PubMed Health⌕ Search

Biomedical subjects

Y Kira

Publications and source records attributed to Y Kira.

At least 37 records · Page 2Linked to original sources
PubMed1996

[Effects of the time interval between the first and second balloon inflations on ischemic preconditioning during percutaneous transluminal coronary angioplasty].

Ischemic preconditioning is an attenuation of myocardial ischemia by repeated brief coronary occlusions observed during percutaneous transluminal coronary angioplasty (PTCA). The effects of the time delay between balloon inflations during PTCA on ischemic preconditioning were investigated in 48 patients with chronic stable angina but no rich collateral vessels. After successful predilatation, two 2-min balloon inflations were performed and the ST segment elevation in the electrocardiogram and chest pain were measured during each balloon inflation and compared. Patients were divided into three groups according to the interval between balloon inflations; 1 min (I1), 2 min (I2) and 5 min (I5). There were no significant differences in ST elevation (3.4, 3.2 and 3.7 mm) and chest pain during the first balloon inflation between these three groups. ST elevation and chest pain were decreased in groups I2 and I5 (2.6 and 2.8 mm) during the second balloon inflation compared with those during the first balloon inflation. However, there was no significant difference in ST elevation and chest pain during the first and second (3.7 mm) balloon inflations in group I1. ST elevation and chest pain were reduced more in group I5 than in I2. These results suggest that an interval of more than 2 min between balloon inflations is necessary to obtain the effect of ischemic preconditioning during PTCA.

Aged↗
PubMed1994

Adenosine as an endogenous mediator of hypoxia for induction of vascular endothelial growth factor mRNA in U-937 cells.

Adenosine induced by hypoxia exerts various effects via different types of receptors. Recently, hypoxia was shown to be a strong inducer of vascular endothelial growth factor, a secreted endothelial cell specific mitogen. In this report, we studied on effects of adenosine on inducibility of VEGF and possible mediation of hypoxia for its induction in U-937 cells. Hypoxia induced expression of VEGF mRNA with an early peak at 1 hour. 5'-N-ethylcarboxamidoadenosine, an adenosine analog, strongly induced VEGF mRNA, which was inhibited by 3,7-dimethyl-1-propargylxanthine (DMPX), an A2-antagonist. The hypoxic induction was inhibited by adenosine deaminase, 7-(beta-hydroxyethyl)theophylline, a non-selective adenosine receptor antagonist and DMPX. These results suggest that the hypoxic induction of VEGF mRNA is mediated by adenosine via A2-receptor in U-937 cells.

Adenosine↗
PubMed1994

Effect of long-term cyclic mechanical load on protein synthesis and morphological changes in cultured myocardial cells from neonatal rat.

We studied the effect of prolonged cyclic mechanical stimulation on protein synthesis and morphological changes in cultured cardiac myocytes isolated from 3-day-old neonatal rats to develop an in vitro model for cardiac hypertrophy induced by a mechanical load. Myocardial cells were cultured on deformative culture plates with M-199 culture medium in the presence or absence of fetal calf serum (FCS), and a cyclic mechanical load was applied for 2 hours up to 15 days. Mechanical stimulation for 2 hours increased the 14C-phenylalanine incorporation rate of myocardial cells, both in the absence and presence of FCS or when the myocardial cells were either beating or arrested with tetrodotoxin. The incorporation rate always increased by mechanical stimulation during 15 days of cell culture as compared to cells that sustained no mechanical stress. The cell size and protein content, which increased gradually with mechanical stimulation and reached a maximum at 10 days, were even greater in the presence of FCS. Within 10 days myocardial cells had aligned in the direction of the maximal cyclic mechanical load. In these cells electron microscopy revealed an increase in the number of myofilaments associated with the development of mitochondria as recognized in the adult myocardial cells. These results indicate that long-term cyclic mechanical loading of cultured myocardial cells may be a good in vitro model for the study of cardiac hypertrophy.

Animals↗
PubMed1994

Rapid induction of vascular endothelial growth factor expression by transient ischemia in rat heart.

Vascular endothelial growth factor (VEGF or vascular permeability factor), a direct-acting, endothelial cell-specific mitogen, has been suggested to be involved in development and maintenance of vasculatures in tumor neovascularization and in normal tissues. To investigate possible roles of VEGF in ischemic hearts, we studied induction of VEGF mRNA by ischemia and hypoxia using coronary artery-ligated hearts in vivo and perfused hearts and cultured myocardial cells in vitro. VEGF mRNA was potently induced by ischemia in the heart in vivo. In perfused hearts, maximum expression was rapidly induced (within 30 min) by transient reversible ischemia (5-10 min of ischemia) and lasted at least 3 h. Induction was also caused by hypoxia, which was confirmed in perfused hearts and cultured myocardial cells. These results suggest that induction of VEGF mRNA is upregulated by oxygen deprivation in the heart and that not only infarction but also chronic ischemia in the clinical setting could induce VEGF as a potent angiogenesis factor to stimulate coronary collateral formation.

Animals↗
PubMed1993

High incidence of mitral and tricuspid regurgitation in patients with Graves' disease detected by two-dimensional color Doppler echocardiography.

With two-dimensional (2D) color Doppler echocardiography, the cardiac and valvular function of 24 consecutive patients with a history of Graves' disease (17 were hyperthyroid and 7 were euthyroid at the time of the examination) were evaluated. The incidences of mitral regurgitation (MR), tricuspid regurgitation (TR) and MR plus TR were significantly higher in the patients with Graves' disease than in the age-matched control group of patients without this disease. In the patients who had signs of congestive heart failure (CHF) while they were hyperthyroid, a significantly higher incidence of severe TR was observed. This is the first report of a 2D color Doppler echocardiography study on the incidences of TR and/or MR in patients with Graves' disease. Our data indicate that in Graves' disease valvular dysfunction can be caused by systemic disorders and that severe TR is a possible risk factor for CHF.

Adult↗
PubMed1989

Pathological analysis of the right ventricular hypertrophy and ventricular interdependence in autopsied hearts with cor pulmonale and pulmonary hypertensive rat hearts.

Thirty autopsied hearts with cor pulmonale and 20 experimental pulmonary hypertensive rat hearts were analysed macroscopically and histometrically. In autopsied hearts with cor pulmonale, right ventricle dilatated in oblique length, and right ventricular wall thickness significantly increased at pulmonary conus (PC) and posterior wall of right ventricle (RVP) compared with that at anterior wall of right ventricle (RVA). Mean diameters of myocardial fibers at PC, RVP, right ventricular side of interventricular septum (IVR) and mid layer of interventricular septum (IVM) significantly increased compared with that at mid layer of left ventricular wall (LVM). The wet weight and the diameter of myocardial fibers in right ventricle (RV) significantly correlated with those in interventricular septum (IVS). In pulmonary hypertensive rats, wet weights of RV and IVS increased significantly with the elevation of mean pulmonary arterial pressure. The diameters of myocardial fibers increased at RVP, RVA, IVR and IVM. There was no significant cardiac hypertrophy in left ventricle (LV), either microscopically or macroscopically. These results suggest that IVS responded morphometrically rather than in concord with RV but not with LV in the cor pulmonale heart.

Adult↗
PubMed1989

Risk factors for the complication of cerebral infarction in Japanese patients with acute myocardial infarction.

The incidence and risk factors for cerebral infarction in Japanese patients with acute myocardial infarction were evaluated. Seven (5.0%) of 140 patients with acute myocardial infarction suffered from cerebral infarction during their initial hospitalization. The incidence was slightly higher than those reported in Western countries. Anterior wall myocardial infarction and a past history of cerebrovascular disease were considered to be probable risk factors for the complication. A beneficial effect of anticoagulant therapy in preventing cerebral infarction in cases of acute myocardial infarction with those risk factors is suggested.

Aged↗
PubMed1987

Biochemical mechanisms of cardiac hypertrophy.

Rapid cardiac growth in adult rats and neonatal pigs involves more efficient use of existing components of the protein synthesis pathway and synthesis of new ribosomes and mRNA to increase the capacity for protein synthesis. Greater efficiency of synthesis can be induced by mechanical perturbations that stretch the ventricular wall, including increased cardiac work and increased ventricular pressure development in beating hearts, and increased aortic and intraventricular pressure in arrested-drained hearts. The biochemical signal linking stretch to more efficient protein synthesis has not been identified. Preferential synthesis of new ribosomes occurs in the first two hours of exposure of Langendorff preparations to high aortic pressure or within four hours after injection of thyroid hormone into normal rats. The rate of protein degradation is either accelerated or unchanged in hypertrophing hearts but is inhibited by induction of cardiac work or high aortic pressure in Langendorff preparations. Overall, increased capacity for, and efficiency of, protein synthesis are the major factors accounting for cardiac growth.

Aging↗
PubMed1987

Aortic perfusion pressure, protein synthesis, and protein degradation.

An increase in aortic pressure from 60 to 120 mm Hg accelerated protein synthesis and inhibited protein degradation in isolated rat hearts perfused as Langendorff preparations. This elevation of aortic pressure raised intraventricular pressure development, coronary flow, and oxygen consumption. The effect of aortic pressure on protein turnover was dissociated from intraventricular pressure development, contractile activity, and oxygen consumption by use of beating-drained and arrested-drained preparations. Results of other experiments argued against coronary flow as a determinant of rates of protein synthesis and degradation. These results indicated that effects of elevated aortic pressure on protein turnover were caused by stretch of the ventricular wall via its engorgement with blood, the so-called erectile properties of the heart or "garden-hose effect." These effects on protein turnover may be of importance in initiating hypertrophy of the heart secondary to pressure or volume overload.

Animals↗
PubMed1986

Aortic pressure as a determinant of cardiac protein degradation.

Mechanical parameters and intracellular mediators that may control protein degradation were studied in isolated rat hearts subjected to increased aortic pressure. Elevation of aortic pressure from 60 to 120 mmHg in Langendorff preparations provided glucose or pyruvate as substrate decreased the rate of protein degradation during the second hour of perfusion. Intracellular contents of ATP or creatine phosphate or the creatine phosphate/creatine ratio did not indicate that energy depletion accounted for these effects. When ventricular pressure development was prevented by ventricular draining, and hearts were arrested with tetrodotoxin, protein degradation still decreased as aortic pressure was raised. The effect of elevated aortic pressure on proteolysis was unchanged when perfusate calcium concentrations were 0.6, 3.0, or 5.1 mM, or when indomethacin or meclofenamate was added to the perfusion buffer. These results provided no evidence to indicate that intraventricular pressure development or cardiac contraction was responsible for the inhibitory effect of increased aortic pressure on protein degradation. Instead, they suggested that stretch of the ventricular wall, as a consequence of increased aortic pressure, could be the mechanical parameter most closely related to the restraint on proteolysis. No evidence was obtained that the lower rate of degradation depended on energy or calcium availability or prostaglandin synthesis.

Adenosine Triphosphate↗
PubMed1986

Mechanical factors affecting protein turnover in isolated rat hearts.

Induction of cardiac work increased protein synthesis in hearts supplied glucose or a mixture simulating normal plasma levels of glucose, insulin, glucagon, lactate, and beta-hydroxybutyrate. During 2 h of perfusion, cardiac work did not accelerate protein synthesis in hearts supplied a mixture of glucose, lactate, and higher concentrations of insulin. Protein degradation was decreased by work in hearts supplied glucose. Nitrogen balance was negative in Langendorff-perfused hearts provided glucose, but was less so in working preparations. Nitrogen balance was zero or positive in working hearts provided the mixture simulating plasma or the mixture of glucose, lactate, and insulin. In Langendorff preparations, increased aortic pressure accelerated protein synthesis during the second hour of perfusion in hearts supplied glucose, glucose plus insulin, or pyruvate. When ventricular pressure development was prevented by ventricular draining or when drained hearts were arrested with tetrodotoxin, protein synthesis still increased as perfusion pressure was raised from 60 to 120 mm Hg. Oxygen consumption increased as aortic pressure was increased in drained, beating hearts, but was unaffected in arrested, drained hearts. These studies indicated that increased aortic pressure and its attendant stretch of the ventricular wall were the mechanical parameter most closely associated with faster rates of protein synthesis.

Animals↗
PubMed1985

Dependence of protein synthesis on aortic pressure and calcium availability.

Increased aortic pressure accelerated protein synthesis in control-beating and arrested-drained hearts supplied with either glucose or pyruvate. Elevation of perfusion pressure from 60 to 120 mm Hg increased oxygen consumption in control-beating but not in arrested-drained preparations. Energy availability, as assessed by adenylate energy charge or creatine phosphate/creatine ratio, or both, was increased in arrested-drained hearts supplied with glucose and perfused at 60 and 120 mm Hg aortic pressure. In control-beating or arrested-drained hearts supplied with pyruvate, energy availability was not improved by elevation of aortic pressure from 60 to 120 mm Hg. An increase of perfusate calcium concentration from 0.5 to 5.0 mM in control-beating Langendorff preparations supplied with glucose and perfused at an aortic pressure of 90 mm Hg doubled oxygen consumption and decreased energy availability, but had no effect on the rate of protein synthesis. In arrested-drained hearts supplied with either glucose or pyruvate and calcium concentrations ranging from 0.5 to 5.0 mM, the rates at 120 mm Hg aortic pressure were 11-25% higher than at 60 mm Hg. These findings provide no evidence to implicate increased oxidative metabolism, energy availability, or extracellular calcium concentration as important factors in the mechanism that accounts for the effects of increased aortic pressure on protein synthesis.

Animals↗