[Surgery of thymoma associated with pure red cell aplasia (PRCA) and hypogammaglobulinemia].
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Biomedical subjects
Publications and source records attributed to M Handa.
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1. To examine the possible participation of the brain iso-renin-angiotensin system in the control of blood pressure, as well as in the regulation of plasma renin activity, saralasin and captopril were injected into the cerebral ventricles of three types of experimental hypertensive rats with different plasma renin profiles. 2. Injection of saralasin and captopril into the cerebral ventricles resulted in a significant decrease in blood pressure of two-kidney, one-clip Goldblatt hypertensive rats (11 +/- 2 and 9 +/- 3 mmHg respectively) and that of spontaneously hypertensive rats (13 +/- 2 and 12 +/- 2 mmHg respectively), but in deoxycorticosterone (DOC)-salt hypertensive rats injection of these two agents showed a significant increase in blood pressure (13 +/- 2 and 12 +/- 3 mmHg respectively). 3. The plasma renin activity was markedly decreased after injection of saralasin and captopril into the cerebral ventricles of two-kidney, one-clip Goldblatt hypertensive rats. Conversely, in DOC-salt hypertensive rats, the plasma renin activity was markedly increased after injection of these two agents. In spontaneously hypertensive rats these agents caused no significant change in plasma renin activity. 4. These findings suggest that the brain iso-renin-angiotensin system participates in the central regulation of blood pressure and may be responsible for modulation of the peripheral renin-angiotensin system.
To investigate the role of the central and peripheral dopaminergic systems in the control of the renin-angiotensin-aldosterone system in conscious rats, dopamine or its antagonist, metoclopramide, was injected intravenously (i.v.) and intracerebroventricularly (i.c.v.). Dopamine (100 micrograms/kg), when injected i.c.v., decreased plasma renin activity (PRA) and plasma aldosterone concentration (PA), while metoclopramide (50 micrograms/kg, i.c.v.) increased both of them. Intravenous administration of dopamine (1 microgram/kg/min) did not produce significant changes in either PRA or PA. In contrast, metoclopramide (500 micrograms/kg, i.v.) increased PA, which was not accompanied by any change in PRA. Blood pressure was decreased by i.c.v. administration of dopamine and increased by i.c.v. injection of metoclopramide, whereas no change in blood pressure was observed when these compounds were administered i.v. Dopamine and metoclopramide, injected i.v. or i.c.v., did not produce significant changes in plasma sodium, potassium and corticosterone concentrations. These results suggest that the dopaminergic system in the brain regulates renin secretion, thereby changing PA. In contrast, dopamine receptors of the adrenal glands may inhibit aldosterone secretion, which is not mediated by changes in the renin-angiotensin system, plasma potassium and ACTH.
In the perfused rat mesenteric vascular bed, the effects of captopril and prostaglandin I2 (PGI2) on the vasoconstrictor responses to norepinephrine or potassium chloride were studied. Captopril or PGI2 in the perfusate attenuated the vascular responses to norepinephrine in a dose-related manner, while these substances had no effect on the vascular contractions induced by potassium chloride. In preparations treated with indomethacin, the inhibitory effect of captopril on the vascular response to norepinephrine was similar to that found in the untreated preparations. These results suggest that, although the effects of captopril on the vascular reactivity is similar to that of PGI2, the direct vascular action of captopril is not mediated by the synthesis of prostaglandins in the vascular bed.
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The intracerebroventricular (i.c.v.) injection of dopamine (50--200 micrograms/kg) produced a dose-dependent decrease in arterial blood pressure in conscious rats. This depressor effect of dopamine was attenuated by the pretreatment with metoclopramide (16.5 micrograms/kg, i.c.v.), a dopamine receptor antagonist. Metoclopramide in higher doses (50 and 150 micrograms/kg), given i.c.v., produced an increase in blood pressure. The pretreatment with dopamine (50 micrograms/kg, i.c.v.) attenuated the pressor effect of metoclopramide. Furthermore, autonomic ganglion blockade with hexamethonium (25 mg/kg, i.v.) almost completely abolished the effects of dopamine and metoclopramide, indicating that these substances were exerting their effects within the central nervous system. These results suggest that the dopaminergic system in the brain is involved in regulation of systemic blood pressure in conscious rats.
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A technical modification in pulmonary venous anastomosis is presented for one-stage bilateral lung autotransplantation in dogs. This method nullified or minimized both narrowing and loss of vascular distensibility due to scar formation at anastomotic line which inevitably resulted in functional defects after the operation. In this new procedure, bilateral pulmonary arteries were anastomosed using angioplastic techniques and both right and left pulmonary veins were sutured orthotopically as a single atrial cuff. Of 11 dogs which underwent one-stage bilateral lung replantation, 6 survived after operation. Sites of vascular anastomoses in the long-term survivors showed no narrowing due to scar formation at autopsy after hemodynamic examination. In these animals rapid and continuing infusion of 2000 to 3000 ml of blood or plasma explander was performed within 15 min through an intraatrial catheter. Various hemodynamic values were measured simultaneously. In the dog with bilateral lung transplants pulmonary arterial pressure showed linear increase with an increase in cardiac output when compared with control animal studies. It could be interpreted from these results that some changes occurred in the mechanism of pulmonary circulation of the transplant.
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