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Biomedical subjects

N Ohya

Publications and source records attributed to N Ohya.

95 records · Page 6Linked to original sources
PubMed1974

Influence of changes in heart rate, aortic pressure and flow rate upon experimental coronary insufficiency.

This study was designed to evaluate the role of heart rate, aortic pressure, and aortic flow in the development of coronary insufficiency following acute coronary stenosis. In dogs, each of these parameters was controlled at a predetermined level while the left anterior descending coronary artery was constricted with a small screw clamp. The critical coronary pressure (CCP), i.e. the pressure below which a rise of left atrial pressure could be detected, was determined at various levels of hemodynamic load. Increases in aortic pressure, elevation of the heart rate and an increase in aortic flow rate were all associated with an elevation of the CCP and an increase in tension-time index (TTI). The changes in CCP were most striking when TTI was increased by aortic flow rate change. These findings suggest that with high aortic pressure, further constriction of coronary artery is required to precipitate coronary insufficiency, that the level of pacing required to induce coronary insufficiency is a useful index in assessing the degree of coronary stenosis, and that an augmentation of aortic flow rate is an important factor in the initiation of coronary insufficiency.

Animals↗
PubMedDate not supplied

Transcatheter arterial embolization for malignant osseous and soft-tissue sarcomas. I. A rabbit experimental model.

PURPOSE: To evaluate the effect of transcatheter arterial embolization (TAE) on metastatic bone tumors in an experimental study. METHODS: Fifteen Japanese white rabbits were transplanted with VX2 sarcoma cells into the iliac crest. In 10 rabbits, the arterial supply to the iliac bone tumors, internal iliac artery and iliolumbar artery were then embolized with particles of gelatin sponge. The therapeutic effect was evaluated by comparison with the natural course of control tumors in the other five rabbits. RESULTS: After TAE, extensive necrosis, fibrosis, and vacuolization within the tumors were confirmed histologically. In the control rabbits, 19% +/- 7% of the entire tumor was found to be spontaneous tumor necrosis; in contrast, the tumors of the TAE group showed necrosis as 62% +/- 22% of the entire tumor. In one TAE group rabbit, no active tumor cell could be detected in the residual tumor. CONCLUSION: TAE was found to be an effective treatment for bone tumors in an experimental model.

Animals↗
PubMedDate not supplied

Beta1-adrenoceptor stimulation by high-dose terbutaline downregulates terbutaline-stimulated alveolar fluid clearance in ex vivo rat lung.

Because high-dose terbutaline and isoproterenol (10(-3) M), beta2-adrenergic agonists, failed to increase alveolar fluid clearance, the mechanisms responsible for this effect were examined in ex vivo rat lungs. An isosmolar 5% albumin solution with Evans blue dye was instilled into the distal airspaces in isolated rat lungs that were then inflated with 100% oxygen at an airway pressure of 8 cm H2O in a 37 degrees C incubator. Alveolar fluid clearance was measured by the progressive increase in dye concentrations over 1 hour. The results indicated that: (1) although 10(-5) M terbutaline or isoproterenol increased alveolar fluid clearance, 10(-3) M terbutaline or isoproterenol did not; (2) both concentrations of terbutaline (10(-5), 10(-3) M) increased intracellular adenosine 3',5'-cyclic monophosphate in cultured type II alveolar epithelial cells; (3) instillation of atenolol, a selective beta1-adrenergic antagonist, in the presence of either 10(-3) M terbutaline or isoproterenol was associated with an increase in alveolar fluid clearance. These results suggested that beta1-adrenoceptor stimulation prevented the normal response to a beta2-adrenergic agonist. To further test this hypothesis, a selective beta1-adrenergic agonist, denopamine, was administered; these results showed that (4) 10(-3) M denopamine, a selective beta1-adrenergic agonist, inhibited the increase in alveolar fluid clearance in the presence of 10(-5) M terbutaline; (5) hypoxia for 2 hours did not alter the effects of terbutaline on alveolar fluid clearance. The mechanism for the inability of the alveolar epithelium to respond to high-dose terbutaline or isoproterenol with the normal upregulation of alveolar fluid clearance in ex vivo rats lungs appears to be mediated by beta1-adrenoceptor stimulation that subsequently suppresses the beta2-adrenergic response.

Adrenergic beta-Agonists↗