Biomedical subjects
Publications and source records attributed to H Mikami.
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We describe a method for determination of guanidino compounds in plasma and erythrocytes. The compounds are separated by liquid chromatography, the concentrations in the effluent being estimated fluorometrically (Trans. Am. Soc. Artif. Intern. Organs 24: 61, 1978). Guanidinoacetic acid, guanidinosuccinic acid, guanidinobutyric acid, guanidine, methylguanidine, taurocyamine, and arginine can be detected and quantitated in both plasma and erythrocytes from healthy individuals. The method was also applied to patients in chronic renal failure. Guanidinosuccinic acid, creatinine, guanidine, and methylguanidine are substantially increased in the plasma and erythrocytes of the uremic patient. Guanidino compounds can be effectively extracted from plasma with 0.5 volume of 300 g/L trichloroacetic acid, from erythrocytes with five volumes of 120 g/L trichloroacetic acid.
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A case with huge cystic disease of the lung was reported. The plain chest X-P revealed several linear shadows in the left middle lung field. Bronchography disclosed multiple cystic lesions located mainly in the left lung. There were also several small cystic lesions in the right lung. No inflammatory findings of the bronchi were found. Difficult problem concerning differential diagnosis between acquired and congenital cystic disease of the lung was discussed.
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Two angiotensin II analogues (AIIA), 1-sarcosine, 8-isoleucine angiotensin II ([Sar, Ile]-AII) and 1-sarcosine, 8-alanine angiotensin II ([Sar, Ala]-AII), were infused in six normal volunteers on high, regular and low sodium diets. The agonist and antagonist activities of these AIIA on blood pressure (BP), plasma aldosterone concentration (PAC), creatinine clearance and plasma renin activity were examined. Both AIIA had agonistic pressor activities in subjects on high and regular sodium diets, [Sar, Ile]-AII being more potent than [Sar, Ala]-AII. Both AIIA caused similar elevation of PAC in subjects on high and regular sodium diets, and an equally fall in PAC in subjects on a low sodium diet. Both AIIA strongly antagonized the rise in BP, the increase in PAC and the reduction of Ccr induced by AII administration in subjects on all three sodium diets. The results indicate that both AIIA can be used to examine the activity of the renin-angiotensin system in patients with hypertension, and they also suggest that AII interaction with its receptors differs in different target tissues.
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.
The role of the sympathetic nervous system (SNS) in essential hypertension was evaluated by examining the response of urinary catecholamines to the intramuscular injection of glucagon in both young and elderly normal subjects (total 16) and in both young and elderly patients with essential hypertension (total 16). Urine was collected for 2 hours before glucagon injection and for 2 and 4 hours after injection, for determination of adrenaline and noradrenaline. The increments of urinary adrenaline and noradrenaline after glucagon injection were significantly higher in young hypertensive than in young normotensive subjects or in normotensive and hypertensive elderly subjects. The observation that the reactivity of the SNS is increased in young patients with essential hypertension lends support to the hypothesis that the SNS is more important in the maintenance of hypertension in the young than in the elderly.
The chromium content was measured in the lungs of chromate workers, obtained at necropsy in six patients and at surgery in two. The mean chromium content of peripheral lung tissue was 36.7 micrograms per gm wet weight (range 0.50 to 130.2 micrograms) and that of the large airways was 0.51 micrograms per gm wet weight (range 0.22 to 0.99 micrograms). These means values were high compared with those from control lungs of a non-chromate exposed lung cancer patients--respectively 0.21 micrograms per gm in lung tissue and 0.11 micrograms per gm in the large bronchi. The longer the exposure period, the higher was the chromium content in the lungs. The concentration of chromium in the upper lobes was significantly higher than that in the lower lobes, suggesting regional differences either in clearance from or deposition in the lung. Moreover, it was apparent that the metal remained in the lungs long after exposure to chromate had ceased
An angiotensin II antagonist, [sacrosine1, isoleucine8] angiotensin II, was infused into thyrotoxic patients. Blood pressure was monitored before and during the infusions to investigate whether the renin-angiotensin-aldosterone system was involved in the maintenance of blood pressure in normotensive and hypertensive thyrotoxic patients. Five out of 17 normotensive patients with hyperthyroidism showed more than a 10 mmHg decrease in mean blood pressure in response to the infusion (responders), while the remaining 12 patients showed no substantial change in blood pressure (non-responders). The infusion caused little change in blood pressure in 8 hyperthyroid patients with systolic hypertension. The mean levels of serum thyroxine, triiodothyronine, plasma renin activity and plasma aldosterone concentration in the normotensive responders were significantly higher than the values in the normotensive non-responders. There were no significant differences in these laboratory values between the hypertensive patients and the normotensive non-responders except that serum triiodothyronine levels were significantly higher in the hypertensive patients. The present study indicates that increased activity of the renin-angiotensin-aldosterone system is involved in the maintenance of blood pressure in most normotensive patients with severe hyperthyroidism, while hypertension in patients with hyperthyroidism is not angiotensin II dependent.
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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