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Biomedical subjects

O Okada

Publications and source records attributed to O Okada.

At least 73 records · Page 4Linked to original sources

[Evaluation of the renal artery in the fetuses with growth retardation and oligohydramnios by two dimensional Doppler ultrasonography].

Renal blood flow dynamics were studied with color and pulsed Doppler ultrasound in 102 normal fetuses at 20 to 40 weeks of gestation, 11 growth retarded fetuses (group A), 15 fetuses with oligohydramnios (group B) and 10 growth retarded and oligohydramniotic fetuses (group C) at 32-40 weeks of gestation. The maximum systolic velocity (VMAX), early diastolic peak velocity (VEA), end diastolic velocity (VED) and resistance index (RIEA:VMAX-VEA/VMAX and RIED:VMAX-VED/VMAX) were measured in the renal artery. VMAX was also measured in the ascending aorta (AO) and pulmonary artery (PA). In the normal fetuses, blood flow velocity increased with gestational age, but VMAX and VEA remained constant after 28 weeks of gestation. The resistance index decreased with gestational age, but RIEA remained constant after 28 weeks of gestation. RIED in groups A and C increased significantly, and VMAX in groups B and C, and VED in group C decreased significantly compared with normal fetuses. VMAX in AO and PA decreased remarkably in the three abnormal groups. It was concluded that the kidneys were poorly perfused in the growth retarded fetuses with oligohydramnios, which may, in part, depend on the decreased stroke volume.

Blood Flow Velocity↗

[Effects of various doses of monocrotaline administration on the development of pulmonary hypertension and its regression in rats].

We observed the time course of hemodynamic and pathological changes after single injection of various dose of monocrotaline (Mct) to investigate the dose-dependent effects on the induction and regression of pulmonary hypertension in rat: A hundred four-week old male Sprague-Dowley rats were divided into five groups and each group, except the control group, received 10 mg, 20 mg, 30 mg or 40 mg/kg Mct, respectively. The experimental periods were nine weeks after monocrotaline injection. At the third, sixth and ninth week after treatment, the survival rate, cardiac catheterization and pathological changes were evaluated. All rats given 30 mg or 40 mg per kg of Mct died within five weeks. In the third week after the treatment, elevation of the right ventricular systolic pressure (RVSP), the grade of right ventricular hypertrophy (RVH) and histological change showed no significant difference among rats receiving 20, 30 or 40 mg/kg Mct injection. Almost all rats given 10 mg or 20 mg/kg Mct survived through the experimental period of nine weeks. Rats given 10 mg per kg of Mct did not develop pulmonary hypertension or pathological abnormalities in the lungs. Rats receiving 20 mg/kg Mct showed transient elevation of RVSP, RVH and pulmonary histological changes in the early phase, but these findings regressed by the ninth week of the experiment. Namely, rats which received 20 mg pr kg of Mct revealed transient elevation of right ventricular systolic pressure, right ventricular hypertrophy and pulmonary histological changes only in the early phase and these changes regressed gradually thereafter. These results indicate some kind of transient and reversible factor may play a role in the development and regression of Mct-induced pulmonary hypertension in rats.

Animals↗