Biomedical subjects

K Kamiya

Publications and source records attributed to K Kamiya.

At least 55 records · Page 3Linked to original sources

PubMed2000

Crohn's disease of the esophagus: report of a case.

We report herein the case of a 27-year-old man with Crohn's disease of the esophagus. The patient presented with large ulcers in the esophagus for which treatment based on a diagnosis of reflux esophagitis was commenced. Although his symptoms were initially resolved, the ulcers did not improve and he was readmitted to hospital 3 months later for progressive heartburn. An esophagoscopy revealed large ulcers in the esophagus, and a colonoscopy revealed a longitudinal ulcer in the terminal ileum. Histological examination of specimens from the terminal ileum showed severe inflammation without granuloma formation, which led to a diagnosis of Crohn's disease. The oral administration of prednisolone and salazosulfapyridine controlled his symptoms and the esophageal ulcers were observed to be healing 2 weeks after this treatment was initiated. A review of the English literature revealed only 77 cases of this disease. Isolated esophageal lesions were reported in ten patients (13.0%), none of which were able to be diagnosed as Crohn's disease preoperatively. Ileocolic lesions developed after esophageal lesions in only five patients (6.5%) including ours. In the remaining 62 patients (80.5%), ileocolic lesions had existed synchronous with or prior to the esophageal lesions. This suggests that ileocolic lesions may often coexist in Crohn's patients with esophageal lesions, and that examination of the terminal ileum must be performed to confirm a diagnosis of Crohn's disease of the esophagus.

Adult↗

PubMed2000

Anomalies of inferior vena cava and left renal vein: risks in aortic surgery.

Although most aortic surgery is now routinely performed without incident, major venous anomalies can cause unexpected bleeding. In the last 6 years, 4 of 166 patients undergoing abdominal aortic surgery at our institution were found to have a major venous anomaly, including a double inferior vena cava (2), a preaortic iliac vein confluence (1), and a circumaortic renal collar (1). The 3 men and 1 woman had a mean age of 62.3 years (range, 56 to 68 years). All four patients underwent surgery for an abdominal aortic aneurysm. Preoperative imaging revealed all of the venous anomalies except for the renal collar. Unexpected venous injuries complicated the operation in one patient who had a double inferior vena cava and an inflammatory abdominal aortic aneurysm and in the patient with the circumaortic renal collar. Major venous anomalies are rarely encountered in patients undergoing aortic surgery. Preoperative assessment and intraoperative awareness are important to prevent unexpected venous injuries. Patients with an anomaly of the left renal vein and an inflammatory abdominal aortic aneurysm are at a particularly high risk.

Aged↗

PubMed2000

Cell-to-cell interaction prevents cell death in cultured neonatal rat ventricular myocytes.

OBJECTIVES: Loss of cardiac cells and the anatomical or functional remodeling of intercellular coupling occur under several pathological conditions. We have assessed the significance of intercellular coupling for cell death. METHODS AND RESULTS: Ventricular cells obtained from 1 day old Wistar rats were cultured. Apoptosis was detected by nick-end labeling. Cells were plated at low and high cell density (3x10(4)/ml and 12x10(4)/ml, respectively). Cultured myocytes died spontaneously by apoptosis in a time dependent manner. The increase of the apoptotic cell population in a culture with high cell density on day 4 (1+/-1.2%, n=4) was significantly lower than that in a culture with low cell density (20+/-5.5%, n=4). The progression of apoptosis in the culture of low cell density was prevented in part after application of the medium extract from the culture of high cell density; the apoptotic cell population on day 6 decreased from 57+/-8.0% (n=4) to 36+/-3.8% (n=4). Treatment of the cultured myocytes at high cell density with antisense oligonucleotide for connexin43 (Cx43) for 24 h on day 2 resulted in a significant decrease in Cx43 expression as judged by Western blot, dye transfer and immunocytochemistry using mouse monoclonal antibody for Cx43. In association with the down-regulation of Cx43, the progress of apoptosis was accelerated; the apoptotic cell population on day 5 in the antisense-treated cultures (27+/-5.7%, n=4) was significantly higher than the sense-treated cultures (5+/-1.1%, n=4). The effect of Cx43 antisense treatment to promote apoptosis was not reversed by application of high cell-density culture medium. CONCLUSIONS: These findings suggest that cell-cell communication through gap junction formation and some humoral factors play important roles in the survival of cultured myocytes.

Actinin↗

PubMed2000

Pacing-induced heart failure causes a reduction of delayed rectifier potassium currents along with decreases in calcium and transient outward currents in rabbit ventricle.

OBJECTIVE: Heart failure in patients and in animal models is associated with action potential prolongation of the ventricular myocytes. Changes in several membrane currents have been already demonstrated to underlie this prolongation. However, information on the two components (I(Kr) and I(Ks)) of the delayed rectifier potassium current (I(K)) in rapid pacing induced heart failure is lacking. METHODS AND RESULTS: Action potentials and whole-cell currents, I(K), I(to1), I(K1), and I(Ca-L) were recorded in apical myocytes of left ventricle from 10 rabbits subjected to left ventricular pacing at 350-380 beats/min for 3-4 weeks and 10 controls with sham operation. Action potential duration at 90% repolarization (APD(90)) was prolonged in myocytes from failing hearts compared to controls at both cycle lengths of 333 and 1000 ms. Both E-4031-sensitive and -resistant components of I(K) (I(Kr), I(Ks)) in myocytes from failing hearts were significantly less than those of control hearts; tail current densities of I(Kr) and I(Ks) following depolarization to +50 mV were 0.62+/-0.05 vs. 0.96+/-0.12 pA/pF (P<0.05), and 0.27+/-0.08 vs. 0.52+/-0.08 pA/pF (P<0.05), respectively. There was no significant difference between control and failing myocytes in the voltage- and time-dependence of activation of total I(K), I(Kr) and I(Ks). The peak of L-type Ca(2+) current (I(Ca-L)) was significantly reduced in myocytes from failing hearts (at +10 mV, -9.29+/-0.52 vs. -12.28+/-1.63 pA/pF, P<0.05), as was the Ca(2+)-independent transient outward current (I(to1); at +40 mV, 4.8+/-0.9 vs. 9.6+/-1.3 pA/pF, P<0.05). Steady state I-V curve for I(K1) was similar in myocytes from failing and control hearts. CONCLUSIONS: Decrease of I(K) (both I(Kr) and I(Ks)) in addition to reduced I(to1), may underly action potential prolongation at physiological cycle length and thereby contribute to arrhythmogenesis in heart failure.

Action Potentials↗

PubMed2000

Influence of excimer laser photorefractive keratectomy on the posterior corneal surface.

PURPOSE: To investigate the influence of excimer laser photorefractive keratectomy on the refraction and geometry of the posterior corneal surface. SETTING: Miyata Eye Hospital, Miyazaki, Japan. METHODS: Thirty-seven eyes of 21 patients with refractive errors of -2.00 to -9.75 diopters (D) were treated with the VISX Twenty-Twenty excimer laser system. The refractive and anteroposterior changes in the posterior corneal surface were measured using scanning-slit corneal topography (Orbscan, Orbtek, Inc.) preoperatively and 1 week and 1 and 3 months postoperatively. RESULTS: Mean posterior corneal refraction was -6.51 D +/- 0. 29 (SD) preoperatively; it decreased to -7.00 +/- 0.49 D, -7.00 +/- 0.55 D, and -6.92 +/- 0.42 D at 1 week, 1 month, and 3 months, respectively (P <.001, Tukey multiple comparison). Mean forward shift of the posterior corneal surface was 29.5 +/- 1.9 microm, 34.4 +/- 3.4 microm, and 54.3 +/- 4.0 microm at 1 week, 1 month, and 3 months, respectively. The amount of posterior corneal refractive change correlated with the degree of forward shift (r= -0.691, P <. 001). The residual corneal thickness correlated with the refractive change (r = 0.524, P <.001) and the forward shift (r = -0.851, P <. 001) of the posterior corneal surface. CONCLUSION: Photorefractive keratectomy induced significant refractive changes in the posterior corneal surface and forward shift of the cornea, both of which correlated with the thinness of the residual cornea.

Adult↗

PubMed2000

The cytoprotective role of lipopolysaccharide-induced nitric oxide against liver damage during early phase of endotoxemia in rats.

Lipopolysaccharide (LPS)-induced endotoxemia produces nitric oxide (NO); however, the role of the NO during endotoxemia is still controversial. The aim of this study was to investigate a role of LPS-induced NO during the early phase of endotoxemia. Wistar rats were intraperitoneally injected with saline or LPS at various doses (0.001, 0.01, or 5 mg/kg), and intra-abdominal NO concentration was determined by chemiluminescence before and after LPS administration at indicated times (1, 2, 6, 10, and 18 h). Serum aspartate aminotransferase and alanine aminotransferase levels were determined and histological examination was performed 10 h after LPS administration to assess liver damage. N(G)-nitro-L-arginine-methyl ester (L-NAME), a nonselective inhibitor of NO synthase, was used to investigate the possible roles of NO during LPS-induced endotoxemia. The intra-abdominal NO concentration was elevated within 2 h and reached a maximal level at 10 h after low doses of LPS injection (0.001 and 0.01 mg/kg) while liver damage was not observed. After high-dose LPS (5 mg/kg) administration, liver damage was observed and intra-abdominal NO was elevated continuously until 18 h. A time course study revealed very similar patterns of intra-abdominal NO increase after the three different dose of LPS at each times points during the first 10 h. Pretreatment of L-NAME inhibited the intra-abdominal NO release and aggravated the liver damage caused by low doses (0.001 and 0.01 mg/kg) of LPS as well as high dose (5 mg/kg) of LPS. Therefore, NO, released during the first 10 h after LPS injection, may play a cytoprotective role in the liver.

Alanine Transaminase↗

PubMed2000

Combination therapy with vascular endothelial growth factor neutralizing antibody and mitomycin C on human gastric cancer xenograft.

Antiangiogenic therapy has been proposed as a new strategy for the treatment of solid tumors. To enhance the therapeutic effect of antiangiogenic agents, combination with conventional anticancer therapy should be investigated. In the present study, we investigated the therapeutic effect of the combination of vascular endothelial growth factor neutralizing antibody (VEGF Ab) and mitomycin C (MMC) on MT-2, a human gastric cancer xenograft. When small pieces of MT-2 were transplanted orthotopically into 62 nude mice, liver metastasis developed 6 weeks after transplantation. The VEGF Ab (100 micro g / mouse) was administered i.p. in the VEGF Ab group (n = 14) and the combination group (n = 16) twice a week from day 10 after transplantation. MMC (2 mg / kg) was administered in the MMC group (n = 16) and the combination group (n = 16) on days 10, 17 and 24 after transplantation. Compared with the control group, in which saline solution was administered i.p., all three treatments inhibited tumor growth significantly and the effects of MMC and combination therapy were potent. Liver metastases were also inhibited significantly by the administration of VEGF Ab alone, MMC alone or combination therapy. Liver metastasis developed in 9 mice of the control group, 3 of the VEGF Ab group, and 4 of the MMC group, but no mice had liver metastasis in the combination therapy group. However a significant body weight loss and a decrease in spleen weight were observed in the MMC and combination groups, with no significant difference between the two groups. These results suggest that combination therapy with VEGF Ab and MMC may be a potent therapy for human gastric cancer.

Adenocarcinoma↗

PubMed2000

Overexpression of vascular endothelial growth factor is responsible for the hematogenous recurrence of early-stage gastric carcinoma.

Vascular endothelial growth factor (VEGF) is crucial for angiogenesis in various malignant tumors. However, it is still unclear whether VEGF is responsible for hematogenous metastasis after the curative resection of gastric carcinoma. In the present study, we evaluated the relevance of VEGF expression to the hematogenous recurrence of stage 1 or 2 primary gastric adenocarcinoma. Among 530 patients, 11 (2.1%) had hematogenous recurrence. Clinicopathological variables were compared between these 11 patients (group R) and 88 patients without intramucosal carcinoma who survived for more than 5 years (group S). Microvessel density (MVD) was assessed immunohistochemically along with VEGF protein expression in all patients from group R and 21 randomly selected patients from group S. There were significant differences in age, tumor size and VEGF expression in tumor tissue between the groups. Positive staining for VEGF protein was observed in all patients of group R, of whom 6 had strongly positive staining. On the other hand, 11 out of 21 patients in group S had positive staining and it was weak in all cases. Both the positive and strongly positive rate were significantly higher in group R than those in group S. There was no significant difference in MVD between the 2 groups (17.7 +/- 11.09/field in group R vs. 14.8 +/- 10. 27/field in group S) and no significant correlation between VEGF expression, MVD and venous invasion, though a weak correlation between the intensity of VEGF staining and MVD was observed (negative staining 12.1 +/- 10.51; weakly positive 16.67 +/- 10.41; strongly positive 19.7 +/- 9.97). Our results suggest that overexpression of VEGF, and not MVD or venous invasion, plays an important role in the hematogenous recurrence of curatively resected gastric carcinoma.

Adult↗

PubMed2000

Rupture of infected pseudoaneurysms in patients with implantable ports for intra-arterial infusion chemotherapy.

Intra-arterial hepatic chemotherapy via implantable reservoirs is being used increasingly. In our department, five patients have undergone emergency surgery since 1991 because of rupture of an infected pseudo-aneurysm at the site of entry of the catheter. Surgical procedures included removal of the catheter and the reservoir, and closure of the affected artery with or without reconstruction. Of these patients, three (60%) died from uncontrollable sepsis. The poor prognosis emphasizes the need, in patients with carcinoma, for strict aseptic technique and hemostasis at the time of catheter placement, and for careful device maintenance.

Adult↗

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↗

PubMed1999

Dynamic character of the complex of human blood coagulation factor VIIa with the extracellular domain of human tissue factor: a normal mode analysis.

As an attempt to investigate the dynamic interactions between plasma serine protease, coagulation factor VIIa (VIIa) and its cofactor, tissue factor (TF), we performed normal mode analysis (NMA) of the complex of VIIa with soluble TF (the extracellular part of TF; sTF). We compared fluctuations of Calpha atoms of VIIa or sTF derived from NMA in the VIIa-sTF complex with those of VIIa or sTF in an uncomplexed condition. The atomic fluctuations of the Calpha atoms of sTF complexed with VIIa did not significantly differ from those of sTF without VIIa. In contrast, the atomic fluctuations of VIIa complexed with sTF were much smaller than those of VIIa without sTF. These results suggest that domain motions of VIIa molecule alone are markedly dampened in the VIIa-sTF complex and that the sTF molecule is relatively more rigid than the VIIa molecule. This may indicate functions of TF as a cofactor.

Amino Acids↗

PubMed1999

Amiodarone: ionic and cellular mechanisms of action of the most promising class III agent.

Amiodarone is the most promising drug in the treatment of life-threatening ventricular tachyarrhythmias in patients with significant structural heart disease. The pharmacologic profile of amiodarone is complex and much remains to be clarified about its short- and long-term actions on multiple molecular targets. This article reviews electrophysiologic effects of amiodarone based on previous reports and our own experiments in single cells and multicellular tissue preparations of mammalian hearts. As acute effects, amiodarone inhibits both inward and outward currents. The inhibition of inward sodium and calcium currents (I(Na), I(Ca)) is enhanced in a use- and voltage-dependent manner, resulting in suppression of excitability and conductivity of cardiac tissues especially when stimulated at higher frequencies and in those with less-negative membrane potential. Both voltage- and ligand-gated potassium channel currents (I(K), I(K,Na), I(K,ACh)) are also inhibited at therapeutic levels of drug concentrations. Acutely-administered amiodarone has no consistent effect on the action potential duration (APD). The major and consistent long-term effect of the drug is a moderate APD prolongation with minimal frequency dependence. This prolongation is most likely due to a decrease in the current density of I(K) and I(to). Chronic amiodarone was shown to cause a down-regulation of Kv1.5 messenger ribonucleic acid (mRNA) in rat hearts, suggesting a drug-induced modulation of potassium-channel gene expression. Tissue accumulation of amiodarone and its active metabolite (desethylamiodarone) may modulate the chronic effects, causing variable suppression of excitability and conductivity of the heart through the direct effects of the compounds retained at the sites of action. Amiodarone and desethylamiodarone could antagonize triiodothyronine (T3) action on the heart at cellular or subcellular levels, leading to phenotypic resemblance of long-term amiodarone treatment and hypothyroidism.

Amiodarone↗

PubMed1999

Carvedilol blocks the repolarizing K+ currents and the L-type Ca2+ current in rabbit ventricular myocytes.

Carvedilol ((+/-)-1-(carbazol-4-yloxy)-3-[[2-(o-methoxyphenoxy)ethyl]am ino]-2-propanol), a beta-adrenoceptor-blocking agent with vasodilator properties, has been reported to produce dose-related improvements in left ventricular function and reduction in mortality in patients with chronic heart failure. However, its electrophysiological effects have not been elucidated. We studied ion channel and action potential modulation by carvedilol in rabbit ventricular preparations using whole-cell voltage-clamp and standard microelectrode techniques. In ventricular myocytes, carvedilol blocked the rapidly activating component of the delayed rectifier K+ current (I(Kr)) in a concentration-dependent manner (IC50 = 0.35 microM). This block was voltage- and time-independent; a prolongation of the depolarizing pulses from a holding potential of -50 mV to +10 mV within the range of 100-3000 ms did not affect the extent of I(Kr) block. Carvedilol also inhibited the L-type Ca2+ current (I(Ca)), the transient outward K+ current (I(to)) and the slowly activating component of the delayed rectifier K+ current (I(Ks)) with IC50 of 3.59, 3.34, and 12.54 microM, respectively. Carvedilol (0.3-30 microM) had no significant effects on the inward rectifier K+ current. In papillary muscles from rabbits pretreated with reserpine, action potential duration was prolonged by 7-12% with 1 microM and by 12-24% with 3 microM carvedilol at stimulation frequencies of 0.1-3.0 Hz. No further action potential duration prolongation was observed at concentrations higher than 3 microM. These results suggest that concomitant block of K+ and Ca2+ currents by carvedilol resulted in a moderate prolongation of action potential duration with minimal reverse frequency-dependence. Such electrophysiological effects of carvedilol would be beneficial in the treatment of ventricular tachyarrhythmias.

Action Potentials↗

PubMed1999

Mutations of a novel human RAD54 homologue, RAD54B, in primary cancer.

Association of breast tumor susceptibility gene products BRCA1 and BRCA2 with the RAD51 recombination protein suggested that cancer could arise through defects in recombination. The identification of NBS1, responsible for Nijmegen breakage syndrome, from the MRE11/RAD50 recombination protein complex also supports this hypothesis. However, our mutation analysis revealed that known members of the RAD52 epistasis group are rarely mutated in human primary cancer. Here we describe the isolation of a novel member of the SNF2 superfamily, characterized with sequence motifs similar to those in DNA and RNA helicases. The gene, designated RAD54B, is significantly homologous to the RAD54 recombination gene. The expression of RAD54B was high in testis and spleen, which are active in meiotic and mitotic recombination. These findings suggest that RAD54B may play an active role in recombination processes in concert with other members of the RAD52 epistasis group. RAD54B maps to human chromosome 8q21.3-q22 in a region associated with cancer-related chromosomal abnormalities. Homozygous mutations at highly conserved positions of RAD54B were observed in human primary lymphoma and colon cancer. These findings suggest that some cancers arise through alterations of the RAD54B function.

Adenocarcinoma↗

PubMed1999

Mutations in the RAD54 recombination gene in primary cancers.

Association of a recombinational repair protein RAD51 with tumor suppressors BRCA1 and BRCA2 suggests that defects in homologous recombination are responsible for tumor formation. Also recent findings that a protein associated with the MRE11/RAD50 repair complex is mutated in Nijmegen breakage syndrome characterized by increased cancer incidence and ionizing radiation sensitivity strongly support this idea. However, the direct roles of BRCA proteins and the protein responsible for NBS in recombinational repair are not clear though they are associated with the recombinational repair complexes. Since RAD51 forms a complex with other members of the RAD52 epistasis group and with BRCA proteins, it is reasonable to ask if alterations of members of the RAD52 epistasis group lead to tumor development. Here we describe missense mutations at functional regions of RAD54 and the absence of the wild-type RAD54 expression resulting from aberrant splicing in primary cancers. Since RAD54 is a recombinational protein associated with RAD51, this is the first genetic evidence that cancer arises from a defect in repair processes involving homologous recombination.

Adenocarcinoma↗

PubMed1999

Orientation change of cardiocytes induced by cyclic stretch stimulation: time dependency and involvement of protein kinases.

UNLABELLED: Mechanical stress has been implicated as one of the growth regulators in the heart. We investigated the effect of cyclic stretch stimulation on morphology and orientation of cultured cardiocytes. Embryonic rat (17 days postcoital) cardiomyocytes cultured on silicone dishes were cyclically stretched to 120% in length at a frequency of 30 cycles/min. After 12 h, in the initial stage of cultivation, cardiocytes and intracellular myofibrils oriented parallel to the stretch direction. When the stretch stimulus was prolonged to 24-48 h, myofibrils that oriented perpendicular to the stretch direction emerged. Furthermore, when the cells were stretched only in the later stage (after 24 h of cultivation), both cells and myofibrils tended to orient perpendicular to the stretch direction. Next we examined the effects of chemical compounds on these phase-related changes in myofibril orientation. None of the drugs tested (H-7, HA-1004, staurosporine, herbimycin A, genistein, GdCl3, and EGTA) blocked the parallel orientation of myofibrils induced by the initial-stage stretch. By contrast, H-7, staurosporine, herbimycin A, and genistein did inhibit almost completely the perpendicular orientation of the myofibrils induced by the late-stage stretch, but HA-1004, GdCl3, or EGTA did not. Immunoblotting study using anti-phsophotyrosine antibody indicated that tyrosine phosphorylation of a protein of about 125 kDa was enhanced in a time-dependent manner by the late-stage stretch, but not by the initial-stage stretch. IN CONCLUSION: the alignment change induced by cyclic stretch depends on the stage of cultivation: with stretch in the initial stage (within 12 h), cells and myofibrils orient parallel to the stretch; with stretch in the later stage (after 24 h), they orient perpendicular to the stretch. The effect of stretch in the later stage is likely mediated by protein kinase C and tyrosine kinase pathways.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1999

Hypoxia inhibits the changes in action potentials and ion channels during primary culture of neonatal rat ventricular myocytes.

Action potentials of rat ventricular myocytes are progressively shortened after birth within several weeks mainly due to a progressive increase in transient outward potassium current (I(to)). On the supposition that an elevation in blood oxygen after birth may contribute to such developmental change, we studied effects of long-term exposure to hypoxia on changes in cardiac action potentials and I(to). Single ventricular myocytes isolated from day-old neonatal rat hearts were cultured in normoxic condition (21% O(2)) for 15 days and served as control. To test the influence of long-term exposure to hypoxia, O(2)tension was reduced to 7.5% at day 6 during culture. In 15-day cells cultured in normoxia, action potential duration (APD) was shortened by 44% (n=11) compared with 5-day cells (n=10); cell capacitance was increased to 2.0-fold. I(to)density was increased by 189-265% (n=11) at voltage levels from -20 to 50 mV without any changes in the kinetics of current inactivation. In 15-day cells cultured in hypoxia, APD was shortened only by 16% (n=6) from control; the increment of cell capacitance was 2.1-fold (n=6). The I(to)increment was limited to 53% (n=8); both inactivation and its recovery of the current was apparently slowed due to the amplification of the slower component. These results suggest that the developmental augmentation of I(to)expression during culture requires oxygen and the increase in I(to)and cell hypertrophy are likely regulated independently.

Action Potentials↗

PubMed1999

Simultaneous repair of arch and abdominal aortic aneurysms. A simple new technique using a temporary bypass graft.

OBJECTIVE: Atherosclerotic aneurysms in the aortic arch are associated with abdominal aortic aneurysms in up to 37% of cases. We have developed a single-stage approach to the repair of both aneurysms using a temporary bypass. SUBJECTS: Since November 1996, 5 patients underwent simultaneous repair of aneurysms in the aortic arch and in the infrarenal abdominal aorta, using a new temporary bypass graft technique. Entire arch replacement with simultaneous abdominal aortic aneurysmectomy was performed in one patient. The other 4 patients underwent distal hemi-arch replacement distal from the orifice of the brachiocephalic artery with simultaneous repair of the abdominal aortic aneurysm. METHOD: For the entire arch replacement procedure, blood flow to all major branches of the aortic arch was established using a bifurcated graft. This graft anastomosed to the ascending aorta was used as the proximal inflow of the temporary bypass graft. For the hemi-arch replacement procedure, the proximal inflow segment of the temporary bypass graft was anastomosed to the brachiocephalic artery. In both cases, the distal outflow segment of the temporary bypass graft was the graft used for repair of the abdominal aortic aneurysm. In order to prevent any clamp injury, Teflon felt was tightly wrapped around the aorta before the clamp was applied. RESULTS: Evaluation of the hemodynamic parameters measured during cross-clamping of the aortic arch revealed stable distal perfusion to the visceral organs and no excessive increase in cardiac afterload. All patients had an uneventful postoperative course and were discharged within 1 month of surgery. CONCLUSION: Our temporary bypass method is recommended for simultaneous replacement of aneurysms in the aortic arch and the abdominal aorta.

Aged↗