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Biomedical subjects

H Moritani

Publications and source records attributed to H Moritani.

13 recordsLinked to original sources
PubMed2001

Pheochromocytoma of the urinary bladder revealed with cerebral hemorrhage.

The case was a 51-year-old man, who has been undergoing treatment with oral medication for hypertension for three years. The patient was admitted to the author's clinic for hemorrhage in the left putamen. He was diagnosed as having primary pheochromocytoma of the bladder from such symptoms as paroxysmal blood pressure elevation after urination, mild increase in catecholamine levels before and after urination, and from the results of 131I-MIBG scintigraphy, and cystoscopy, and underwent excision of the bladder tumor. Upon endocrinological examination, only mild increases in catecholamine levels were found. Therefore, constant monitoring of blood pressure and 131I-MIBG scintigraphy were useful for a definitive diagnose.

Catecholamines↗
PubMed2000

YM-53601, a novel squalene synthase inhibitor, reduces plasma cholesterol and triglyceride levels in several animal species.

The aim of this study was to evaluate the potency of YM-53601 ((E)-2-[2-fluoro-2-(quinuclidin-3-ylidene) ethoxy]-9H-carbazole monohydrochloride), a new inhibitor of squalene synthase, in reducing both plasma cholesterol and triglyceride levels, compared with 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor and fibrates, respectively. YM-53601 equally inhibited squalene synthase activities in hepatic microsomes prepared from several animal species and also suppressed cholesterol biosynthesis in rats (ED(50), 32 mg kg(-1)). In guinea-pigs, YM-53601 and pravastatin reduced plasma nonHDL-C (=total cholesterol - high density lipoprotein cholesterol) by 47% (P<0.001) and 33% (P<0.001), respectively (100 mg kg(-1), daily for 14 days). In rhesus monkeys, YM-53601 decreased plasma nonHDL-C by 37% (50 mg kg(-1), twice daily for 21 days, P<0.01), whereas the HMG-CoA reductase inhibitor, pravastatin, failed to do (25 mg kg(-1), twice daily for 28 days). YM-53601 caused plasma triglyceride reduction in hamsters fed a normal diet (81% decrease at 50 mg kg(-1), daily for 5 days, P<0.001). In hamsters fed a high-fat diet, the ability of YM-53601 to lower triglyceride (by 73%, P<0.001) was superior to that of fenofibrate (by 53%, P<0.001), the most potent fibrate (dosage of each drug: 100 mg kg(-1), daily for 7 days). This is the first report that a squalene synthase inhibitor is superior to an HMG-CoA reductase inhibitor in lowering plasma nonHDL-C level in rhesus monkeys and is superior to a fibrate in significantly lowering plasma triglyceride level. YM-53601 may therefore prove useful in treating hypercholesterolemia and hypertriglyceridemia in humans.

Animals↗
PubMed1999

Establishment of a long-surviving murine model of myocardial infarction: qualitative and quantitative conventional microscopic findings during pathological evolution.

Ongoing basic molecular analyses are being performed in mice, and a simple long-surviving murine model of myocardial infarction (MI) would be very useful in this regard. Although a few studies have induced MI in mice by coronary artery ligation, the induction involves a complex technique and has a relatively high mortality rate. In addition, the identification of the basic pathological sequence is essential to the interpretation of experimental results. We developed a simple technique for the induction of MI in mice and examined qualitative and quantitative conventional microscopic findings during the pathological evolution over a 28-day observation period. Male BALB/c mice weighing approximately 25-30 g were anesthetized and then ventilated with a positive pressure ventilator. The heart was exposed by thoracotomy. Left coronary artery occlusion was performed by thermocoagulation using a thermocoagulation knife at the level of the tip of the left atrium. After establishing this surgical method, we used it to induce MI in 71 mice. The operative and postoperative mortality rates of this model were 5.6% (4/71) and 12.6% (9/71), respectively. In 3 (5.2%) of the 58 surviving mice, the area of infarct was not sufficient. The infarct area in the remaining 55 mice was 40 +/- 9% of the entire perimeter of the left ventricle. Conventional microscopic examinations with hematoxylin-eosin and Masson-trichrome staining disclosed that all of the characteristic histopathological features of MI occurred 1-2 days earlier than those in rats. Our surgical technique provides a sufficient infarct area, with an acceptable mortality rate. The present study clarified the histopathological sequence in this long surviving murine MI model.

Animals↗
PubMed1999

Reperfusion accelerates the distribution of type I and III collagen messenger RNA expression after acute myocardial infarction: in situ hybridization in experimental infarction in rats.

BACKGROUND: The effects of reperfusion on the time-dependent appearance and distribution of type I and III collagen messenger RNA (mRNA) expression had not hitherto been examined. OBJECTIVE: To compare the sequential changes in the extent of distribution of type I and III collagen mRNA expression in reperfused infarct hearts of rats with those in unreperfused infarct hearts. METHODS: Using an experimental rat model of infarction, we examined type I and III collagen mRNA expression with specific rat pro alpha 1 (I) and human pro alpha 1 (III) collagen riboprobes by in-situ hybridization. Reperfusion was established after a 2 h coronary ligation that produced complete necrosis of the myocytes. RESULTS: Positive signals both for alpha 1 (I) and for alpha 1 (III) collagen mRNA appeared in the infarct peripheral zone 12 h after coronary ligation both of the reperfused and of unreperfused hearts. The spread of signal into the infarct central zone occurred 1-2 days earlier for the reperfused hearts than it did for the unreperfused hearts. The difference between the distributions of signals for the reperfused and unreperfused hearts became obscure on day 14. No notable difference between the extents of signal distribution for alpha 1 (I) and alpha 1 (III) collagen mRNA was obtained. We observed intense signals from spindle-shaped mesenchymal cells (myofibroblasts and fibroblasts) located between surviving myocytes in the marginal zone of the infarct. No myocyte exhibited signals both for alpha 1 (I) and for alpha 1 (III) collagen mRNA. CONCLUSION: In the present study, using in-situ hybridization, we demonstrated that reperfusion accelerates the distribution of expression both of alpha 1 (I) and of alpha 1 (III) collagen mRNA in the infarct zone after acute myocardial infarction in rats.

Animals↗
PubMed1998

Expression of type XVII collagen alpha 1 chain mRNA in the mouse heart.

The type XVII collagen alpha 1 chain has been identified as a component of the type I hemidesmosome, and is thus thought to play a role in extracellular matrix (ECM) maintenance and signal transduction between the cell and the ECM. We examined the expression of type XVII collagen alpha 1 chain mRNA in the mouse heart by Northern blot analysis and determined the sequential changes of its expression in different developmental stages of the heart using the reverse transcriptase-polymerase chain reaction (RT-PCR) method. Northern blotting: Total RNA was extracted from 10 adult mouse hearts by the guanidine/cesium method. Hybridization was performed with mouse cDNA for alpha 1 (XVII) collagen. RT-PCR: Total RNA was extracted from 7 embryos, 4 neonates and 8 adult mice. Reverse transcription was performed using oligo-dT primer and MMLV. Amplification was carried out in alpha 1 (XVII) collagen and glyceraldehyde 3-phosphate dehydrogenase (GAPDH). GAPDH served as an internal control. Northern blotting revealed a 5.6 kb signal that was identical to that of the alpha 1 (XVII) of skin and transformed keratinocyte reported previously. The sequences of the PCR products were also identical to those reported. The normalized expression ratios of alpha 1 (XVII) were 0.91 +/- 0.20 in the embryonic heart, 0.36 +/- 0.20 in the neonatal heart and 0.96 +/- 0.21 in the adult heart. In conclusion, we identified the expression of type XVII collagen alpha 1 chain mRNA in the mouse heart, suggesting that the type I hemidesmosome is located in the heart. The results of the RT-PCR at different developmental stages of the heart suggest that type XVII collagen contributes not only to cardiogenesis in the embryonic stage but also to maintenance of architecture and function in the adult heart.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Changes in extracellular matrix components in cardiomyopathic Syrian hamster, BIO 14.6.

We examined changes in the distribution of extracellular matrix components in the myocardium of cardiomyopathic Syrian hamsters (BIO 14.6). Fibronectin, laminin, and type IV collagen, and type I and III collagens were immunohistochemically stained by the avidin-biotin-peroxidase complex method, using a polyclonal antibody for each component. Hearts obtained from 4 stages of BIO 14.6 cardiomyopathy were examined. Peri- and endomysial fibrosis increased as the disease progressed. Replacement and meshwork (perimysial fibrosis penetrating the intercellular space) fibrotic lesions appeared beginning in the 2nd stage, ie, the fibrotic and healing stage. All of the components examined, ie, fibronectin, laminin and type IV collagen, and type I and III collagens, were present in various fibrotic lesions and played a significant role in fibrotic changes throughout all of the stages of the disease. No primary deficit of any of these components was seen. An increased distribution of fibronectin was observed in both the enlarged peri-and endomysial spaces beginning in the initial stage, ie, the necrotic stage, when myocyte hypertrophy was inconspicuous, and distribution throughout the myocardium increased further as the disease progressed. Laminin and type IV collagen in the fibrotic lesions were not restricted to the myocyte membrane. Type III collagen was distributed in replacement and meshwork fibrotic lesions, and the extent of its distribution increased in proportion to that of type I collagen. The continuous increases in the distribution of fibronectin, laminin and type III collagen indicate that fibrotic changes occurred continuously in this model.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Reperfusion hastens appearance and extent of distribution of type I collagen in infarct zone: immunohistochemical study in rat experimental infarction.

BACKGROUND: The effects of reperfusion on time-dependent alteration of type I collagen have not been examined. OBJECTIVES: We compared the sequential changes in the appearance and distribution of type I collagen in reperfused infarct rat hearts to those in non-reperfused hearts. METHODS: Using an experimental rat model of infarction, we performed immunohistochemical staining with a polyclonal antibody to type I collagen by the avidin-biotin-peroxidase method. Reperfusion was established after 2-h coronary ligation that produced complete necrosis of myocytes. RESULTS: In reperfused hearts, type I collagen appeared in the peripheral zone of the infarct at day 2, which was 1 day earlier than in non-reperfused hearts. The extent of distribution of type I collagen in reperfused hearts was comparable to that observed approximately 1 day later in non-reperfused hearts. CONCLUSION: Reperfusion can accelerate collagen matrix formation compared with that in non-reperfused hearts after acute myocardial infarction.

Animals↗
PubMed1994

Silent zone on Lorenz plots of the ventricular response before termination of paroxysmal atrial fibrillation--report of a case.

An ambulatory 24 h Holter electrocardiogram was recorded during paroxysmal atrial fibrillation in a 67-year-old man. His paroxysmal atrial fibrillation terminated spontaneously approximately 12 h after the start of recording. The RR variability of this Holter recording was studied using Lorenz plots, frequency domain analysis, and time domain analysis. A silent zone appeared on the Lorenz plots beginning a few hours before the termination of his attack. The coefficient of variance (CV) and the power of the high-frequency component of RR variability (HF) gradually increased toward the termination. The silent zone was closely related to the functional refractory period of the atrioventricular node estimated from the Lorenz plots, and the functional refractory period was significantly correlated with the CV and HF power of RR variability. This case suggests that a silent zone on Lorenz plots reflects increased parasympathetic tone. In addition, such a silent zone may be useful for predicting the course of paroxysmal atrial fibrillation and for evaluating the role of the autonomic nervous system in this condition.

Aged↗
PubMed1993

Progression of left ventricular enlargement in patients with hypertrophic cardiomyopathy: incidence and prognostic value.

A total of 51 patients with hypertrophic cardiomyopathy (HCM) were followed for at least 3 years (mean follow-up period 6.5 years) by serial M-mode and two-dimensional echocardiography. An increase of the left ventricular diastolic dimension (LVDd) to > or = 55 mm with a decrease in the left ventricular ejection fraction (LVEF) to < 55% was observed in eight (15.7%) patients (progressive disease group). In five of these eight patients, the LVDd was > or = 60 mm and the LVEF was < 40%. Ventricular enlargement was closely related to mortality and death due to congestive heart failure occurred in three of these patients. No deaths occurred among the 37 patients without significant progression of ventricular enlargement (nonprogressive group). The annual changes of LVEF and LVDd in the progressive disease group were larger than in the nonprogressive group (LVEF -0.18 +/- 1.45 vs. -2.46 +/- 1.47 %/year; LVDd 0.22 +/- 0.81 vs. 1.43 +/- 0.77 mm/year). An increment in LVDs occurred earlier than the enlargement of the LVDd. Therefore, close attention to the LVDs seems to be important to detect early left ventricular morphological changes in HCM. In summary, this study indicates that HCM patients include a subgroup with symptoms resembling dilated cardiomyopathy, in whom the left ventricle enlarges with hypofunction and in whom there is high mortality due to congestive heart failure.

Adult↗
PubMed1992

cDNA cloning of mitochondrial delta 3, delta 2-enoyl-CoA isomerase of rat liver.

A 1.08 kbp cDNA encoding rat liver mitochondrial delta 3, delta 2-enoyl-CoA isomerase (ECI) of 298 amino acid residues (Mr 32,895) was isolated from rat liver lambda gt11, lambda gt10 cDNA libraries by the combination of an immunochemical method with a rabbit-antibody against rat liver ECI and a plaque hybridization method. The deduced amino acid sequence from the cDNA indicates that ECI is synthesized with an amino-terminal extrasequence of 35 amino acid residues and processed to the mature enzyme (Mr 29,256).

Amino Acid Sequence↗
PubMed1992

Family of a patient with serum cholinesterase deficiency.

A-39-year-old man was admitted to our hospital because of a markedly decreased level of serum cholinesterase found incidentally by a blood test. Detailed examination did not reveal severe liver disease, malignant tumor, infection or organophosphate compound poisoning. Investigation of three generations of his family revealed two homozygous and five heterozygous family members with the cholinesterase deficiency gene E1s indicating familial serum cholinesterase deficiency.

Adult↗