the source is surrounded by sinks is advantageous to the prey. When the dispersal rate is low, effects of the spatial structure may exceed those of the number of sinks. In brief, productivity in patches and patterns of connectivity between patches differentially influence persistence of populations in different trophic levels.

Animals↗

PubMed1999

Surgery for descending thoracic aortic anastomotic aneurysms with a temporary external bypass method.

The surgical treatment of descending thoracic aortic anastomotic aneurysms is technically challenging. The purpose of this study was to evaluate the use of a temporary external bypass method as an intraoperative measure in the surgical treatment of anastomotic aneurysms of the descending thoracic aorta. An analysis of five consecutive patients who had undergone surgery for a collective seven descending thoracic aortic anastomotic aneurysms in our university hospital over a period of 14 years was conducted. A temporary bypass technique was used as an intraoperative measure in all the operations, four of which were performed with a right axillary to left external iliac artery bypass, while other sites were used in the remaining three. Systemic heparinization was able to be avoided in six operations and was markedly reduced in the remaining one. Although the major postoperative complication was coagulated hemothorax after six procedures, all patients recovered well and are still alive after a mean follow-up period of 8.2+/-1.5 (SEM) years. The results of this analysis led us to conclude that our temporary bypass method for treating descending thoracic aortic anastomotic aneurysm prevented the risks of anticoagulant administration for circulatory support, which contributed to the success of the operation. This method can be used as adjunct treatment for anastomotic aneurysms in the descending thoracic aorta.

Adult↗