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Biomedical subjects

H Ijichi

Publications and source records attributed to H Ijichi.

At least 163 records · Page 9Linked to original sources
PubMed1981

Sympathetic and pressor hyperresponsiveness to intracisternal injections of hypertonic NaCl in DOCA hypertensive rats.

Blood pressure and sympathetic nerve activity were recorded before and after intracisternal injections of hypertonic NaCl solution in urethane anesthetized normotensive and deoxycorticosterone acetate (DOCA) hypertensive rats. Dose dependent pressor effects were recorded by intracisternal injections using normotensive Wistar rats. And the early phase of responses which were significantly depressed by blocking alpha-adrenergic receptors with phentolamine, accompanied by increased frequency of sympathetic nerve firing. Pressor responses and acceleration of the rate of sympathetic nerve firing produced by intracisternal injections of hypertonic NaCl were appreciably larger in DOCA hypertensives whose basal sympathetic nerve activity was elevated significantly than in normotensive rats. Pressor responses to intravenous injection of norepinephrine were also augmented, but responses to intracisternal injection were augmented more than those to norepinephrine injection. These findings suggest that sodium sensitive site which connects to pressor systems supposedly located around lower brain stem could be hypersensitive and eventually contribute to peripheral sympathetic hyperactivity in DOCA hypertension.

Animals↗
PubMed1981

Clinical study on increased serum thyroxine-binding globulin in cancerous state.

Serum thyroxine-binding globulin (TBG) in 169 patients with various cancers was determined by radioimmunoassay (RIA). Eleven patients showed a high serum TBG level (greater than 35 micrograms/ml). Two of them had been treated with estrogen for prostate cancer. One patient had high serum TBG with serum hepatitis. Another 8 cases had normal liver function and also normal levels serum estrogen. Thus, about 4.7% (8/169) of the cancer patients had high serum TBG and mild hyperthyroxinemia caused by unknown mechanisms. The high TBG level in these patients continued until just before death, or in some cases decreased to normal after removal of cancer tumors by operation. Cancer is occasionally associated with an increase in serum TBG. Although the mechanism is not clear, the increased TBG in the cancerous state in interesting and has significance as a tumor marker.

Adult↗
PubMed1981

[Analysis of left to right ventricular stroke count ratio by gated radionuclide angiocardiography: detection and quantitation of valvular regurgitation and shunts (author's transl)].

The stroke count ratio (SC ratio: SCL/SCR) for left to right ventricular enddiastolic-endsystolic count differences was obtained from LAO multi-gated cardiac blood pool scintigrams for quantitative assessment of valvular regurgitation and shunts. SC ratio, 1.48 +/- 0.24 (mean +/- S.D.) in 21 normal subjects, was decreased in 7 patients with atrial septal defects (ASD) and in one with isolated tricuspid regurgitation (TR), and increased in 15 patients with aortic regurgitation (AR) and in 6 with mitral regurgitation (MR). In post-surgical reassessment of 3 patients, the ratio was restored in normal range. Comparison between SC ratio and angiographic estimates of regurgitation revealed good agreement. Regurgitant fraction (RF) in AR or MR and shunt ratio (SR) in ASD were calculated by the formula: RF = 1-1.48/SC ratio, and SR = 1-SC ratio/1.48, respectively. These were derived by assuming that an excess of stroke counts was due to regurgitant or shunt flow and that the coefficient in counting ventricular radioactivity was 1.48. Agreement was found between RF or SR measured by this formula and by the invasive method. This method permits noninvasive quantitation in patients with valvular regurgitation and shunts without complicated computer procedures.

Aortic Valve Insufficiency↗
PubMed1980

Effect of trapidil on prostacyclin generation of arterial wall.

Prostacyclin (PGI2) has been reported to be a labile but potent inhibitor of platelet aggregation and a powerful vasodilator. This paper reports the effect of trapidil on PGI2 generation in rat aorta by means of bioassay system. The aortic ring was incubated in 0.05 M Tris HCl buffer (pH 7.5) for 10 min. This incubation medium was added into human PRP, and then incubated at 37 degrees C for 2 min., and ADP was added. PGI2 activity was assayed by the inhibitory percentage of ADP induced platelet aggregation. When the aortic ring was incubated in a medium containing trapidil, PGI2 generation was accelerated. This acceleration was inhibited by pretreatment with indomethacin. Moreover, the aortas of rats intravenously injected with 30 mg/kg of trapidil were incubated in the same way, and PGI2 activity in the medium was estimated. More potent PGI2 activity was observed in the aortas of rat treated with trapidil compared with the controls. These results indicate that acceleration of PGI2 generation from aorta by trapidil is involved in the mode of action of this drug of thrombus formation.

Animals↗
PubMed1980

Effect of sodium loading and depletion on vascular reactivity and prostacyclin generation.

In order to estimate the modulatory activity of Prostacyclin (PGI2) to the vascular reactivity, pressor responses to angiotensin II (A II) and noradrenaline (NA) and PGI2 generation aorta were measured using the rats of sodium loading or of sodium depletion. On the sodium loading, the blood pressure increased gradually and plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were decreased. The pressor responses to A II and NA were enhanced by sodium loading. The PGI2 generation of aorta was enhanced at the initial stage of sodium loading and decreased thereafter. The increased generation of PGI2 may represent the adaptive mechanism for the attenuation of the sustained elevation in blood pressure. It sodium depletion, the pressor responses to A II and NA were decreased, and PRA and PAC were elevated. PGI2 generation of aorta was also increased. These findings suggested that PGI2 could participate in blood pressure control mechanism on sodium loading and depletion.

Aldosterone↗