Biomedical subjects

T Ban

Publications and source records attributed to T Ban.

At least 37 records · Page 2Linked to original sources

PubMed1997

[A successful surgical repair of congenital mitral stenosis due to commissural papillary muscle fusion].

A case of congenital mitral stenosis, patent ductus arteriosus, pulmonary hypertension was reported. At one year of age, the patient underwent surgical division of PDA because of persistent left heart failure. She went well after the operation. At seven year of age, she was readmitted to our hospital for easy fatigability. The cardiac catheterization revealed remarkably elevated pulmonary arterial pressure and pulmonary capillary wedged pressure. She underwent a surgical intervention for the mitral stenosis at eight year of age. At operation, the mitral valve exhibited the characteristics of type IIc according to Carpentier's classification: thickened and dysplastic leaflet, extremely short chordae tendanae fused with papillary muscles, obliteration of interchordal space and hypertrophic two papillary muscles. We replaced the valve with 23 mm Carbomedicus prosthetic valve because it seemed to be difficult to repair the native valve satisfactorily without residual stenosis or insufficiency. Her postoperative course was uneventful and the pulmonary arterial pressure and pulmonary capillary wedged pressure decreased remarkably one year after the operation.

Child↗

PubMed1997

In vivo testing of a magnetically suspended centrifugal pump designed for long-term use.

The life of currently-available centrifugal pumps is limited to no more than three days. As a magnetically suspended centrifugal pump (MSCP) contains no shaft or seal, it could be expected to have a longer life expectancy. The MSCP was evaluated in a chronic animal model using eight adult sheep. Left ventricular assist with the MSCP was instituted between the left atrium and the descending aorta. The flow rates ranged from 2.5 to 6.0 L/min. The duration of the experiments ranged from 14 to 60 days. No mechanical failure occurred. The plasma free hemoglobin levels remained within an acceptable range (3-19 mg/dL). No reduction in the counts of red blood cells or platelets was observed. Thrombus formation within the MSCP was recognized in one pump. The main reason for termination was thromboembolism derived from the circuits. Three types of regulation methods (constant rotational speed, constant motor current, and controlled motor current) were also investigated. Regulation by a constant motor current mode altered the pressure-flow (P-Q) characteristics, and thereby, a steadier pump flow was obtained compared with regulation in the constant rotational speed mode. Moreover, the controlled motor current mode can change the P-Q relationship. These results demonstrate that the MSCP is a promising device for long-term use.

Animals↗

PubMed1996

Reperfusion causes significant activation of heat shock transcription factor 1 in ischemic rat heart.

BACKGROUND: The myocardial protective role of heat shock protein (HSP) has been demonstrated, and there has been increasing interest in stress response in the heart. We examined the DNA-binding activity of heat shock transcription factor (HSF), by which the transcription of heat shock genes is mainly regulated, during heat shock or ischemia/reperfusion in isolated rat heart. METHODS AND RESULTS: Rat hearts were isolated and perfused with Krebs-Henseleit buffer by the Langendorff method. Whole-cell extracts were prepared for gel mobility shift assay using oligonucleotides containing the heat shock element, which is present upstream of all heat shock genes. Induction of mRNAs for HSP70, HSP90, and GRP78 (glucose-regulated protein) was examined by Northern blot analysis. Although the activation of HSF during global ischemia was weak and rapidly attenuated, postischemic reperfusion induced a significant activation of HSF. In addition, although HSP70 mRNA was hardly induced during ischemia, its burst induction was detected during postischemic reperfusion. Supershift assays using specific antisera for HSF1 and HSF2 revealed that ischemia/reperfusion as well as heat shock induced the activation of HSF1 in hearts. Although the expression of HSP70 mRNA during heat shock was more vigorous than the expression during ischemia/reperfusion, the induction of HSP90 mRNA in postischemic reperfusion was significantly greater than that in heat shock. CONCLUSIONS: Our findings demonstrated that reperfusion causes a significant activation of HSF1 in ischemia-reperfused heart. The striking contrast between the induction of HSP70 mRNA and that of HSP90 mRNA suggests the presence of regulatory mechanisms other than HSF.

Animals↗

PubMed1996

Analysis of right ventricular function during bypass of the left side of the heart by afterload alterations in both normal and failing hearts.

This study investigated the mechanism of right ventricular failure during bypass of the left side of the heart by precisely assessing right ventricular function with use of a conductance catheter. Bypass of the left side of the heart was established with a centrifugal pump in 10 mongrel dogs weighing 11 to 19 kg. Right ventricular function during left heart bypass was evaluated by two parameters that were both derived from measurement of relative change in right ventricular volume by the conductance catheter technique. One parameter was the right ventricular end-systolic pressure-volume relationship as a load-independent index, and the other was the peak right ventricular pressure-right ventricular stroke volume relationship as a "force-velocity relationship." These parameters were measured in both normal and failing hearts while afterload was increased by bilateral intrapulmonary balloon inflation. Moreover, changes in these relationships were observed by varying assist ratios of left heart bypass from 0% to 100%. Failing heart models were induced by normothermic aortic clamping for 20 minutes. The right ventricular end-systolic pressure-volume relationship in normal hearts did not change, irrespective of the assist ratio of left heart bypass, whereas that in failing hearts decreased from 4.25 +/- 1.41 mm Hg/ml without bypass of the left side of the heart to 3.53 +/- 1.30 mm Hg/ml after 100% assist of left heart bypass (p < 0.05). In the peak right ventricular pressure-right ventricular stroke volume relationship, right ventricular stroke volume was almost constant in normal hearts when afterload was increased regardless of the assist ratio of left heart bypass. Moreover, right ventricular stroke volume was maintained at a higher level during bypass of the left side of the heart compared with that without left heart bypass. However, that slope of the relationship in failing hearts was inversely linear and became significantly steeper after 100% assist of bypass of the left side of the heart compared with that without left heart bypass (-0.131 +/- 0.042 versus -0.051 +/- 0.038, p < 0.005). Therefore ++these two slopes of the relationship intersected at a point that was considered the critical point of afterload during bypass of the left side of the heart. In other words, right ventricular stroke volume was decreased by 100% left heart bypass above the critical point of afterload. In conclusion, this study demonstrates not only that bypass of the left side of the heart results in an increase in right ventricular stroke volume in both normal and failing hearts at the physiologic range of afterload, but also that right ventricular function against higher afterload is impaired by 100% assist of bypass of the left side of the heart in failing hearts.

Animals↗

PubMed1996

Influence of hepatic mitochondrial redox state on complement biosynthesis and activation during and after cardiopulmonary bypass operations.

We have proposed the hazardous phenomena associated with cardiopulmonary bypass (CPB) are due to metabolic derangement by hepatic mitochondrial dysfunction during and after CPB. On the contrary, complement activation and consumption during CPB is reported to be related to the morbidity associated with cardiac surgery. To determine the significance of the hepatic mitochondrial function on the morbidity of cardiac surgery, we measured the serum levels of complements (C3 and C4), activated complements (C3a and C4a), and the arterial ketone body ratio (AKBR), which reflects the hepatic mitochondrial redox state, in 30 patients undergoing CPB. The AKBR, which was at a normal level preoperatively, dropped to a critical level after the initiation of CPB and remained at a low level during the CPB, returning to the preoperative level on the second postoperative morning in a time dependent fashion. The patients group were assigned to two groups according to their AKBR on the first postoperative morning. Group I consisted of patients whose AKBR had recovered to above 0.7 on the first postoperative morning (n = 16). Group II consisted of the rest of the patients (n = 14). The serum complement concentration had considerably decreased by the end of bypass, but recovered in a time-dependent fashion after CPB. The group I patients (C3: 71% of its preoperative value, C4: 85% of its preoperative value) recovered their complements more quickly than the group II patients (C3: 56% of its preoperative value, C4: 54% of its preoperative value). However, the serum C3a and C4a concentrations increased by the end of bypass (C3a: 806% of its preoperative value, C4a: 341% of its preoperative value). The activated complements were significantly higher in the group II patients (C3a: 124% of its preoperative value, C4a: 236% of its preoperative value) than in the group I patients (C3a: 75% of its preoperative value, C4a: 113% of its preoperative value) on the first postoperative morning. It is suggested that hepatic mitochondrial function is related to recovering the complements and to reducing the activated complements after CPB.

Adolescent↗

PubMed1996

Protection against reperfusion-induced arrhythmias by human thioredoxin.

Adult T-cell leukemia-derived factor (ADF), identified in the supernatant of adult T-cell leukemia (ATL) cell culture, is a human homologue of thioredoxin and consists of 104 amino acids; it has two redox-active half-cysteine residues in an exposed active center. Human thioredoxin has many biological activities, including growth promotion, cell activation, and a catalase-like radical scavenging activity. We examined the protective effect of human thioredoxin (h-thioredoxin) against reperfusion-induced arrhythmias in an isolated rat heart model with 10-min regional ischemia followed by 30-min reperfusion. Male Wistar rats were assigned to six groups: a control, a superoxide dismutase (SOD 8 x 10(4) IU/L), and a catalase group (1 x 10(6) IU/L), and three groups treated with h-thioredoxin [approximately .01 microM (TRX-I group), approximately 0.1 microM (TRX-II group), and approximately 1 microM (TRX-III group)]. In the early reperfusion period, h-thioredoxin reduced the incidence of ventricular fibrillation (VF) to 8% in the TRX-II group (p < 0.01) from the control value of 75%. SOD and catalase reduced the incidence of VF to 43 and 33%, respectively (NS). During the entire reperfusion period, the incidence of VF in the SOD group was 79%, as compared to 83% in the control group. In the catalase and TRX-II groups, the incidence of VF was significantly reduced to 42 and 25%, respectively. These findings indicate that SOD failed to protect against the reperfusion-induced arrhythmias. h-Thioredoxin exerted a protective effect against these arrhythmias; a concentration of approximately 0.1 micro was the most effective.

Animals↗

PubMed1996

A new magnetically suspended centrifugal pump: in vitro and preliminary in vivo assessment.

To overcome problems derived from the shaft within the conventional centrifugal pump, we have been developing a new centrifugal pump, namely a magnetically suspended centrifugal pump (MSCP), which has no shaft and operates as a noncontacting and bearingless pump. The impeller is suspended magnetically between the magnetic bearing and the driving motor. Hemolysis tests were performed in comparison with the Biopump (BP80, BioMedicus). The index of hemolysis (IH) was significantly lower in the MSCP than in the Biopump. In addition, a smaller gap in the MSCP induced lower hemolysis. In preliminary studies using mongrel dogs, the layer of thrombus adherent to the impeller was observed in a few hours, which impaired the pumping efficiency. However, by using an impeller coated with silicone, no aggregations of platelets or fibrin on the impeller were observed in 24 h of continuous pumping. In conclusion, the MSCP had a gentler influence on blood cells than the Biopump, and the impeller coated with silicone may contribute to the long-term pumping of the MSCP.

Animals↗

PubMed1996

Natriuretic peptide receptors in human artery and vein and rabbit vein graft.

Natriuretic peptides elicit their biological effects by elevation of cGMP through activation of two biologically active receptors: natriuretic peptide A receptor, which shows high affinity to atrial and brain natriuretic peptides, and natriuretic peptide B receptor, which is specific to C-type natriuretic peptide. To elucidate the implications of the natriuretic peptide system in arteries and veins, we examined the cGMP production in response to atrial and C-type natriuretic peptide and gene expressions of biologically active natriuretic peptide receptors in human gastroepiploic artery, internal mammary artery, and saphenous vein. Atrial natriuretic peptide augmented cGMP production more potently by one order of magnitude in arteries than in veins. C-type natriuretic peptide stimulated cGMP production weakly and equally in these vessels. Analyzed by reverse transcription-polymerase chain reaction, gene expression of natriuretic peptide A receptor was four times more abundant in arteries than in veins. Gene expression of natriuretic peptide B receptor was approximately the same between these vessels. We also studied the responsiveness to atrial and C-type natriuretic peptide in rabbit jugular vein grafted into carotid artery. In arterialized vein grafts 4 weeks after operation, the effects of atrial and C-type natriuretic peptides on cGMP production did not change from those in jugular veins. In conclusion, atrial natriuretic peptide stimulates cGMP production more potently in arteries than in veins due to the preferential expression of natriuretic peptide A receptor in arteries. These observations support the distinct roles of natriuretic peptides in cardiovascular homeostasis.

Aged↗

PubMed1996

Thyrotropin induces G1 cyclin expression and accelerates G1 phase after insulin-like growth factor I stimulation in FRTL-5 cells.

We have investigated the mechanism by which TSH pretreatment potentiates insulin-like growth factor I (IGF-I)-induced DNA synthesis in FRTL-5 cells. As previously described, pretreatment with TSH increased IGF-I-induced DNA synthesis, suggesting that the effect of TSH is mediated through the cAMP pathway. TSH and A kinase activators required at least 12 h to precondition cells to respond to IGF-I stimulation. The presence of cycloheximide abolished the effect of TSH to increase IGF-I-induced DNA synthesis. When the time course of thymidine uptake after IGF-I addition was studied, TSH pretreatment increased the maximum DNA incorporation and shortened the G1 phase interval. These results indicated that some proteins induced by TSH are required for the effect of TSH on IGF-I activity, and the proteins are important for cell cycle progression. Cyclins are key regulators of the cell cycle; therefore, we investigated the expression of cyclins D1 and E after TSH stimulation. TSH- and A kinase-activating agents increased the expression of cyclins D1 and E after 24 h. The same amounts of cyclins D1 and E induced by IGF-I were increased after TSH pretreatment. TSH pretreatment induced the expression of G1 cyclin in FRTL-5 cells, and IGF-I caused the accumulation of enough G1 cyclins to drive the cell cycle from G1 to S phase in a short time, which accounts for the effect of TSH on IGF-I induced DNA synthesis.

Animals↗

PubMed1996

Action potential duration-stabilizing action of taurine in guinea pig ventricular myocytes.

To examine taurine actions on the rate of repolarization of action potentials (AP), L-type Ca2+ (ICa), late outward K+ (Ik) and the inward rectifier currents as affected by the external Ca2+ concentrations ([Ca2+]o), whole-cell voltage-clamp and current-clamp experiments were conducted in guinea pig ventricular myocytes. At a high (3.6 mM) [Ca2+]o, 10 mM taurine suppressed both ICa and IK, shortened AP duration and decelerated the rate (-dV/dt) of terminal repolarization of AP. In contrast, at a low (0.9 mM) [Ca2+]o, taurine intensified both ICa and IK, lengthened AP duration and accelerated -dV/dt. However, at either [Ca2+]o, the resting membrane potential was slightly hyperpolarized, and the inward rectifier, current examined by the ramp-pulse protocol remained unaffected by taurine. Taurine is suggested to maintain a stable AP duration by altering the inward Ca2+ and IK in the opposite directions, depending on [Ca2+]o. The relevance of the stabilizing action of taurine on the AP duration to its reported anti-arrhythmic efficacies is discussed.

Action Potentials↗

PubMed1996

Kinetic mechanism of Na+ channel depression by taurine in guinea pig ventricular myocytes.

To examine effects of taurine on the kinetics of the Na+ channel current (I(Na)), action potentials and whole-cell Na+ currents were recorded from single ventricular myocytes of guinea pigs. Kinetic parameters for the activation and inactivation of I(Na) were determined in accordance with the first-order kinetic model. Changes in the kinetic parameters were assessed before and after taurine exposure (5-50 mM). While taurine at concentrations higher than 10 mM decreased the peak I(Na) by ca. 15%, the agent did not alter the reversal potential and the maximum Na+ conductance (GNa). Taurine shifted the steady-state inactivation (h(infinity)) curve toward the negative potential direction and decreased the slope of h(infinity). Concomitantly, the slope of the steady-state activation (m(infinity)) was also slightly decreased and the rate of inactivation in the large potential region (-40 to -30 mV) slightly increased, whereas the rate of the activation appeared to remain unchanged. It is suggested that taurine alters the surface charge of the membrane and reduces the number of charges moving upon activation and inactivation of channels, thereby reducing I(Na).

Action Potentials↗

PubMed1996