[Redistribution pattern of exercise stress myocardial scintigraphy: its correlation to coronary-arteriographic findings].
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Biomedical subjects
Publications and source records attributed to H Hama.
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Bilateral nephrectomy in the rats deprived of water for 46 h markedly reduced plasma angiotensin II concentrations (P less than 0.001), but it was without effect on extremely low levels of the hormone in the hypothalamic tissue. These results may suggest that the activity of a possible intrinsic brain renin-angiotensin system is not influenced by that of the kidney-plasma renin-angiotensin system.
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The replantation of 4 digits of 1 hand was attempted in a patient who had completely amputated his fingers at the level of the metacarpophalangeal joints. Anastomosis of the severed ends of the third common volar digital artery proved to be successful not only in re-establishing arterial circulation in the middle and ring fingers but also in the index and little fingers, as evidenced by survival of the digits and as evaluated by postoperative angiography. The reasons for this success are discussed in light of anatomic studies.
The effects of intraventricular injection of Sar1-Ala8-angiotensin II (A specific antagonist of angiotensin II) on the plasma vasopressin level increased by intraventricular injection of angiotensin II and by water deprivation (46 h) were examined in conscious male rats with an indwelling cannula in the third cerebral ventricle. Blood samplings were made by decapitation and the plasma level of vasopressin was determined by radioimmunoassay. Twenty-five, 50 or 100 ng of angiotensin II produced significant (P less than 0.05) increase in plasma vasopressin level 90 sec after the injection. The effect of 50 ng of angiotensin II was inhibited significantly (P less than 0.05) at least with 100 ng of Sar1-Ala8-angiotensin II given 2 min before the injection of angiotensin II. The dehydrated rats to which 1000 ng of Sar1-Ala8-angiotensin II was given 5 min before the decapitation showed the significantly (P less than 0.05) lower median plasma vasopressin level than that of the dehydrated controls. No significant difference in plasma osmolality was noted between them. These results suggest that the plasma vasopressin response to intraventricular angiotensin II is produced via angiotensin II receptors in the brain and that Sar1-Ala8-angiotensin II inhibits the effect of endogenous angiotensin II on plasma vasopressin level under dehydration.
A case is reported in which roentgenograms of the lumbar spine showed a vertical cleft in the superior articular process of the L-5 vertebra. The cleft seemed to be of no clinical significance.
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As the greater part of the immunoreactive angiotensin II in cerebrospinal fluid has been suggested to be angiotensin III, a comparison was made between the effects on vasopressin release of angiotensin II and angiotensin III administered into the third cerebral ventricle in conscious male rats. The blood samples were collected 90 seconds after the injection of angiotensin II or angiotensin III by means of decapitation. Plasma vasopressin (microU/ml) extracted and determined by radioimmunoassay were 2.3 +/- 0.8, 6.7 +/- 5.0, 14.0 +/- 2.2, 16.3 +/- 4.3 and 20.7 +/- 2.5 (mean +/- SEM), respectively following the injection of 0, 10, 25, 50 and 100ng of angiotensin II. The increases in plasma vasopressin produced by angiotensin II 25, 50 and 100ng were statistically significant (p less than 0.05). On the other hand, plasma vasopressin following the injection of 22.7 and 45.4ng of angiotensin III, which are equimolar to 25 and 50ng of angiotensin II each, were 14.9 +/- 2.7 and 16.3 +/- 5.6, respectively. No significant difference was found between the effect on plasma vasopressin of angiotensin II and that of angiotensin III at the dose level of 24.3 or 48.6 p. mol. These data indicate that angiotensin III is equipotent to angiotensin II in terms of vasopressin release when administered into the third cerebral ventricle. The possible role of angiotensin III in the brain on vasopressin secretion is discussed.
Adenomata taken from 25 patients with primary aldosteronism were observed by electron microscopy. The cells in the adenoma had a well developed agranular endoplasmic reticulum but granular endoplasmic reticulum was not prominent. Most of the mitochondria resembled those in the cells of the zona glomerulosa, suggesting that the adenomata which caused primary aldosteronism are derived from this zone. Spironolactone bodies were found in the cells of the adenoma from a patient who received spironolactone. Their appearance was identical to that described in previous reports.
Rat salivary glands were examined by an indirect immunofluorescence technique using anti-angiotensin II antiserum. Cells reacting with the antiserum were found in the convoluted granular tubules of the submaxillary gland. In view of the previous reports that renin was isolated from the rat submaxillary gland and that cells with a renin-like immunoreactivity were demonstrated in the convoluted granular tubules of the gland, the present study suggests that a set of substances forming the renin-angiotensin system may be present in this gland.
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