Biomedical subjects

S Morooka

Publications and source records attributed to S Morooka.

At least 55 records · Page 3Linked to original sources

PubMed1998

[Echocardiographic observation of appearance and progression of mitral annular calcification in a patient with familial obstructive hypertrophic cardiomyopathy].

A 37-year-old man with familial hypertrophic obstructive cardiomyopathy (HOCM) developed mitral annular calcification (MAC) during the follow-up period. At the age of 23 years, a systolic murmur and electrocardiographic abnormality including giant T wave inversion were detected incidentally. His elder brother also had HOCM. Catheterization disclosed a left ventricular outflow pressure gradient of 25 mmHg and thickened interventricular septum. Echocardiography showed asymmetric septal hypertrophy and systolic anterior motion of the mitral valve. The patient was followed up by repeated echocardiography from age 37 years and the onset of MAC (2 mm in thickness) was found at age 48 years. One year later, the MAC had progressed markedly (5 mm) without other remarkable changes in the M-mode echocardiogram, except mitral regurgitation (at age 41 years), left ventricular apical as well as posterior wall hypertrophy (age 43 years) and left atrial enlargement (age 46 years). The left ventricular inflow velocity at the atrial contraction period decreased significantly concomitantly with MAC. MAC is a rare complication in young and middle aged patients. The onset and progression of MAC is still obscure in HOCM. This patient showed that sudden onset and rapid progression of MAC can occur in young patients with HOCM.

Adult↗

PubMed1997

Characterization of a novel iodocyanopindolol and SM-11044 binding protein, which may mediate relaxation of depolarized rat colon tonus.

Studies under blockade of alpha-, beta1-, and beta2-adrenoreceptors revealed a good correlation between the responses of rat colon relaxation of depolarized tonus and of rat adipocyte lipolysis elicited by catecholamines or BRL-37344, a selective beta3-adrenoreceptor agonist, suggesting beta3-adrenoreceptor stimulation. In contrast, SM-11044, a nonselective beta-adrenoreceptor agonist, stimulated colon relaxation more efficiently than lipolysis; its effects were differently antagonized by cyanopindolol with pA2 values of 8.31 in colon and of 7.32 in adipocytes. Binding studies in rat colon smooth muscle membranes using [125I]iodocyanopindolol under blockade of adrenaline and serotonin receptors revealed the existence of a single class of sites (Kd = 11.0 nM, Bmax = 716.7 fmol/mg protein). The specific binding was saturable and reversible and was displaced by SM-11044 but not by BRL-37344, isoproterenol, noradrenaline, adrenaline, serotonin, nor dopamine. This binding site was photoaffinity labeled using [125I]iodocyanopindolol-diazirine. The labeling was prevented by SM-11044 but not by BRL-37344. The amino-terminal amino acid sequences of the high performance liquid chromatography-purified peptides generated by enzymatic and chemical cleavages of the affinity labeled 34-kDa protein confirmed that the novel iodocyanopindolol or SM-11044 binding protein of rat colon smooth muscle membranes is different from known adrenaline, serotonin, or dopamine receptors. Its functional role might include the relaxation of depolarized colon.

Adipocytes↗

PubMed1997

Expressions of P-selectin- and HSP72-like immunoreactivities in rat brain after transient middle cerebral artery occlusion.

The role of an adhesion molecule such as P-selectin may be important in the pathogenesis of stroke. However, temporal, spatial and cellular profiles of the expression of such a protein have not been fully studied. Change of immunoreactive P-selectin was examined in rat brain after transient middle cerebral artery (MCA) occlusion in comparison with that of 72 kDa heat shock protein (HSP72) which is a well known marker of cell injury. Western blot analyses were performed to ensure the selective detection of immunoreactive P-selectin and HSP72 proteins with each antibody using brain samples before and after ischemia. Temporal, spatial and cellular changes of immunohistochemical expressions of P-selectin and HSP72 were evaluated with rat brain sections at 2 and 8 h, and 1, 3 and 7 days of reperfusion after 1 h of MCA occlusion (MCAO). Hematoxylin-eosin (HE) staining was performed to evaluate brain cell damage at 3 and 7 days of reperfusion. Western blot showed a single band at molecular weights of 140 and 72 kDa for P-selectin and HSP72, respectively, only after ischemia. No significant band was observed without primary antibody. P-selectin-like immunoreactivity was not normally present in rat brain sections. However, it was expressed mainly in the post-capillary venules of the cerebral cortex and caudate in the MCA territory with a peak at 8 h to 1 day. The expression was diminished by 3 days of reperfusion. An immunoreactive HSP72 was scarcely present in the cerebral cortex and caudate of the sham control brain. However, the protein was induced in neurons of the MCA territory. The HSP72 induction was gradually intensified from 8 h with peaks at 1 day in the cortex and at 3 days in the caudate. The immunoreactivity decreased by 7 days. Histopathological study with HE staining showed no evident cell damage at 3 and 7 days of reperfusion. The present results indicate that temporal, spatial and cellular differences were present in the expressions of immunoreactive P-selectin and HSP72 proteins. P-selectin was expressed from an earlier stage of reperfusion in post-capillary venules, and the expression became maximum at the same time both in the cerebral cortex and caudate. In contrast, HSP72 induction began later in neurons and reached maximum at a different time between the cortex and caudate.

Animals↗

PubMed1997

Postischemic expression of P-selectin immunoreactivity in rat brain.

Change of immunoreactive P-selectin was examined in rat brain after transient middle cerebral artery (MCA) occlusion (O) with anti-P-selectin monoclonal antibody using brain samples of sham control and after ischemia. Temporal, spatial, and cellular changes of immunohistochemical expressions of P-selectin were evaluated with rat brain sections at 2 and 8 h, 1, 3, and 7 days of reperfusion after 1 h of MCAO. Western blot showed a single band at molecular weight of 140 kDa for P-selectin after ischemia. P-selectin immunoreactivity was not normally present in rat brain sections. However, it was expressed mainly in the post-capillary venules of the cerebral cortex and caudate in the MCA territory with a peak at 8 h-1 day. The expression was diminished by 3 days of reperfusion. The present results indicate that P-selectin was expressed from an earlier stage of reperfusion in post-capillary venules, and the expression became maximum at the same time both in the cerebral cortex and caudate.

Animals↗

PubMed1997

Impaired left ventricular diastolic filling occurs in diabetic patients without atherosclerotic coronary artery disease.

Using left ventriculography, left ventricular diastolic function was studied in 24 diabetic patients who had angina pectoris without atherosclerotic large-vessel coronary artery diseases (group A, 14 patients with exercise-induced ischemic ST-T changes as seen during electrocardiogram; group B, 10 patients without such changes). In groups A and B, the global peak filling rate was significantly less than that in control patients without diabetes or cardiac diseases. The ratio of the global time to the peak filling rate to the diastolic time was higher in both groups A and B than in the control groups. However, the total of time differences, defined as the sum of the time differences between global time to the peak filling rate and each of the three regional time to the peak filling rate, was greater in group A than in either group B or the control patients. Total time difference was similar in group B and the controls. Left ventricular diastolic filling was impaired in diabetic patients without large-vessel coronary artery disease. Impaired diastolic filling was present regionally in patients with ischemic ST-T change but globally in those without such change.

Adult↗

PubMed1997

Effect of enalapril maleate on cerebral blood flow in patients with chronic heart failure.

The effect of enalapril on cerebral blood flow (CBF) was studied in 11 patients with chronic heart failure (NYHA II or III, dilated cardiomyopathy in 6 and old myocardial infarction in 5). CBF was evaluated by analyzing the Patlak-Plot curve obtained from radionuclide angiography with technetium-99m hexamethylpropylene amine oxime (99mTC-HM-PAO). Cardiac index (CI) and stroke volume (SV) were simultaneously measured by impedance cardiography. These measurements were performed before and at four weeks after daily administration of 5 mg enalapril. The stroke volume, cardiac index, and heart rate were not significantly changed after four weeks of enalapril administration. However, CBF was increased by 6.5% from 36.72 +/- 4.66 to 39.13 +/- 5.65 mL/100g/min (P < 0.05). These results suggest that enalapril increased cerebral blood flow, which was not related to increased cardiac output in congestive heart failure. Patlak-Plot analysis of radionuclide angiography using 99mTC-HM-PAO may be available for quantitative assessment of brain perfusion.

Aged↗

PubMed1997

Evaluation of myocardial viability using sequential dual-isotope single photon emission tomography imaging with rest TI-201/stress Tc-99m tetrofosmin in the prediction of wall motion recovery after revascularization.

In patients with coronary artery disease (CAD), differentiation between severely ischemic but potentially viable myocardium and irreversibly infarcted tissue is clinically important, particularly when revascularization procedures are considered. Although thallium (TI) cardiac imaging has been shown to be a good tool for investigating myocardial viability in CAD, this tracer shows physical limitations, such as a low photon energy and long half-life. We assessed the results of a rest TI-201/stress Tc-99m tetrofosmin protocol in subjects with prior anterior myocardial infarction. All of the patients had an akinetic or dyskinetic area and more than 75% stenosis in the left anterior descending artery. All of the patients underwent revascularization after the examination. We evaluated the improvement in wall motion after revascularization using the centerline method with contrast left ventricular angiography. Fourteen patients showed reversible defects with the rest TI-201/stress Tc-99m tetrofosmin protocol or in additional TI-201 24 h redistribution images. All 14 patients showed a significant improvement in wall motion after revascularization. Dual-isotope rest TI-201/stress Tc-99m tetrofosmin single photon emission tomography data, acquired separately, may give fast and complete information about myocardial perfusion during stress and at rest, and on about myocardial viability.

Aged↗

PubMed1997

Leukocyte kinetics in the pulmonary microcirculation: observations using real-time confocal luminescence microscopy coupled with high-speed video analysis.

To quantitatively assess blood cell kinetics in the intact pulmonary microcirculation, in which arterioles, venules, and capillaries are exceedingly intricate and densely convoluted, we recently developed a real-time confocal laser luminescence microscope with a high-speed analysis component. The system has the capacity to yield confocal images of rapidly moving cells at a rate of 1000 frames/second and at sufficiently high degrees of magnification. Applying this novel method to isolated perfused rat lungs, we estimated the endothelial distributions of constitutively expressed intercellular adhesion molecule-1 (ICAM-1) and P-selectin and also studied leukocyte hemodynamic behavior in the pulmonary microvasculature under conditions in which ICAM-1, P-selectin, and L-selectin were inhibited, respectively, by 1A29 (monoclonal antibody to rat ICAM-1), ARP2-4 (monoclonal antibody to rat P-selectin), and fucoidin (competitive inhibitor of both P- and L-selectin). The results were compared with those obtained with a nonconfocal microscope using conventional epiluminescence. Intertwined microvessel networks in the lung were clearly distinguishable in confocal images but not in conventional nonconfocal views. ICAM-1 was perceptibly expressed along venular and capillary but not arteriolar endothelium, whereas P-selectin was undetectable in all microvessels examined. Leukocytes were not firmly adhered to venular or arteriolar endothelial cells. Leukocyte rolling was recognized more frequently along arteriolar walls than along venular walls and was suppressed in arterioles by L-selectin inhibition but not by either ICAM-1 or P-selectin inhibition. In capillaries, transient and sustained arrest of leukocytes occurred at physiologic shear rates. Inhibition of ICAM-1 or P-selectin had no remarkable effect upon either transient or sustained entrapment of leukocytes in capillaries. In conclusion, physiologic and biologic characteristics of pulmonary microvessels appear to be quite different from those of the systemic microcirculation.

Animals↗

PubMed1997

[Successful surgical treatment of aortic regurgitation due to annuloaortic ectasia and mitral regurgitation caused by tendon rupture in a case of osteogenesis imperfecta].

A 54-year-old man presented with osteogenesis imperfecta complicated with both aortic regurgitation due to annuloaortic ectasia and mitral regurgitation secondary to tendon rupture. He had spinal and carpal deformities in his childhood, and heart murmurs were identified at the age of 25. He was admitted complaining of dyspnea on effort. His height was 142 cm and his weight was 46 kg. He had kyphosis, scoliosis and carpal deformity. Blue sclera was not observed. Chest radiography showed cardiomegaly and lung congestion. Echocardiography showed annuloaortic ectasia, mild aortic regurgitation, and serious mitral regurgitation due to postero-apical tendon rupture. Bone deformity and his statues were indicative of osteogenesis imperfecta. He received modified Bentall and mitral valve replacements.

Aortic Valve Insufficiency↗

PubMed1997

Fulminant hepatic failure due to cardiac tamponade associated with mixed connective tissue disease.

We describe a 42-year old Japanese woman with mixed connective tissue disease (MCTD) who developed fulminant hepatic failure and hepatic encephalopathy. Massive pericardial effusion accompanying cardiac tamponade was shown by echocardiography. The hepatic failure was considered to be caused by a low cardiac output state because of cardiac tamponade, which might be due to cardiac involvement of MCTD. This is a rare case, showing an unusual progressive course in MCTD.

Adult↗

PubMed1997

Tricuspid valve infectious endocarditis associated with dental treatment.

A 52-year-old man with neither congenital heart disease nor history of drug abuse had a spiking fever after dental treatment and was diagnosed with pneumonia at a local clinic. He was treated with antibiotics and his fever went down. Ten months later, he had again pyrexia and suffered from congestive heart failure. He admitted to our hospital and tricuspid valve endocarditis was proved by echocardiography. He was treated with penicillin. However, during the treatment, he developed a pulmonary embolism. So he underwent surgical treatment. We should take dental treatment into account one of predisposing causes of tricuspid endocarditis.

Anti-Bacterial Agents↗

PubMed1996

Expression of polymorphonuclear leukocyte adhesion molecules and its clinical significance in patients treated with percutaneous transluminal coronary angioplasty.

OBJECTIVES: This study evaluated the role of neutrophil adhesion molecules LFA-1 (CD11a/CD18), Mac-1 (CD11b/CD18) and p150,95 (CD11c/CD18) in patients undergoing percutaneous transluminal coronary angioplasty (PTCA). BACKGROUND: Several recent studies have suggested that cell adhesion molecules on both neutrophils and vascular endothelial cells play an important role in the process of tissue inflammation. METHODS: Thirty-eight patients (30 men, 8 women; mean [+/-SE] age 56 +/- 5 years, range 38 to 76) with single-vessel coronary artery disease of the left anterior descending artery underwent coronary angioplasty. Peripheral blood was sampled at baseline before, immediately after and 12, 24, 48 and 144 h after PTCA. The expression of CD18, CD11a, CD11b and CD11c on the surface of polymorphonuclear leukocytes was examined by flow cytometry with monoclonal antibodies. RESULTS: In patients without subsequent restenosis, there was no change in mean channel fluorescence intensity (MFI) of CD18 at each sampling time. However, in the patients with restenosis, the MFI of CD18 significantly increased at 48 h after PTCA (from 57 +/- 6 to 73 +/- 8, p = 0.0008). The MFI of CD11b increased slightly at 48 h after PTCA in patients without restenosis (from 584 +/- 121 to 735 +/- 114, p = 0.037). In patients with restenosis, the MFI of CD11b was slightly increased at 24 h after PTCA (from 586 +/- 122 to 768 +/- 214, p = 0.018) and significantly increased at 48 h after PTCA (to 1,534 +/- 268, p = 0.0006). The expression of CD11a and CD11c did not change at any sampling points after PTCA in either of the two patient groups. Percent change in the expression of CD18 at 48 h after PTCA (from baseline) and that of CD11b were correlated (r = 0.73, p = 0.0008) in patients with restenosis. CONCLUSIONS: Inflammatory stimuli within the coronary vessels associated with coronary angioplasty may upregulate Mac-1 expression on the surface of polymorphonuclear leukocytes. This process may be more marked in patients who experience later restenosis. Thus, activation of neutrophil adhesion molecule Mac-1 at 48 h after PTCA may have value as a predictor of subsequent restenosis.

Adult↗

PubMed1996

An impaired carotid sinus distensibility and baroreceptor sensitivity alter autonomic activity in patients with effort angina associated with significant coronary artery disease.

Baroreceptor sensitivity and carotid sinus distensibility were lower in patients with angina associated with significant coronary artery disease than in patients with vasospastic angina. Baroreceptor sensitivity was significantly correlated with carotid sinus distensibility in both groups of patients.

Angina Pectoris↗

PubMed1996

Cross-linking of the ninth consensus repeat domain of P-selectin (GMP-140, CD62P) with a monoclonal antibody enhanced leukocyte adhesive activity.

P-selectin (GMP-140, CD62P) is a member of the selectin family of cell adhesion molecules expressed on the cell surface of platelets and endothelial cells, which mediates leukocyte adhesion via carbohydrate ligands. We now report that a monoclonal antibody (mAb), recognizing the ninth consensus repeat domain of the human P-selectin molecule, enhanced the adhesion activity of neutrophils to platelets, whereas the monovalent Fab fragment of the mAb did not exert this effect. The enhancement by the mAb was thought to result from cross-linking of the P-selectin molecules. The results indicated that cross-linking adjacent to the transmembrane domain of P-selectin enhanced the cell adhesion activity.

Antibodies, Monoclonal↗

PubMed1996

Relationship between regional abnormality of left ventricular rapid filling and coronary microcirculation disturbance in hypertrophic cardiomyopathy.

BACKGROUND AND HYPOTHESIS: To investigate the mechanism of regional left ventricular diastolic filling disturbance in hypertrophic cardiomyopathy (HCM), we assessed the relationship between abnormalities of regional ventricular rapid filling and regional coronary microcirculation using radionuclide ventriculography and exercise 201thallium (201TI) myocardial scintigraphy with sector analysis. METHODS: Thirty patients with HCM and 14 patients with atypical chest pain syndrome (controls) were studied. Left ventricular images (left anterior oblique view) were obtained by electrocardiogram-gated 99mtechnetium radionuclide angiography and were divided into three sectors radiating from the geometric center. The time-activity curves and their first derivative curves were analyzed, and the peak filling rate (PFR), the ratio of the time-to-peak filling rate per diastolic interval (TPFR/T) were calculated for the global left ventricle and for the lateral and septal sectors. Exercise stress 201TI myocardial scintigraphy was also performed, and early and delayed images were obtained. The regional washout rate (WR) was then evaluated for the lateral and septal sectors. RESULTS: In HCM patients, the regional PFR in the septal sector (corresponding to the region of hypertrophic myocardium) was 285 +/- 76%/s, and was significantly lower than that in the controls (398 +/- 90%/s, p < 0.01). The regional TPFR/T in the septal sector (32 +/- 10%) was prolonged compared with the value of 21 +/- 5% in the controls (p < 0.05). The regional WR in the septal sector was 21 +/- 9%, and was significantly lower than that in the controls (43 +/- 5%, p < 0.01). Moreover, regional WR correlated positively with regional PFR (r = 0.5, p < 0.05) and showed a weak negative relationship with regional TPFR/T (r = -0.4, p < 0.07) in the septal sector. CONCLUSIONS: These results suggest that regional impairment of rapid filling might be related to a disturbance of the coronary microcirculation in HCM.

Cardiomyopathy, Hypertrophic↗

PubMed1996

Effect of SM-12502 on disseminated intravascular coagulation (DIC) in tumor-bearing rats.

To investigate the role of PAF in tumor-associated disseminated intravascular coagulation (DIC), we have established the tumor-induced DIC model in rats and examined the effect of PAF-antagonist as compared with commonly used anti-DIC drugs. Four days after the intraperitoneal inoculation of rat ascites hepatoma AH-130, DIC-like hematological parameter changes such as decrease in platelet count, prolongation of PTT and increase in FDP were observed. In addition, serum levels of GOT and GPT were increased, indicating that liver injury was provoked. PAF-antagonist SM-12502 inhibited the development of DIC (PT, PTT and FDP) and liver injury. These results indicate that PAF plays an important role in tumor-associated DIC as well as accompanying organ failure.

Alanine Transaminase↗

PubMed1996

Tc-99m tetrofosmin myocardial perfusion SPECT after dipyridamole combined with low-level exercise in the diagnosis of coronary artery disease.

Tc-99m tetrofosmin is a lipophilic, cationic perfusion imaging agent that changes to Tl-201 in detecting coronary artery disease during exercise testing. The purpose of this study is to evaluate the usefulness of Tc-99m tetrofosmin dipyridamole stress imaging combined with low level exercise for the detection of coronary artery disease. We examined 42 patients and 10 normal volunteers who also underwent coronary angiography. A one-day protocol was used: in the stress study, 296 MBq of tetrofosmin was injected and in the rest study 888 MBq was injected. After intravenous administration of dipyridamole (0.142 mg/kg/min for 4 minutes), the patient was exercised on a bicycle ergometer for 3 min (25 Watts). Tetrofosmin was injected 2 minutes after dipyridamole infusion during the exercise. Single photon emission computed tomographic images were obtained 30 minutes after the tracer injection. Images were interpreted as abnormal in 36 of 42 patients with coronary artery disease, and normal in all of 10 normal volunteers. The overall sensitivity of detection of coronary artery disease was 83.3% and the normalcy rate was 100%. The diagnostic values for the detection of significant stenosis in the three major arteries were: LAD sensitivity 83%, specificity 92%; LCX sensitivity 47%, specificity 91%; RCA sensitivity 75%, specificity 83%. Of the 66 arteries with more than 50% stenosis, 48 arteries were correctly identified. Of the 36 with more than 70% stenosis, 31 were identified. Scintigraphic evidence of multivessel disease was found in only 9 patients (50%). A protocol of Tc-99m tetrofosmin SPECT combined with low level exercise after dipyridamole is therefore useful for the detection of the coronary artery disease.

Adult↗

PubMed1996

Role of P-selectin in the early stage of the Arthus reaction.

P-selectin is rapidly translocated to the surface of endothelial cells and platelets following exposure to chemical mediators such as histamine, thrombin and complement factors. The Arthus reaction is caused by vascular injury which is initiated by the local deposition of the immune complex followed by the activation of complement and release of chemical mediators. In this report, the role of P-selectin in the early stage of reverse passive Arthus reaction in rat using monoclonal antibodies (mAbs) against rat P-selectin will be investigated. Intravenous administration of the mAb ARP2-4 significantly attenuated paw edema 1 h after challenging it with antigen by 31.5% (1 mg/kg) and 44.7% (3 mg/kg), respectively. Edema formation was also reduced by sulfatide (73.1%, 50 mg/kg) and inositol hexakisphosphate (InsP6) (72.9%, 30 mg/kg), which have been reported to block P-selectin-mediated neutrophil adhesion. Moreover, neutrophil accumulation into the inflammatory site in the Arthus reaction was inhibited by anti-P-selectin mAb. P-selectin expression was detected along vessel walls prior to neutrophil accumulation, as determined by immunohistochemical staining using the antibody. In addition, the expression of P-selectin mRNA was induced 4 h after deposition of immune complex. From these results, we concluded that P-selectin plays an important role in the pathogenesis of the Arthus reaction especially in the early stage by recruiting neutrophils into sites of inflammation.

Animals↗