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Maurizio GUAZZI, Alvise POLESE, Fabio MAGRINI, Cesare FIORENTINI
1973Volume 14Issue 2 Pages
97-103
Published: 1973
Released on J-STAGE: December 25, 2008
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In a comparative trial practolol was found to be quite superior to propranolol in the treatment of spontaneous angina pectoris. Propranolol did not reduce the number of anginal attacks in the 24 hours, as evaluated through the patients' charting and continuous electrocardiographic recording, and induced exaggerated bradycardia as well as clinical and hemodynamic signs of poor cardiac performance. In the same patients practolol achieved complete disappearance of the anginal attacks, and returned cardiac function to quite satisfactory levels. The forcedly low doses might be one of the possible reasons of the failure of propranolol.
The attacks of the angina here investigated occurred at rest and in absence of any detectable eliciting factor. They were not triggered by circulatory modifications interfering with the oxygen requirement of the heart. These findings make the favorable therapeutic response to betablockade of difficult interpretation on the basis of the mechanisms usually indicated for the antianginal action of these drugs, and suggest that some other, still unknown effect must be at work.
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H. V. Srinivas, J. A. Antani
1973Volume 14Issue 2 Pages
104-109
Published: 1973
Released on J-STAGE: December 25, 2008
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The clinical profile of 11 cases of puerperal cardiomyopathy is presented.
Poor socioeconomic condition and malnutrition were observed in all the patients and its importance as an etiological factor is discussed.
A brief review of the etiopathogenesis with relevant literature is mentioned.
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Keishi ABE, Tetsuo SAITO, Yoichi OTSUKA, Haruki AOYAGI, Nobuo IROKAWA, ...
1973Volume 14Issue 2 Pages
110-125
Published: 1973
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During the last 10 years, 7 hypertensive patients due to segmental renal ischemia or infarction among total 48 cases of renovascular hypertension have been observed in our clinic.
These 7 cases of renal arterial branch stenosis consist of 5 men and 2 women. The youngest case was aged 12 and the oldest 31. Their blood pressures were ranged from 160-225mmHg in systolic and from 84 to 150 in diastolic. Abnormal intravenous pyelogram was found in 4 out of 7 cases. So far as our experience was concerned, clinical features, urinalysis, radioisotope renography, renoscintigraphy and split renal function study were of little value for screening of the patients with renal arterial branch stenosis. However, angiography and provocation test of renin secretion are the best tools for making diagnosis of this type of hypertension. Surgical treatment including nephrectomy and revascularization relieved the hypertension in 5 patients. Antihypertensive drugs were given in one of 5 operated cases and in 2 non-operated cases. Six out of 7 patients remained normotensive.
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IV. Effect of Calcium Chloride and Potassium Chloride on Myocardial Hemodynamics and Clearance of 86Rubidium
Atul R. LADDU, Pitambar SOMANI, Harold F. HARDMAN
1973Volume 14Issue 2 Pages
126-134
Published: 1973
Released on J-STAGE: December 25, 2008
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The effect of a constant intracoronary infusion of potassium chloride and calcium chloride upon myocardial hemodynamics and clearance of
86Rubidium in the heart was studied in the isolated supported dog heart preparation (ISHP). In the ISHP with a constant coronary blood flow, potassium chloride in doses up to 4mg/min had no significant effect upon either the myocardial hemodynamics (MH), clearance of
86Rubidium (C
86Rb) or the capillary transport coefficient, PS. Calcium chloride in small doses had no effect upon the MH, C
86Rb or PS. A higher dose of calcium chloride (4mg/min) produced an increase in myocardial contractile force, left ventricular peak systolic pressure, myocardial oxygen consumption and a decrease in C
86Rb and PS. Pretreatment of the ISHP with practolol (0.25mg/Kg), an agent which blocks adrenergic β-receptors, did not modify the effects of calcium chloride upon the MH, C
86Rb or PS. It is concluded that the effects of calcium chloride are exerted directly, independent of a β-receptor mediation.
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Koshiro FUKIYAMA
1973Volume 14Issue 2 Pages
135-139
Published: 1973
Released on J-STAGE: December 25, 2008
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A small amount of angiotensin not to cause a significant elevation of systemic arterial pressure was infused into vertebral arteries of dogs anesthetized with morphine and α-chloralose. Electrical stimulation of carotid sinus nerve caused a smaller reduction in arterial pressure and heart rate during the period of angiotensin infusion than the control period. Arterial pressure response to occlusion of the common carotid artery was not affected by the infusion of angiotensin. The results suggest that angiotensin may sensitize medullary vasomotor centre in a manner of suppressing the tonic inhibition of baroreceptor reflex, resulting in an increase of central sympathetic vasomotor outflow.
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Kurakazu SHIMIZU, Manabu YAMAMOTO, Yawara YOSHITOSHI
1973Volume 14Issue 2 Pages
140-145
Published: 1973
Released on J-STAGE: December 25, 2008
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An activity of prostaglandin (PG)-like substances was measured in venous blood and renal medullary tissue of dogs. The PG-like substances were extracted by silica gel column chromatography and their activity was measured by rat vasodepressor bioassay. The activity of PGE-like substance both in renal venous blood and medulla was greater in saline infused dogs than in control, non-infused dogs. The possibility was discussed that the increased activity of PGE in kidney may be involved in the mechanisms of natriuresis in saline-loaded animals.
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Tsuneaki SUGIMOTO, James L. ALLISON, Arthur C. GUYTON
1973Volume 14Issue 2 Pages
146-153
Published: 1973
Released on J-STAGE: December 25, 2008
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The time course and mode of deterioration of the heart under prolonged maximal work load were studied in open-chest dogs, the hearts of which were loaded at maximal cardiac output while the aortic pressure was kept constant. During the period of loading, the maximal level of cardiac output that could be attained was relatively stable for 30min to 1 hour and then began to fall suddenly and rapidly. This terminal deterioration appeared to be caused by mechanical factors, possibly over-distention of the heart, rather than by fatigue of the muscle
per se.
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Proceedings of VIII Annual Scientific Meeting of the Council for the Spontaneously Hypertensive Rat October 8, 1972, Nagasaki
Tetsuya INATOME, Yutaka FURUTA, Susumu YORIFUJI, Akinobu NAGAOKA, Hisa ...
1973Volume 14Issue 2 Pages
154-155
Published: 1973
Released on J-STAGE: December 25, 2008
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Tetsuya INATOME, Yutaka FURUTA, Susumu YORIFUJI
1973Volume 14Issue 2 Pages
156
Published: 1973
Released on J-STAGE: December 25, 2008
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Akinobu NAGAOKA, Hisashi IWATSUKA, Ziro SUZUOKI, KOZO OKAMOTO
1973Volume 14Issue 2 Pages
157-158
Published: 1973
Released on J-STAGE: December 25, 2008
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Kiro SHIMAMOTO, Akio TERAOKA, Hisashi IWATSUKA, Ziro SUZUOKI
1973Volume 14Issue 2 Pages
159
Published: 1973
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Kioko KAWAI, Hideo TSUCHIYAMA, Hajime SUGIHARA
1973Volume 14Issue 2 Pages
160-161
Published: 1973
Released on J-STAGE: December 25, 2008
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Yukio YAMORI, Akira OOSHIMA, Kozo OKAMOTO
1973Volume 14Issue 2 Pages
162-164
Published: 1973
Released on J-STAGE: December 25, 2008
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1) Neither significant differences in plasma corticosterone level at rest nor marked differences in its diurnal variation except for a possible displacement of the peak in female SHR were observed between spontaneously hypertensive rats (SHR) and normotensive rats (NR). 2) Response in plasma corticosterone to various stress loadings was not increased in SHR, but rather decreased under certain conditions in comparison with NR. 3) Biological half-life of plasma corticosterone determined from the decline in exogenously loaded corticosterone in adrenalectomized rats was not significantly different between SHR and NR. 4) Analysis of adrenal venous steroid profile in SHR and NR under the maximum stimulation by ACTH showed that the conversion ratio from progesterone to DOC was decreased in SHR. 5) These results indicate that there probably is no acceleration of synthesis and metabolism of adrenal corticosterone itself in SHR compared with NR, and raised a possibility of relative impairment of 21-β-hydroxylase in SHR. A speculated compensatory metabolic pathway from progesterone via 18- or 17-α-hydroxylation as well as the substrain difference in steroidogenesis in relation to vascular vulnerability still remains to be clarified by further study.
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Yasuyuki MOROTOMI, Kenjiro TANAKA, Teruo OMAE
1973Volume 14Issue 2 Pages
165-167
Published: 1973
Released on J-STAGE: December 25, 2008
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Kumiko SHIONO, Hirofumi SOKABE
1973Volume 14Issue 2 Pages
168-169
Published: 1973
Released on J-STAGE: December 25, 2008
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Nagao KAJIWARA, Yoshiko KOBAYASHI, Akira MURAKAMI, Jun HASHIDA, Takahi ...
1973Volume 14Issue 2 Pages
170
Published: 1973
Released on J-STAGE: December 25, 2008
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Masayori OZAKI
1973Volume 14Issue 2 Pages
171
Published: 1973
Released on J-STAGE: December 25, 2008
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Yoshikiyo KUDO, Hiroshi KUMAGAI, Akira SASAKI, Yutaka UMEHARA
1973Volume 14Issue 2 Pages
172-173
Published: 1973
Released on J-STAGE: December 25, 2008
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Fumitada HAZAMA, Akira OOSHIMA, Kazuhiko TOMIMOTO, Kozo OKAMOTO
1973Volume 14Issue 2 Pages
174-176
Published: 1973
Released on J-STAGE: December 25, 2008
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(1) There were definite differences in incidence of the hypertensive vascular changes in the brain and kidneys among the substrains of SHR.
(2) The loading of sodium chloride in drinking water accelerates the development of hypertensive vascular changes and sequential pathological changes in the brain and kidneys of SHR.
(3) The substrains A
3 and C of SHR have a peculiar nature with regard to cerebrovascular diseases. A
3 develops spontaneously cerebrovascular diseases with a high incidence, and shows the highest incidence of the changes among various substrains by salt loading. The substrain C shows the lowest incidence of cerebrovascular diseases in the nontreated animals as well as in the NaCl group. This substrain does not appear to be salt-sensitive.
(4) These facts suggest that inherited factors play an important role in developing hypertensive vascular diseases.
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Further Study
Hitoshi TANIJIRI, Masakazu IKEDA, Chujiro KASHII, Tadasu TAKATSU
1973Volume 14Issue 2 Pages
177-178
Published: 1973
Released on J-STAGE: December 25, 2008
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Supplementary experiments to the previous one were performed to complete the chronological observation of the development of cardiac hypertrophy in SHR from birth to the age of 1 year. So far, the increased activity of β-HBDH in SHR seems not to be a genetic strainspecific character, but to be pertinent to the development of its cardiac hypertrophy, because the activity of β-HBDH was not increased in the early suckling SHR, and its increased activity was also seen in the elder control rats.
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Kyuzo AOKI, Kazuhiro TAZUMI, Iwao SATO, Yoshimi KOBAYASHI, Kiyoharu TA ...
1973Volume 14Issue 2 Pages
179-180
Published: 1973
Released on J-STAGE: December 25, 2008
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A Study with a Scanning Electron Microscope
Kimiho IRINODA, Shigeki TAKAHASHI
1973Volume 14Issue 2 Pages
181
Published: 1973
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An Animal Model for Hypertension Research
KOZO OKAMOTO
1973Volume 14Issue 2 Pages
182-183
Published: 1973
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The Sixth Case in the Literature and Discussion
Yoshihisa OKUDA, Takakazu TSUNEDA, Akira MORISHIMA, Shinsaku MATSUMOTO ...
1973Volume 14Issue 2 Pages
184-191
Published: 1973
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A case of a 29-year-old man with abnormal shadow of the heart complicated with bacterial endocarditis and hemiplegia is presented.
Cardiac catheterization and angiography revealed a right coronary artery to left ventricle fistula which was saccularly dilated and tortuous. This is the sixth case in the literature.
The literature is reviewed and shortly discussed.
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1973Volume 14Issue 2 Pages
e1
Published: 1973
Released on J-STAGE: December 25, 2008
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