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Biomedical subjects

M Hiroe

Publications and source records attributed to M Hiroe.

At least 91 records · Page 5Linked to original sources
PubMed1996

Time- versus frequency-domain analysis in predicting cycle length of inducible ventricular tachycardia after myocardial infarction.

To determine whether time- and frequency-domain analyses differ in their ability to predict sustained ventricular tachycardia (VT) induced by programmed ventricular stimulation, 60 consecutive patients with myocardial infarction and 30 healthy control subjects were evaluated. Programmed ventricular stimulation using three extrastimuli and signal-averaged ECG recordings were performed in patients with myocardial infarction. Of the 60 patients, sustained monomorphic VT (SMVT) with cycle length (CL) > or = 250 ms (slow SMVT) was inducible in 9, and SMVT with CL < 250 ms (fast SMVT) was inducible in 9. The durations of the filtered QRS (f-QRS) at each high-pass filter (25, 40, and 80 Hz) and the low amplitude signal (LAS) at 25-Hz high-pass filtering were significantly longer in the slow SMVT group than in the fast SMVT, no VT, or normal control group. The root-mean-square voltages at 25-Hz and 80-Hz high-pass filters in the slow SMVT group were significantly lower than in the fast SMVT, no VT, or normal control group. There was no significant difference in time-domain variables among fast SMVT, no VT, and normal control groups. The CL of the induced sustained VT was significantly correlated with the durations of f-QRS and LAS. Concerning frequency-domain variables (area ratio and factor of normality), there was no significant difference between slow and fast SMVT groups. Both the slow and fast SMVT groups had a significantly higher area ratio and a significantly lower factor of normality than the group with no VT or the normal control subjects. In conclusion, there were significant correlations between time-domain variables and CL of SMVT, while there was no correlation when using frequency-domain parameters.

Cardiac Catheterization↗
PubMed1996

Selective radiofrequency catheter ablation of the slow pathway for common and uncommon atrioventricular nodal reentrant tachycardia.

The utility of selective radiofrequency catheter ablation of the slow pathway for the treatment of common and uncommon atrioventricular nodal reentrant tachycardia (AVNRT) was studied in 110 consecutive patients, 94 with slow-fast form common AVNRT, and 11 and 5, respectively, with the fast-slow and slow-slow forms of uncommon AVNRT. Ablation sites were determined by mapping a late and spiky "slow pathway potential" in the posterior right atrial septum in common AVNRT, and also the earliest retrograde atrial activation over the retrograde slow pathway in uncommon AVNRT. AVNRT was successfully eliminated in all patients with a mean number of radiofrequency pulses of 2.9 +/- 3.0 and a mean total energy applied of 3536 +/- 2996 joules. There were no early or late complications, except for transient AV block for 15 sec immediately after energy application in one common AVNRT patient, and no recurrence of AVNRT in a mean follow-up period of 24 +/- 13 months. There were no significant differences between common and uncommon AVNRT in success rate, mean application number and total energy applied. However, the AVN physiology post-ablation was different. Slow pathway conduction was eliminated in only 32% of the patients post-ablation in common AVNRT, while it was elininated in 100% in uncommon AVNRT. Selective radiofrequency catheter ablation of the slow pathway can cure common and uncommon AVNRT effectively and safely. Common AVNRT can be eliminated irrespective of the persistence of slow pathway conduction, while uncommon AVNRT can be eliminated by the eradication of slow pathway conduction.

Adolescent↗
PubMed1996

Large right ventricular myxoma in a 79-year-old male.

A 79-year-old male, admitted because of severe dyspnea on exertion, showed echocardiographic findings of a large tumor in the dilated right ventricle. The right ventricular outflow tract was nearly occluded by the tumor mass, and the mass was attached to the interventricular septum by a pedicle. The tumor removal operation was successful. The size of the tumor was 40 mm x 90 mm, and the weight 70 g. Microscopic findings showed typical myxomatous tissue with high cellularity, and no malignancy was observed. This is the oldest reported patient with right ventricular myxoma which was cured by operation.

Aged↗
PubMed1996

Uptake of indium-111-anti-intercellular adhesion molecule-1 monoclonal antibody in the allografted rat lung during acute rejection.

BACKGROUND: Although many methods for detection and quantification of allograft rejection of the lung have been explored, only histologic diagnosis by lung biopsies has gained widespread acceptance. To examine whether indium-111-anti-intercellular adhesion molecule-1 monoclonal antibody imaging can noninvasively detect acute lung rejection, we measured the uptake of this radiopharmaceutical in lung tissue and with scintigraphy in orthotopically transplanted rat lungs. METHODS: The left lung transplant model was used with Lewis- to Wistar-King rat allografts and Lewis isograft controls. Lungs were harvested 2,3,4,5,6, and 7 days after transplantation. The transplanted and native lungs were removed 24 hours after injection of the radiotracer, weighed, and counted in a gamma well counter; uptake ratios of the transplanted or native lungs were then calculated, and scintigraphy was performed. RESULTS: Histologic rejection scores by the grading system of the International Society for Heart and Lung Transplantation at 2,3,4,5,6, and 7 in the allografts were 1.2 +/- 0.2, 2.3 +/- 0.6, 3.0 +/- 0.5, 3.7 +/- 0.4, and 4, and 4, respectively. The uptake ratios of the allografts 3,4, and 5 days after transplantation were significantly higher than the values of the respective isografts and correlated with histologic rejection grades. However, 6 days after transplantation, uptake ratios of allografts decreased and did not correlate with histologic grades. On days 3,4, and 5 after transplantation, the tracer uptake within the allografts was visualized by means of scintigraphy. CONCLUSIONS: We conclude that indium-111-anti-intercellular adhesion molecule-1 monoclonal antibody increased during mild to moderate acute lung rejection. An abnormal scintigram with this radiotracer suggests that lung biopsy should be performed to exclude lung rejection.

Animals↗
PubMed1996

[Effects of nicorandil on coronary collateral circulation depend on the donor arteries].

The effects of nicorandil on coronary collateral circulation during exercise-induced ischemia were compared between the different donor arteries in 13 patients with effort angina, 7 with complete obstruction of the left anterior descending artery (LAD) with well-developed collateral vessels from the right coronary artery (RCA) (LAD group), and 6 with complete occlusion of the RCA (segment 2-3) with well-developed collateral vessels from the LAD (RCA group). Initial percentage thallium (%TI) uptake (thallium-201 single photon emission computed tomography) and washout rate were measured in the anterior, septal and posterior regions during ergometer exercise. The submaximal treadmill exercise test was also performed using a cardiopulmonary monitoring system to measure Vo2 at anaerobic threshold (AT). After the controls were obtained, nicorandil (15 mg/day) was administered for 4 weeks, during which ergometer exercise and treadmill exercise tests were carried out repeatedly. A significant improvement of initial %TI uptake on exercise was observed in the LAD group with nicorandil therapy, but no improvement was shown in the RCA group. The AT significantly increased after nicorandil treatment in the LAD group (13.9 +/- 0.38-->16.8 +/- 1.18 ml/min/kg), reflecting the improvement of cardiac function through the increased collateral flow. However, in the RCA group, it remained unchanged, suggesting no improvement of cardiac function. Nicorandil was effective to increase collateral flow from the RCA, but ineffective on that from the LAD. Nicorandil is an effective coronary dilator and is reported to affect both large and small coronary arteries. The effect on the collateral circulation is dependent on the donor artery supplying different areas. The vasodilator effect of nicorandil is mainly on the LAD, which is large enough to supply blood to a wider area of the heart, rather than the RCA.

Adult↗
PubMed1995

Molecular cloning of a novel serine/threonine kinase, MRK, possibly involved in cardiac development.

We have isolated a novel member of putative serine/threonine kinase from a rat heart cDNA library using polymerase chain reaction methods. The novel kinase is transcribed as 2.6 kb mRNA encoding for a protein of 629 amino acids with the C-terminal non-catalytic portion. Amino acids analysis revealed that the N-terminal catalytic domain is 87% identical to the male-germ cell associated kinase (MAK), a cdc2-related serine/threonine kinase found to promote meiosis during spermatogenesis. Therefore, we designated this novel kinase as the MAK-related kinase (MRK). MRK protein, with a molecular weight of 66 kD, was shown to phosphorylate itself and the exogenous substrates, histone H1 and myelin basic protein. In addition, phosphoamino acid analysis confirmed the serine/threonine-specific protein kinase activity of MRK. Although MRK was ubiquitous in adult rat tissues, the expression of MRK protein in embryos was restricted primarily to embryonic myocardium during early organogenesis. This finding suggests that MRK may be a participant in cardiac development.

Amino Acid Sequence↗
PubMed1995

Effects of nicorandil on kinetics of oxygen uptake at the onset of exercise in patients with coronary artery disease.

The beneficial effects of coronary vasodilators on exercise capacity in patients with angina pectoris are well known. However, their effects on oxygen uptake (VO2) kinetics at the onset of exercise have not been elucidated. The present study was undertaken to determine the acute effects of nicorandil, a newer coronary vasodilator, on the kinetics of VO2 at the onset of exercise in patients with ischemic heart disease. Ten patients with significant coronary stenosis performed constant mild-intensity cycle exercise (32 +/- 3 W) for 6 minutes after oral administration of 10 mg of nicorandil or an identical placebo in a double-blind, crossover manner. Nicorandil had no effect on resting heart rate, blood pressure, or VO2. However, the time constant for the increase in VO2 during constant work rate exercise was significantly shorter (the kinetics of VO2 were faster) after administration of nicorandil than after placebo (46.5 +/- 13.3 vs 51.1 +/- 11.9 seconds; p = 0.039). The increase in VO2 at 6 minutes compared with 3 minutes of constant work, which reflects the VO2 kinetics, also was reduced with nicorandil (3.8 +/- 37.9 vs 27.5 +/- 27.1 ml/min; p = 0.022). Nicorandil was found to increase the rate of VO2, increase during the onset of constant work rate exercise, probably as a result of an improved response in cardiac output. Analysis of VO2 kinetics provides new and useful parameters for the evaluation of circulatory adjustments at the onset of exercise in patients with ischemic heart disease.

Adult↗
PubMed1995

Evaluation of exercise capacity using submaximal exercise at a constant work rate in patients with cardiovascular disease.

BACKGROUND: Symptom-limited incremental exercise tests are used to estimate the severity of cardiovascular disease and the patient's daily activity. However, there is a need for objective parameters for submaximal exercise. To test the hypothesis that a decrease in maximal exercise capacity can be estimated by oxygen uptake (VO2) kinetics, we measured the time constant of VO2 both during the onset of constant work rate exercise at 50 W and during recovery from this exercise and compared it with data obtained during maximal exercise in patients with cardiovascular disease and in normal subjects. METHODS AND RESULTS: A total of 34 patients with cardiovascular disease and 14 normal subjects performed 6 minutes of 50-W constant work rate exercise and an incremental exercise test to the symptom-limited maximum on a cycle ergometer. VO2 was calculated from respiratory gas analysis on a breath-by-breath basis. The time constant of VO2 during the onset of 50-W exercise was 61.4 +/- 15.2 seconds in patients with cardiovascular disease, significantly longer (the kinetics of VO2 were slower) than that in normal subjects (48.8 +/- 10.4 seconds, P = .008). The time constant of VO2 during the onset of exercise was significantly negatively correlated with peak VO2 (r = -.67) and maximal work rate (r = -.66). The time constant during recovery, which did not differ significantly from that of exercise, was also prolonged in patients with cardiovascular disease; it showed a negative correlation with peak VO2 (r = -.63) and maximum work rate (r = -.54). CONCLUSIONS: The time constant of VO2 during and after recovery from 50 W of constant work rate exercise, which does not require the subject's maximal effort, is a useful and objective measure of exercise capacity in patients with mild to moderate cardiovascular disease.

Adult↗
PubMed1995

Differential localization of atrial natriuretic peptide and skeletal alpha-actin messenger RNAs in left ventricular myocytes of patients with dilated cardiomyopathy.

OBJECTIVES: This study was designed to determine whether atrial natriuretic peptide and skeletal alpha-actin messenger RNAs (mRNAs) are co-localized in ventricular myocytes of patients with dilated cardiomyopathy. BACKGROUND: Atrial natriuretic peptide and skeletal alpha-actin are known as augmented genes with cardiac hypertrophy. However, the expression and localization of both genes in chronic failing heart remain unclear. METHODS: Left ventricular biopsy specimens were obtained from 14 patients with dilated cardiomyopathy. Atrial natriuretic peptide and skeletal alpha-actin mRNAs were detected by in situ hybridization with specific sulfur-35 uridine triphosphate-labeled RNA probes in the serial sections. RESULTS: Atrial natriuretic peptide mRNA was detected in 10 patients, and intense signals were localized in the myocytes located in the subendocardium and around the interstitial fibrous area. By contrast, skeletal alpha-actin mRNA was homogeneously detected in all myocytes in seven patients. By left ventriculography, patients with skeletal alpha-actin-positive findings had a lower ejection fraction (37.1 +/- 6.0%) than those with negative findings (46.3 +/- 5.8%, p < 0.05), but atrial natriuretic peptide mRNA expression was not related to left ventricular function. CONCLUSIONS: These results indicate that the expression of atrial natriuretic peptide and skeletal alpha-actin mRNAs are not always co-localized in the left ventricle of patients with dilated cardiomyopathy and suggest that the mechanisms of the regulation of these two genes in the chronic failing heart are different.

Actins↗
PubMed1995

Distribution of mRNAs for natriuretic peptides in RV hypertrophy after pulmonary arterial banding.

It has been unclear whether the increases in transcript accumulation for atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) during pressure overload are caused by the direct hemodynamic stress imposed on the myocytes or mediated by systemic hormonal factors. We examined the levels and regional distributions of ANP and BNP mRNAs in the hypertrophied right ventricle produced by experimental coarctation of main pulmonary artery (PA) in rats and compared them with those of skeletal alpha-actin mRNA, which is known to be a genetic marker for cardiac hypertrophy. In this experimental model, the left ventricle was free from the influence of pressure overload. By Northern blot analysis, remarkable increases in mRNAs for ANP and BNP, as well as skeletal alpha-actin, were observed in the right ventricle at 1 day after PA banding. Changes of expression of these genes were minimal in the left ventricle. ANP mRNA levels in the right ventricle increased further at days 3 and 7, whereas BNP mRNA remained at its day 1 level through 7 days. Increased expression of ANP, BNP, and skeletal alpha-actin mRNAs occurred exclusively in the right ventricular (RV) free wall and in the junctional region between the RV free wall and the interseptal wall as determined by in situ hybridization. These data suggest that local stimuli caused by hemodynamic overload induce cardiac hypertrophy and its associated increases in ANP and BNP expression in the RV free wall.

Actins↗
PubMed1995

Restricted usage of T cell receptor V alpha-V beta genes in infiltrating cells in the hearts of patients with acute myocarditis and dilated cardiomyopathy.

Prolonged myocardial cell damage initiated by acute myocarditis is thought to be one of the most important etiology of dilated cardiomyopathy. To investigate the immunological mechanisms involved in the pathogenesis of dilated cardiomyopathy, we analyzed the phenotypes of infiltrating cells and examined the expression of perforin in infiltrating cells in the hearts of patients with dilated cardiomyopathy as well as acute myocarditis. We also examined the expression of HLA and intercellular adhesion molecule-1 (ICAM-1) in myocardial tissue of these patients. Furthermore, to evaluate the antigen specificity of infiltrating T cells and persistence of viral genomes in the myocardial tissue, we analyzed the expression of T cell receptor (TCR) V alpha and V beta genes as well as enterovirus genomes by PCR. We found infiltration of perforin-expressing killer cells and enhanced expression of HLA class I and ICAM-1 in the myocardial tissue. We also found that the repertoires of TCR V alpha as well as V beta gene transcripts were restricted, indicating that a specific antigen in the hearts was targeted. Because no enterovirus genomes were detected in all patients, it is strongly suggested that a cell-mediated autoimmune mechanism triggered by virus infection may play a critical role in the pathogenesis of dilated cardiomyopathy. However, we could not exclude the possibility that viruses other than enteroviruses could be pathogenic in these patients.

Acute Disease↗
PubMed1995

Natriuretic peptides inhibit angiotensin II-induced proliferation of rat cardiac fibroblasts by blocking endothelin-1 gene expression.

The present study was aimed to test the role of endothelin-1 (ET-1) as a possible autocrine/paracrine growth factor for cardiac fibroblasts, and to examine its interaction with cardiac natriuretic hormones. Expression of preproET-1 (ppET-1) mRNA by cultured cardiac fibroblasts from neonatal rats was demonstrated by Northern blot analysis using cDNA for rat ppET-1 as a probe. Angiotensin II (ANG II) and ET-1 transiently (30 min) increased steady-state ppET-1 mRNA levels in cardiac fibroblasts. Both ET-1 and ANG II significantly stimulated [3H] thymidine incorporation into cardiac fibroblasts, whose effects were dose-dependently inhibited by an ETA receptor antagonist (BQ123), BQ123 also inhibited both ET-1- and ANG II-induced ppET-1 mRNA expression. Both atrial and brain natriuretic peptides (ANP, BNP), which activate particulate guanylate cyclase, inhibited ppET-1 mRNA expression and [3H]thymidine incorporation stimulated by ANG II and ET-1. Sodium nitroprusside, a soluble guanylate cyclase activator, and 8-bromocyclic GMP, a membrane-permeable cGMP derivative, similarly inhibited ppET-1 mRNA expression and [3H]-thymidine incorporation. BNP was more potent than ANP to inhibit ANG II- and ET-1-stimulated DNA synthesis, whereas BNP and ANP were almost equipotent in stimulating cGMP generation in cardiac fibroblasts. Our data demonstrated that ANG II and ET-1 upregulate ET-1 gene expression in rat cardiac fibroblasts partly via cyclic GMP-dependent mechanism, and that natriuretic peptides inhibit ANG II-stimulated proliferation of cardiac fibroblasts, possibly by inhibiting ET-1 gene expression. Our data suggest the possible role of endogenous ET-1 as an autocrine/paracrine growth factor for cardiac fibroblasts and its close interaction with natriuretic peptides in the regulation of cardiac fibrosis.

Angiotensin II↗
PubMed1995

[Exercise testing in cardiac patients].

Symptom-limited incremental exercise tests have been used, to estimate the severity of cardiovascular disease and the patients' daily activity. However, there is a considerable amount of interest in obtaining submaximal measurements of aerobic function rather than parameters requiring maximal exercise effort. We compared the parameters obtained during the incremental exercise with those during the 6 minutes of moderate constant work rate exercise. Peak oxygen uptake (VO2) and the anaerobic threshold were significantly decreased in patients with cardiovascular disease as compared to normal subjects. The slope of the increase in carbon dioxide output (VCO2) to the increase in VO2 (delta VCO2/delta VO2) above the anaerobic threshold was significantly increased and the slope of the increase in VO2 to the increase in work rate (delta VO2/delta WR) was significantly decreased in patients with cardiovascular disease. The anaerobic threshold was found to occur at the work rate above which left ventricular function decreased during exercise in these patients. The time constant of VO2 during and following recovery from 6 minutes of 50 watts of constant work rate exercise was significantly longer (the kinetics of VO2 were slower) in patients with cardiovascular disease than in normal subjects. The time constant of VO2 was significantly negatively correlated with peak VO2 and maximum work rate obtained during the incremental exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Anaerobic Threshold↗
PubMed1995

Plasma human brain natriuretic peptide in chronic renal failure.

Brain natriuretic peptide (BNP) is a polypeptide hormone which is homologous with atrial natriuretic peptide (ANP). Since the 2 hormones partially share common secretory regulation we simultaneously assessed plasma BNP and ANP in patients with chronic glomerulonephritis without apparent cardiac involvement. Blood samples were taken from patients with serum creatinine (Cr) 0.5-1.2 mg/dl (normal renal function), patients with Cr > 1.2 mg/dl (chronic renal failure) and dialysis patients. BNP did not correlate with serum Cr, which indicated our antibody did not recognize accumulated metabolites due to decreased renal function. BNP and ANP decreased after dialysis-(p < 0.01). Changes of BNP during HD correlated with changes in body weight (p < 0.05). Plasma BNP concentrations were 12.0 +/- 22.0 pg/ml in patients with normal renal function, 17.6 +/- 23.4 pg/ml in chronic renal failure, and 91.5 +/- 93.5 in dialysis patients (p < 0.05 compared with patients with normal renal function). Plasma BNP/ANP ratios were 0.507 +/- 0.646 in patients with normal renal function, 0.392 +/- 0.842 in chronic renal failure, and 0.573 +/- 0.431 in dialysis patients (p < 0.05, compared with chronic renal failure). Increased ANP in chronic renal failure and dialysis indicates volume overload on atrium. In contrast, BNP increased only in dialysis patients, which indicates differences of hemodynamic stress in chronic renal failure and dialysis. We conclude that simultaneous measurements of plasma BNP and ANP further discriminate salt-water and hemodynamic abnormalities in dialysis patients.

Adult↗
PubMed1994

Two isoforms of a chloride channel predominantly expressed in thick ascending limb of Henle's loop and collecting ducts of rat kidney.

Complementary DNAs encoding rat kidney chloride channels (ClC-K2L and ClC-K2S) were isolated by a polymerase chain reaction cloning strategy. Degenerate primers were designed based on the significant amino acid identity of the previously cloned chloride channels (ClC-0, -1, -2, and -K1). The 687-amino acid protein encoded by ClC-K2L is about 80% identical to rat ClC-K1 and about 40% identical to ClC-0, -1, and -2. ClC-K2S encodes a 632-amino acid protein in which 55 amino acids containing the putative second membrane-spanning domain of ClC-K2L are deleted. Chloride currents induced by both clones were very similar in terms of inhibitor sensitivity and anion selectivity (Br- > I- > Cl- >> cyclamate-). Northern blot with total ClC-K2L as a probe under high stringency revealed its message predominantly in kidney, especially in the outer and inner medulla. Reverse transcription polymerase chain reaction technique using microdissected nephron segments revealed that the main site of expression of both clones in kidney was the thick ascending limb of Henle's loop and collecting ducts, where the existence of a variety of chloride channels and their importance for maintaining body fluid homeostasis have been demonstrated. These results suggest that ClC-K2L and -K2S are chloride channels in the thick ascending limb and collecting ducts and may be important routes for transcellular chloride transport like ClC-K1.

Amino Acid Sequence↗
PubMed1994

Insulin-like growth factor-II induces hypertrophy with increased expression of muscle specific genes in cultured rat cardiomyocytes.

In the present study, we examined whether insulin-like growth factor-II (IGF-II) induces hypertrophy of cultured neonatal rat cardiomyocytes. IGF-II (10(-7) M) increased the cell surface area of, and the protein content in, cardiomyocytes after 48 h-exposure. IGF-II dose-dependently (10(-10)-10(-7) M) stimulated protein synthesis as evaluated by [3H]leucine incorporation; the maximum response was 1.7-fold increase over control at 10(-7) M. Since the response of cardiac hypertrophy is characterized by enhanced expression of muscle specific genes, effects of IGF-II on steady-state levels of mRNA for myosin light chain 2 (MLC2), troponin I and alpha-actin isoforms (skeletal and cardiac isoforms) were evaluated by Northern blot analysis. IGF-II (10(-7) M) increased mRNA levels for MLC2, troponin I and skeletal alpha-actin, as early as 60 min with a maximum response after 6 h, whereas cardiac alpha-actin mRNA levels were unaffected. Calcium channel blocker, nicardipine, inhibited IGF-II-stimulated skeletal alpha-actin mRNA levels, however, inhibitor of protein kinase C, H-7, unaffected. These results suggest that IGF-II plays a potential role in cardiac hypertrophy.

Animals↗