[Myocardial uptake of thallium-201 in rat with cardiac hypertrophy].
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Biomedical subjects
Publications and source records attributed to H Ijichi.
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To evaluate differences in systolic global and regional performances of the left ventricle during exercise, multi-stage submaximal exercise echocardiography was used for 21 patients with hypertrophic cardiomyopathy (HCM) and 14 patients with systemic hypertension (HT), whose interventricular septa (IVS) were nearly the same in thickness (HCM; 16.5 +/- 2.4 mm, HT; 15.4 +/- 1.7 mm, NS). The data were compared with those of 18 normal subjects (N). During exercise, end-diastolic dimension (EDD) was increased in all three groups; however, there was no statistical differences among the three groups either at rest or during exercise. End-systolic dimension (ESD) was significantly decreased during exercise in HT (29.3 +/- 5.8 at rest to 28.1 +/- 5.8 mm at the peak exercise, p less than 0.05) and N (from 30.3 +/- 3.3 to 25.7 +/- 3.0 mm, p less than 0.001). On the other hand, ESD of HCM at rest, which was less than those of the other two groups, did not decrease with exercise (from 25.1 +/- 4.5 to 25.6 +/- 4.6 mm, NS), and rather they increased (more than 2 mm) during exercise in seven patients. The % shortening fraction (%SF) increased from rest to exercise both in HT (35.6 +/- 7.9% to 40.1 +/- 9.6%, p less than 0.001) and in N (from 35.1 +/- 4.2 to 45.9 +/- 4.7%, p less than 0.001). However, in the HCM group, the %SF, which was significantly greater at rest than in the other two groups, did not increase during exercise (42.5 +/- 6.8 to 42.5 +/- 8.8%, NS). In addition, in seven of 21 patients with HCM, the %SF increased more than 5% at the peak exercise. At rest, systolic wall thickening (%WT) of the IVS equally reduced both in HCM and HT. It increased in HT from 20.8 +/- 9.3% at rest to 24.6 +/- 12.7% at the peak exercise (p less than 0.05), but did not change in HCM (from 16.6 +/- 9.6% to 16.3 +/- 7.0%, NS). At rest, %WT of the left ventricular posterior wall (LVPW) was significantly greater in HCM than in HT. During exercise, it increased in HT (from 43.1 +/- 15.9% to 61.9 +/- 20.5%, p less than 0.01), but did not increase in HCM (from 81.0 +/- 27.7% to 85.5 +/- 29.6%, NS).(ABSTRACT TRUNCATED AT 400 WORDS)
A 41-year-old male was diagnosed as acute lymphocytic leukemia (ALL) in November, 1982 and partial remission was obtained by a combination chemotherapy of LVP, DVP ABOP and VAMP. In January, 1983, peripheral blood showed an increasing number of leukemic cells and he was readmitted to our hospital. WBC count in the peripheral blood was 13,200/mm3 and an 82% ratio of leukemic cells was observed. Bone marrow aspiration showed a hypercellularity of 89.4% leukemic cells. High-dose Ara-C therapy was started at a dose of 3 g/m2 i.v. every 12 hours for 6 days. Leukemic cells in peripheral blood were rapidly decreased in number, and the nucleated cell count of bone marrow was also reduced after 3 weeks of treatment, however 95% of leukemic cells remained. Low-dose L-asparaginase was then supplemented at a dose of 2000 U for 3 days, and 2 months later complete remission was achieved. The side effects associated with this high-dose Ara-C therapy were nausea, vomiting, diarrhea, fever and conjunctivitis, although these were tolerable. These observations suggest that high-dose Ara-C combined with L-asparaginase should be added to the treatment of leukemia which is refractory to conventional chemotherapy.
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Clinical effects of sequential administration of high-dose cytosine arabinoside with L-asparaginase were studied in 5 cases of refractory acute leukemia and 2 cases of non-Hodgkin's lymphoma. A total 12 courses were carried out on these 7 patients and complete remission was obtained in 2 courses and partial remission in 3 courses. Two cases of lymphoma with pleural effusion or CNS invasion achieved partial and complete remission, respectively. The side effects associated with this sequential therapy were nausea, vomiting, diarrhea, fever and conjunctivitis, although these were tolerable. These observations suggest that high-dose cytosine arabinoside combined with L-asparaginase is a useful regimen for refractory leukemia and lymphoma.
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To assess differences in left ventricular (LV) performance between mitral regurgitation (MR) and aortic regurgitation (AR), exercise echocardiography was performed for 12 patients with MR and 18 patients with AR, and the results were compared with those of 11 normal subjects. These patients with LV volume overloads were all in the NYHA class I or II. There were no differences in age or sex distributions between the two groups. Symptom-limited submaximal exercise was performed on an ergometer in the supine position. The results obtained were as follows: LV dimensions at end-diastole (EDD) and end-systole (ESD) were greater in the diseased groups than in the normal group. Resting EDD and ESD showed no differences between the MR and the AR groups. There were no differences in exercise-induced increases in heart rates or elevations of systolic blood pressures among the three groups. During exercise, EDD increased and ESD decreased in the normal group, and similar results were obtained for the MR group. However, in the AR group, EDD and ESD remained unchanged. Ten of the 18 patients with AR had decreased ESD, and eight had unchanged or increased ESD during exercise. Resting shortening fractions were equally distributed among the three groups. During exercise, the shortening fractions were significantly increased in the normal and the MR groups. In the AR group, shortening fractions remained at resting values, with variable responses in individual cases. Systolic wall thickening of the interventricular septum and the LV posterior wall showed similar responses of shortening fractions. The relation between the peak systolic wall stress index (PSSI) and ESD, or PSSI and the shortening fraction revealed that exercise induced an afterload mismatch of LV performance in some patients with AR. Thus, though resting LV performances did not differ from each other, an afterload mismatch is more easily induced with exercise in patients with AR than in patients with MR. This may be one of the cause of the different clinical courses in these two groups with LV volume overloads.
Thallium-201 double dose scintigraphy was applied to exercise to estimate the coronary blood flow reserve of the left and right ventricles and this was compared with the degree of coronary artery stenosis. As an index of coronary reserve we measured the rate of change of blood flow distribution (delta F) calculated from the change in myocardial radioactivity following thallium-201 injections, once at rest and once during exercise. With submaximal exercise the increases in delta F of the left ventricle were less in patients with ischemic heart disease than in the control subjects, and were less as the number of diseased coronary vessels increased. The increases of delta F of the right ventricle were less in patients with stenosis of the proximal portion of the right coronary artery than in patients without stenosis and in the control subjects. The more severe the stenosis of the proximal portion of the right coronary artery, the smaller the delta F of the right ventricle. These results indicate that evaluation of the delta F in the left and right ventricles is useful in estimating coronary artery stenosis.
Although angiotensin II, ACTH and potassium are generally acknowledged as major factors in regulating the influences on aldosterone secretion, it has recently been reported that dopamine is a potent inhibitor of aldosterone secretion in man and animals. In the present study, we investigated the effect of two kinds of dopaminergic receptor antagonists, metoclopramide and sulpiride, on plasma aldosterone concentration (PAC) and serum prolactin (PRL) in man. Normotensive volunteers and patients with hypopituitarism were injected with metoclopramide (10 mg i.v.) or sulpiride (10 mg i.m.). In normal volunteers, metoclopramide increased both PAC and PRL levels, and showed a maximum level at 30 minutes after injection. In patients with hypopituitarism, PAC tended to increase without change of PRL, which suggested that the increase in PAC by metoclopramide might have a direct inhibitory effect on the dopaminergic receptor in the adrenal gland. Moreover another antagonist, sulpiride also increased PRL but contrary tended to decrease PAC. These results suggested that PRL responses to both inhibitors were mediated by dopaminergic antagonist activity at the level of pituitary receptors. However dopamine-induced modulation of aldosterone secretion may be different from that of PRL at dopaminergic receptors. These results suggested that modulatory inhibition of aldosterone secretion by dopamine may be affected by difference of affinity of dopamine to receptor as organ specificity, or different affinity of metoclopramide and sulpiride to adrenal dopamine receptor.(ABSTRACT TRUNCATED AT 250 WORDS)
Taking advantage of the fact that the distribution of Thallium-201 in an organ almost parallels the blood flow to the organ, we devised a non-invasive method of simultaneously determining blood flow and its distribution in human organs. With this method, we investigated the effect of exogenous prostaglandin E1 (PGE1) on the central and peripheral circulation. Scintigraphy was performed after two injections of 201Tl chloride, one at rest and one after the administration of PGE1 or saline. In eight subjects given PGE1 (0.2 microgram X kg-1 X min-1, iv), blood pressure fell, whereas both heart rate and cardiac output rose. The fractional distribution was increased in the heart (+13.3 +/- 2.98%, mean +/- SD), but decreased in the liver (-10.2 +/- 1.95%) and gastro-intestinal tract (-7.09 +/- 2.65%). No significant change was observed in the kidneys or leg. The blood flow in all these organs was increased. In the six control subjects given saline, there was no change in these central and peripheral haemodynamics. Thus, the intravenous infusion of PGE1 in man causes uneven blood flow distribution in heart, liver, kidney, gastro-intestinal organs and leg muscles, despite increased blood flow to all these organs. The method used in this study is relatively non-invasive and useful in evaluating organ blood flow in man, and seems to be widely applicable to physiological and pharmacologic research.
Increased sympathetic nervous system activity and vasopressin release has been demonstrated in established DOCA-salt hypertension in the rat. To determine the importance of these mechanisms in centrally-mediated pressor responses in this model of hypertension, both awake rats and rats anaesthetised with urethane were given intracerebroventricular injections of carbachol. The systolic blood pressure after implanting a silicon rubber mould containing DOCA, and with subsequent substitution of 1% saline in tap water, increased from 112 +/- 3 mmHg to a stable 188 +/- 7 mmHg by the end of 4 weeks, measured using a tail-cuff method. The blood pressure consistently became elevated when carbachol was injected into the cerebral ventricles of awake rats. Of the three groups of normotensive rats (NTR), sham-operated rats (SHAM) and DOCA-salt hypertensive rats (DOCA), the magnitude of the pressor phase was largest in the DOCA rats. The heart rate in all three groups of rats decreased similarly. When the rats were later anaesthetised with urethane to allow recording of abdominal sympathetic nerve activity, the carbachol injections caused biphasic blood pressure responses and sympathetic nerve discharge consisting of initial vasodepression and sympathetic nerve inhibition of short duration. This was followed by a sustained pressor phase accompanied by a corresponding increase in sympathetic nerve activity. The magnitude of the pressor response was again larger in the DOCA than in the SHAM rats. Spinal section abolished the initial depressor phase but did not much affect the sustained pressor phase.(ABSTRACT TRUNCATED AT 250 WORDS)
Pulmonary varix is rare, only 53 cases having been reported. A brief review of the literature is given. Because its radiologic appearance may be indistinguishable from mediastinal or pulmonary lesions, pulmonary angiography is necessary to avoid exploratory thoracotomy, mediastinoscopy, and unnecessary antituberculous therapy.
Central cardiovascular effects of the sodium-potassium adenosine triphosphatase (Na+, K+-ATPase) inhibitor, ouabain, were investigated by injecting it intracerebroventricularly (ICV) using conscious Wistar rats. Ouabain, 0.1-10 micrograms injected ICV, produced dose-related pressor responses attaining peak elevations after about 5 min. To investigate the underlying mechanisms of these central pressor responses, angiotensin II blockers were injected ICV before the injections of ouabain. 1-Sar, 8-Ile angiotensin II (ang IIa), 50 micrograms, given 3 min before the ouabain, abolished the pressor responses to ouabain, 5 micrograms. Angiotensin I converting enzyme inhibitor (CEI, captopril), 100 micrograms, also significantly attenuated the pressor responses to ouabain. Since previous results with ICV injections of ouabain suggested that the pressor responses are mediated via a release of brain angiotension II, and the site of action of brain angiotensin II is believed to be the anteroventral third ventricle (AV3V) area of the brain, ICV injections of ouabain were repeated using rats whose AV3V areas had been destroyed electrically. The pressor responses were smaller in the AV3V lesioned rats than in sham-operated rats. The abdominal sympathetic nerve activity was recorded using three conscious, normotensive Wistar rats. ICV injections of ouabain, 5 micrograms, elicited pressor responses as described above and these were accompanied by a corresponding increase in the nerve firing, lasting for 5-7 min. These responses were again abolished by pretreatment with an angiotensin II antagonist. These results suggest that centrally administered ouabain elicits vasopressor responses which increase peripheral sympathetic nerve activity.(ABSTRACT TRUNCATED AT 250 WORDS)
Potassium supplementation attenuated the development of hypertension in DOCA-salt rats but did not affect blood pressure in control rats. However, it caused a decrease in body weight in both groups of rats. Sympathetic nerve and pressor responses either to electrical stimulation of the hypothalamus or to intracisternal injections of hypertonic NaCl were enhanced in DOCA-salt rats but were normalized by KCl supplementation. Since the pressor responses to injected norepinephrine or tyramine remained unaltered by KCl treatment, a peripheral inhibition of cardiovascular reactivity was considered unlikely. Pretreatment with methyclothiazide also attenuated the elevation in blood pressure but did not affect the responsiveness to hypothalamic stimulation; hence increased natriuresis or diuresis alone could not account for the effects induced by KCl. These findings are consistent with the conclusion that KCl supplementation attenuates the development of DOCA-salt hypertension in rats by acting on the central nervous system to reduce sympathetic output.