Search PubMed⌕ Search

Biomedical subjects

J Ando

Publications and source records attributed to J Ando.

At least 109 records · Page 6Linked to original sources
PubMed1987

The effect of fluid shear stress on the migration and proliferation of cultured endothelial cells.

We have examined the effect of shear stress on the regenerative response of cultured vascular endothelial cells by using a fluid shear apparatus designed in our laboratory. The shear stress was created on the endothelial cell layer of a fetal calf and grown confluently in a culture dish by whirling the medium, with a rotating disk placed on the fluid surface. The effect of the shear load (0.3-1.7 dyn/cm2) over 24 hr was evaluated by counting the number of regenerated cells in a denuded area that had been created by mechanically removing some cells before rotating the medium. The cell number observed in the denuded area after the exposure to shear stress was about twice as great as that of the static control. The difference was statistically significant (P less than 0.01 to P less than 0.05). Cell migration and proliferation occurred more prominently in the downstream portion of the flow than in the upstream part. The cell number in the downstream portions correlated significantly with the intensity of the applied shear stress (P less than 0.05). These results indicate that shear stress can stimulate the migration and proliferation of endothelial cells.

Animals↗
PubMed1986

Binding of [3H]nitrendipine to cardiac and cerebral membranes from normotensive and renal, deoxycorticosterone/NaCl and spontaneously hypertensive rats.

The properties of [3H]nitrendipine binding to cardiac and cerebral membranes from normotensive Wistar-Kyoto (WKY) and renal (RHR), deoxycorticosterone/NaCl (DOCA-HR) and spontaneously hypertensive (SHR) rats were investigated. The maximal numbers of binding sites (Bmax) in the striatum, thalamus and hippocampus for SHR increased by 21.4-40.0, 28.1-40.4 and 21.4-34.1% of the numbers in WKY, but the apparent dissociation constants (KD) in the cerebral membranes differed very little between WKY and SHR. In the cardiac membranes, KD and Bmax values differed very little between WKY and SHR. In the RHR and DOCA-HR, the Bmax values in the striatum, thalamus and hippocampus were similar to those of WKY. These findings suggest that the increase in Bmax of [3H]nitrendipine in the striatum, thalamus and hippocampus of SHR may play a part in the development and maintenance of high blood pressure in SHR.

Animals↗
PubMed1986

Responsiveness of hypophyseal-adrenocortical axis to repetitive administration of synthetic ovine corticotropin-releasing hormone in patients with isolated adrenocorticotropin deficiency.

The primary lesion site in isolated ACTH deficiency was studied in three patients by examining the responses of immunoreactive ACTH to insulin-induced hypoglycemia, lysine vasopressin, and synthetic ovine corticotropin-releasing hormone (CRH). In all patients, no significant changes in immunoreactive ACTH followed insulin-induced hypoglycemia or lysine vasopressin. Fifty micrograms (greater than or equal to 1 microgram/kg BW) of CRH administered as an iv bolus dose daily for 6 consecutive days elicited no significant increase in plasma immunoreactive ACTH, beta-lipotropin, or cortisol levels in all patients. Eight iv bolus injections of 0.63 microgram/kg BW CRH at 4-h intervals also failed to induce a significant response of immunoreactive ACTH to an iv bolus dose of 1 microgram/kg CRH at 36 h in one patient. In contrast, a single bolus dose of 50 micrograms CRH induced a response of plasma immunoreactive ACTH in a patient with Cushing's disease and a patient with Addison's disease. The present results suggest that the primary lesion of isolated ACTH deficiency is not the hypothalamus, but, rather, is located in pituitary ACTH-secreting cells.

Addison Disease↗
PubMed1986

Calcium channel, Ca++ mobilization, and mechanical reactivity of estrogen- and progesterone-treated rat uterus.

Properties of [3H]nitrendipine binding, high K+- and Ca++-induced contractions and the inhibition of high K+-induced contractions by verapamil were investigated in the uterine preparations isolated from rats treated with estrogen or progesterone or both. In [3H]nitrendipine binding experiments using crude membrane fractions, treatment with estrogen alone or estrogen+progesterone significantly lowered the KD; There was very little change in the Bmax. In the Ca++-depleted, high K+-containing medium, only the progesterone-, and estrogen----progesterone-treated uteri produced contractions. The estrogen-, estrogen----progesterone-, and estrogen+progesterone-treated uteri showed decreases in concentrations of Ca++ required for the maximal contractions. In the estrogen- and estrogen+progesterone-treated uteri, the dose-response curves by verapamil were shifted to the left in a parallel manner. These findings suggest that estrogen appeared to increase the affinity of calcium channels and increase transmembrane influx of Ca++, leading to enhancement of contractions, whereas progesterone might increase the Ca++ storage in the intracellular sites.

Animals↗
PubMed1985

Alterations in myocardial perfusion during painless ST-segment depression in patients with angina pectoris.

In order to determine whether painless ST changes represent myocardial ischemia, we studied regional myocardial perfusion in patients with angina pectoris who showed painless ST-segment depression during a treadmill exercise test. Twenty-one patients were evaluated by myocardial imaging using thallium-201 injected intravenously during exercise when painless ST-segment depression was evident. The same examination was repeated in 5 of the above patients when they showed ST-segment depression with chest pain. Myocardial images obtained during painless ST-segment depression revealed perfusion defects in 15 of 21 patients (71%). Images obtained during ST-segment depression with chest pain showed perfusion defects in all 5 patients (100%) including 3 patients who demonstrated no defects during painless ST-segment depression. In these 5 patients, the ST-segment depression associated with pain was significantly greater than that without pain (3.4 +/- 1.1 vs 2.1 +/- 1.1 mm, p less than 0.01). These results suggest that the majority of episodes of painless ST-segment depression occurring during exercise are accompanied by regional myocardial perfusion abnormalities and that transient painless ST-segment depression in patients with angina pectoris might represent less severe myocardial ischemia.

Adult↗
PubMed1985

[Right ventricular dysplasia and dilated cardiomyopathy observed by radionuclide images].

Four cases of right ventricular dysplasia (RVD) and 28 cases of dilated cardiomyopathy (DCM) were studied. RVD was characterized clinically by syncope, sustained recurrent ventricular tachycardia with left bundle branch block patterns on the surface electrocardiogram, and right heart failure. Furthermore, moderate to severe dilatation of the right ventricle and depressed right ventricular function were apparent on radionuclide angiography. However, left ventricular dilatation and depressed left ventricular function were documented in DCM. Right ventricular volume was proportional to left ventricular volume in DCM, however, right ventricular volume was disproportionately greater in RVD. On the T1-201 perfusion image, left ventricular perfusion defects were delineated in 10 of 26 patients with DCM, and in one of four RVD patients. During two to eight year follow-up periods, six patients died suddenly five of whom had left ventricular perfusion defects. However, in 19 patients without left ventricular perfusion defects, only one sudden death was observed. A connecting link between sudden death and left ventricular perfusion defect is suggested.

Cardiac Volume↗
PubMed1985

[Hypertrophic obstructive cardiomyopathy with extensive myocardial fibrosis: case report with autopsy].

An autopsy case of hypertrophic obstructive cardiomyopathy with extensive myocardial fibrosis is reported in a 43-year-old male. His mother died suddenly at 55. At the age of 39 the patient felt fatigue and feverish sensation followed by dyspnea and palpitation on exertion. He responded to beta-blocker and was discharged on the 51st hospital day. He died suddenly during his work three years and one month after discharge. The heart weighs 700 g. The thickness of the ventricular septum measures up to 3.2 cm, and that of the left ventricular posterior wall 2.2 cm. Subaortic endocardium is moderately thickened. Many patchy fibroses of various sizes and broad linear fibroses are mainly observed in the ventricular septum and in the left ventricular free wall. Microscopic examination shows severe fascicular disarray of hypertrophied myocardial fibers in the ventricular septum and in a part of the left ventricular anterior wall. Pericardial fibrosis, granulation tissue with many capillaries, and slight lymphocytic infiltrate are also noted. These findings suggest that the patient have both congenital hypertrophic cardiomyopathy and myocarditis. There are following possibilities as regards the relation between the two: first, haphazard association of cardiomyopathy with myocarditis; secondly, myocarditis triggered the onset or progression, or both, of cardiomyopathy. He also had liver cirrhosis, probably alcoholic, which appears to accelerate the progression of myocardial disarray and fibrosis.

Adult↗
PubMed1984

Myocardial perfusion and left ventricular performance during exercise-induced ST-segment depression in apparently healthy subjects.

Ischemic-like ST-segment depression seen during exercise in apparently healthy subjects has previously been noted, but the cause of this change is unknown. The aim of this study was to investigate the pathophysiology of this electrocardiographic change. Ten healthy subjects who developed an electrocardiographic "ischemic" pattern of ST change during treadmill exercise testing were studied. All subjects underwent both thallium-201 myocardial perfusion imaging and radionuclide angiocardiography at rest and during exercise at a time when abnormal ST changes appeared, and demonstrated a normal homogeneous pattern of thallium-201 distribution on both rest and exercise images. Overall, left ventricular ejection fraction rose from 0.60 +/- 0.06 (mean +/- SD) at rest to 0.65 +/- 0.07 with exercise. None of the subjects had regional wall motion abnormalities at rest or during exercise. These results are different from the findings observed in patients with coronary heart disease and angina pectoris in whom regional abnormalities in both perfusion and left ventricular performance have been noted during exercise. Therefore it would seem that myocardial ischemia is not likely to be a tenable explanation for the electrocardiographic "ischemic" changes in these apparently healthy subjects.

Adult↗
PubMed1983

Adrenergic regulation of estradiol uptake and cyclic GMP content in rat uterus.

The presence of adrenergic regulation of estradiol uptake in rat uterus was studied by using alpha- and beta-adrenergic blockers in normal or Ca2+-free Tyrode's solution at 30 degrees C in vitro. Cyclic GMP content was also investigated under these conditions. By the stimulation with noradrenaline (4 X 10(-7) M), Ca2+-dependent 3H-estradiol uptake was increased in both cytosol and nuclear fractions. These increases were blocked in the presence of phentolamine (4 X 10(-7) M) but not by propranolol (4 X 10(-7) M). Increase in uterine cyclic GMP contents were shown under the condition in which 3H-estradiol uptake was stimulated. These results suggest that adrenergic alpha-stimulation increased uterine estradiol uptake and that consequently, increased estradiol-receptor complexes elevated uterine cyclic GMP levels. The changes in uterine cyclic GMP may serve as an index of estrogen action.

Animals↗
PubMed1983

Pharmacological effects of flurazepam and diazepam on isolated canine arteries.

The effects of flurazepam and diazepam, benzodiazepine derivatives, on contractions (or contractures) induced by Ca++, K+ or norepinephrine were examined in the isolated canine coronary artery and thoracic aorta. Ca++-Induced contraction was evoked by cumulative addition of CaCl2 to Ca++-depleted K+-depolarizing solution; K+: and norepinephrine-induced contractions were evoked by cumulative addition of KCl and norepinephrine, respectively, to the medium. Flurazepam and diazepam (1 X 10(-5), 3 X 10(-5) and 1 X 10(-4) M for coronary artery; 3 X 10(-5) and 1 X 10(-4) M for thoracic aorta) shifted the dose-response curves for KCl downwards in a non-competitive manner, and shifted the dose-response curves for CaCl2 to the right in a competitive manner. Ca++-Induced contracture was inhibited completely by addition of flurazepam or diazepam (1 X 10(-4) M), and the inhibition was reversed dose-dependently by addition of CaCl2. Flurazepam and diazepam (3 X 10(-5) and 1 X 10(-4) M) shifted the dose-response curves for norepinephrine both rightwards and downwards in the thoracic aorta. These findings suggest that flurazepam and diazepam inhibit Ca++-influx into the cells (Ca++-antagonistic effect), causing relaxation and inhibition of K+-, Ca++-, or norepinephrine-induced contraction (or contracture) of the vascular smooth muscle.

Animals↗
PubMed1983

[Nuclear medicine].

Explore the source record for details and available documents.

Coronary Disease↗