Ten elderly hypertensives (4 men, 6 women) were studied before and after 8-week administration of 20mg/day slow-release nifedipine. Systemic and regional hemodynamic data were measured using a pulsed Doppler technique. Slow-release nifedipine reduced mean arterial pressure, while cardiac output remained unchanged, resulting in a decrease in total peripheral resistance. None of common carotid, vertebral, celiac, superior mesenteric, renal, or terminal aortic flow changed significantly before or after administration of slow-release nifedipine. Pharmacokinetic parameters were as follows: Cmax, 59.1ng/ml; AUC, 288.2ng hr/ml; Tmax, 3.4hr; tl/2, 5.5hr. There was a direct relationship between the concentration of slow-release nifedipine and its depressor effect. Slow-release nifedipine had no influence on humoral factors such as plasma renin activity, angiotensin II, aldosterone, atrial natriuretic peptid, noradrenaline or adrenaline. Slow-release nifedipine may provide desirable hemodynamic effects in elderly hypertensives.

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The interrelation of the aluminum content and aging change of the nerve cells was studied with special reference to the neurofibrillary tangle (NFT) and occurrence of senile plaque (SP), in 15 autopsied brains (cerebrum) of non-demented elderly subjects varying in age from 75 to 101 years old and 10 cases of non-demented non-elderly adult subjects. 1) In the brain of non-demented non-elderly adult subjects, the aluminum content of the hippocampus was 14.4±1.39ppb and that of the cortex of the frontal lobe was 20.4±2.54ppb. In the brain of the non-demented elderly subjects, the aluminum content of the hippocampus was 401.7±60.05ppb and that of the cortex of the frontal lobe was 373.29±72.35ppb. Comparison of the two groups showed obviously higher levels in the latter group, being 28 times in the hippocampus and 19 times in the cortex of the frontal lobe. 2) The histochemical demonstration of the aluminum localization by the Morin method disclosed the positive fluorescence reaction along the part of the disintegrating neurofibrillary tangle and amyloid core in the senile plaques of non-demented elderly subjects. In the normal brain tissue, positive fluorescence reaction was observed in the wall of the capillary vessels of the blood brain barrier, perivascular glial supporting tissues, the nuclei of the astrocytes and nuclei, nucleoli of the nerve cells partially. No fluorescence reaction was observed in the non-demented adult subjects. 3) Morphologically, the appearence of the neurofibrillary tangle was noted in some cases of non-demented elderly group with higher aluminum levels. Classical and diffuse type senile plaques were dispersed in the 1st to 4th zone of the cortex of the frontal lobe. However, diffuse type senile plaques in the hippocampus appeared to a lesser extent. Neurofibrillary tangles were slightly noted in the cortex of the frontal lobe, however marked increase was confirmed in the CA1 to CA3 zones of the hippocampus. Ultrastructurally, paired helical filaments (PHF) were noted in the neurofibrillary tangle constituent and the increase of amyloid fibrils in senile plaques was confirmed. In this study, high levels of the aluminum content of the brain were confirmed in the non-demented elderly subjects. Moreover, the histochemical demonstration of aluminum localization by the Morin method disclosed a positive fluorescence reaction along the sites of neurofibrillary tangles and amyloid core in the senile plaques of non-demented elderly subjects. Based on these observations, the accumulation of aluminum plays a role in the appearence of neurofibrillary tangles and increase of senile plaques suggesting the possible mechanism of interaction with the causative factor of senile dementia of the Alzheimer type (SDAT).

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This longitudinal study was performed to clarify the relation between brain atrophy and common carotid hemodynamcis. A total of 147 patients, including 70 males and 77 females, who had neither neurologic deficits nor organic lesions on computed tomography of the brain, were enrolled in this study. The ages of the patients ranged from 47 to 76 years (mean: 62 years) at the first diagnosis of brain atrophy. The patients were divided into three groups: 66 controls without hypertension or diabetes mellitus (Group I), 60 with hypertension (Group II) and 21 with both hypertension and diabetes mellitus (Group III). Brain atrophy was diagnosed by caudate head index (CHI). Mean blood flow volume (BF) at the right common carotid artery was measured by an ultrasonic quantitative flow measurement system. Both CHI and BF were measured twice at a mean interval 6.5 years. Increment in CHI per year (ΔCHI) and decrement in mean blood flow volume per year(ΔBF) were calculated. ΔCHI of Group I and Group II had a significant relation with aging. ΔCHI of Group III showed a larger increase than that of both Group I and Group II in subjects in the sixties. ΔCHI had a significant relation with ΔBF in each group. These results indicate that complication of both HT and DM, or decrement in mean blood flow volume may cause brain atrophy to progress.

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VCAP chemotherapy combined with natural interferon-α (HBLI) was performed on elderly patients over 65 year with multiple myeloma (MM), and its clinical effects were compared with those of VCAP chemotherapy without HLBI on elderly MM and also with those of HLBI-VCAP and VCAP combination therapy on non-elderly MM. Sixteen elderly and 21 non-elderly patients received HLBIVCAP combination therapy, whereas 12 elderly and 21 non-elderly patients were treated with VCAP chemotherapy alone. The remission rate (CR+PR) was 81% for the elderly HLBI-VCAP group, 58% for the elderly VCAP group, 90% for the non-eldrely HLBI-VCAP group, and 76% for the non-elderly VCAP group. While the median survival time was 54 months for the elderly HLBI-VCAP group and 13.5 months for the elderly VCAP group, it was 70 months for non-elderly HLBI-VCAP group and 34.5 months for the non-elderly VCAP group. The survival time in the elderly HLBI-VCAP group was significantly longer than that in the elderly VCAP group. Therefore, improvement of survival in cases treated by interferon was much better in the elderly group than in the non-elderly group. These results indicate that HLBI-VCAP combination therapy is beneficial for the treatment of elderly MM.

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A 71-year-old male was admitted to our hospital due to progressive dyspnea. The right lung of this patient was replaced by multiple bulous lesions including giant bullae. He had severe deterioration of lung function and gas exchange. He did not complete the pre-operative examinations for thoracic surgery, but improvement in ventilatory function was expected after bullectomy. After multiple bullectomy, this case showed marked improvements in lung function and gas exchange, subsequently his dyspnea improved, as did his activities of daily living. These lung functional improvement may have resulted not only from the mechanical advantage of diaphragmatic motion due to removal of space-occupying lesion of the lung, but also from the reduction of tough fibrous adhesion between the lung and the parietal pleura which had impaired smooth lung movement. Thorough evaluation of operative indications is necessary before surgery in aged patients with lung diseases

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