Endurance time and fatigue in static contractions.
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Biomedical subjects
Publications and source records attributed to K Iwanaga.
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The effects of human interferon on the growth of xenografted human tumors were studied. Human lymphoblastoid interferon (IFN) was administered intraperitoneally to nude mice with yolk sac tumors of the ovary (YST-1 and YST-2) and endometrial carcinoma (AD-19). IFN inhibited the growth of YST-1 tumor at a dose of 1.0 X 10(6)u/kg/day for twenty one days, and AD-19 tumor at a dose of 1.0 X 10(6)u/kg/day for twenty eight days. On the other hand, IFN failed to inhibit the growth of YST-2 tumor at a dose of 1.0 X 10(6)u/kg/day for eight days. The coefficient of correlation between tumor volume and serum alpha-fetoprotein of tumor-bearing mice was 0.51 in YST-1 and 0.42 in YST-2. No morphologic difference was observed between tumor cells from IFN-treated mice and control tumor-bearing mice. No severe weight loss of tumor-bearing mice was recognized after treatment with IFN. From these results, the usefulness of IFN for clinical treatment was suggested.
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The effect of age on the levels of active and trypsin-activatable inactive plasma renin was examined in 41 normal subjects and 54 patients with essential hypertension, during recumbency and after stimulation with furosemide and ambulation. Active renin levels in supine subjects and patients decreased with age. Inactive renin levels did not change with age in normal subjects, whereas in hypertensive patients they decreased with age. Following stimulation with furosemide and ambulation, the levels of active renin increased but the responsiveness to stimulus decreased with age in both groups. In contrast, inactive renin levels slightly increased after furosemide administration and ambulation, resulting in increased proportion of active to total renin. These data show that an acute stimulation with furosemide and ambulation affects mainly the active form of plasma renin, and the effect of age on inactive plasma renin in normal subjects may be different from that in patients with essential hypertension.
The effect of aging on urinary kallikrein excretion (UkalV) was investigated in 54 normal subjects, 11-88 yr old, and 37 patients with essential hypertension, 17-82 yr old. Urinary sodium, potassium, and aldosterone excretion (U(Ald)V) were also measured in these subjects. Urinary sodium and potassium excretion in both normal subjects and hypertensive patients did not significantly change with aging. In normal subjects, U(kal)V (r = 0.45; P less than 0.001) and U(Ald)V (r = 0.58; P less than 0.01) significantly decreased with increasing age. U(kal)V was positively correlated with U(Ald)V (r = 0.44; P less than 0.001). In contrast, the hypertensive patients had a significant decrease with age in U(Ald)V (r = -0.36; P less than 0.05), but no significant age-related change in U(kal)V. No significant correlation between U(kal)V and U(Ald)V was observed in the hypertensive patients. In individuals less than 60 yr old, there was no significant difference in U(kal)V values between normal subjects and hypertensive patients. Hypertensive patients more than 60 yr old excreted more urinary kallikrein than normal subjects of the same age group (P less than 0.05). In conclusion, the age-related decrease of U(kal)V in normal subjects may be due to the reduced activity of the renin-angiotensin-aldosterone system. It remains to be elucidated whether the absence of the age-related decrease in U(kal)V in hypertensive patients is related to the pathogenesis or pathophysiology of essential hypertension.
The effect of age on active and cryoactivatable inactive plasma renin levels was examined in 58 normal subjects and 58 patients with essential hypertension during recumbency and after stimulation with furosemide and ambulation. Active renin levels declined with age in both supine subjects and patients. Inactive renin levels did not change with age in normal subjects, while in hypertensive patients they decreased with age. Following stimulation with furosemide and ambulation, the levels of active renin increased but its responsiveness to the stimulus decreased with age in both groups. In contrast, inactive renin was not significantly influenced by furosemide administration and ambulation. These data show that an acute stimulation with furosemide and ambulation affects mainly the active form of plasma renin, and that the effect of age on inactive plasma renin in normal subjects may be different from that in patients with essential hypertension.
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Effects of new anticancer drug Cis-platinum dichloride (CPDD) on yolk sac tumor were studied. Human yolk sac tumor serially transplanted in BALB/c nude mice (YST-1) was used as material in this experiment. Two administration methods of CPDD were examined and compared. 1) CPDD 5 mg/kg X 1 day X 4 2) CPDD i mg/kg X 5 days X 4. Tumor size was measured and serum AFP of nude mice was determined by radioimmunoassay method during experiments. At the end of experiments, treated tumor was resected and examined by light and electron microscopy. Results as follows: 1. CPDD was active in regressing yolk sac tumor at doses of 5 mg/kg given as a single treatment and doses of 1 mg/kg given daily for five days. It appeared that CPDD showed higher activity against tumors by daily injections at doses of 1 mg/kg. 2. Close correlation was recognized between tumor size and serum AFP of nude mice ((r = 0.93, p less than 0.001). Serum AFP of tumor-bearing nude mice revealed to be a useful marker of yolk sac tumor also in nude mice as in human patient. 3. Effect of CPDD on tumor cells was confirmed by light and electron microscopy.
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Captopril was given for treatment of hypertension alone or in combination with diuretics to 32 patients for 1- to 4-mo periods. The decrement of mean blood pressure after 1 and 2 mo correlated with pretreatment plasma renin activity (PRA) and the response of blood pressure to infusion of an angiotensin II antagonist. These correlations were no longer apparent after 4 mo of treatment. When subjects with a decrement of mean blood pressure that exceeded 13 mm Hg were compared with nonresponders, responders not only had higher control PRA and higher PRA at 1 mo of treatment, but also had decreased plasma aldosterone levels, decreased urinary aldosterone excretion, and increased serum postassium levels that persisted over the 4 mo of observation. The reduction of plasma aldosterone correlated with the fall of mean blood pressure. Urinary kallikrein, catecholamines, electrolytes, and endogenous creatinine clearance did not change in response to treatment. These findings indicate that the antihypertenisve activity of captopril on long-term administration probably depends in part on the blockade of angiotensin II, but other mechanisms cannot be excluded.
5 alpha-dihydrocortisol has been reported to amplify the mineralocorticoid activity of aldosterone. In this study 5 alpha-dihydrocortisol was administered to unilaterally nephrectomized rats treated with 11-deoxcorticosterone acetate (DOCA) and sodium chloride to examine its potentiating effect on the elevation of blood pressure in these animals. Subcutaneous administration of DOCA at two dose levels (40 microgram and 100 microgram/100 g of body weight 3 times a week) resulted in a significant rise in blood pressure when compared with controls given no DOCA. However, concomitaut injection of 5 alpha-dihydrocortisol (300 microgram/100 g of body weight 3 times a week) with both doses of DOCA did not accelerate the development or potentiate the severity of the hypertension in a 4 week period. Furthermore, administration of 5 alpha-dihydrocortisol did not cause a further decrease in plasma renin activity or a greater increase in urinary kallikrein excretion than those observed after DOCA alone. Thus, 5 alpha-dihydrocortisol does not potentiate DOCA in the production of low renin hypertension in unilaterally nephrectomized salt-loaded rats.
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