Thirty mongrel dogs investigated in the present study were divided into two groups according to age. The young group consisted of 15 dogs that were less than 4 years old and the old group included 15 dogs of 4 years or older. Changes in bronchial muscular tone were estimated by the pneumatic balance resuscitator (Burns valve) which can provide a direct measurement of variations in the exchangeable air volume. Small doses of acetylcholine and serotonin injected directly into bronchial arteries caused bronchial constriction both in the young and old group, but it was significantly smaller with the same dose among the old group than the young group. Adrenaline caused bronchial dilatation following its direct administration into bronchial arteries and the old group appeared to show smaller responses than the young group with the same dose. Quantitative measurements of bronchial wall components were made on sections of right lungs obtained from five dogs of each group. Calculated percentile ratios of bronchial muscle area over total wall area were significantly smaller among the old group than the young group and this result was taken to be compatible with decreased responsiveness of the airway to various drugs as observed among the old group. Although qualitative and involutionary changes of bronchial muscle were observed among old dogs, morphological appearance of the goblet cell of the bronchial epithelium and bronchial glands in the wall was not discriminatory in both groups.
Thirty mongrel dogs investigated in the present study were divided into two groups according to age. The young group consisted of 15 dogs that were less than four years old and the old group involved 15 dogs of four years or older. The thoracotomized dogs were maintained on a pneumatic resuscitator operating at a constant pressure during the experiment. The bronchial artery was perfused with normal saline through a small aortic sac at a constant pressure after its complete separation from systemic circulation. Direct and continious measurement of the bronchial arterial flow with an electric magnetic flow meter enabled changes in the bronchial vascular tone to be estimated without systemic effects. Small doses of adrenaline and angiotensin injected directly into the bronchial artery caused its constriction markedly both in the young and the old group, whereas administration of serotonin and acetylcholine in small doses into the bronchial artery resulted in its dilatation in the two group. Each of these constrictive and dilative reactions to the drug was more notable with larger doses in the same group. The old group appeared to show smaller changes in bronchial arterial tone with the same dose of each drug than the young group, but the difference between these two groups is not statistically significant. Morphological changes with age in bronchial artery was also assessed in the two group by making quantitative measurements of medial thickness on sections of lungs obtained from six dogs of each group. Medial thickness of bronchial arteries, expressed as percentile ratio over external diameter, was not significantly different between the young and the old group. Such changes as vacuolization, hiatus formation in the media and intimal thickning with narrowed cavity were characteristic of bronchial arteries observed in lungs from old dogs.
The present experiment was conducted in thirty dogs to investigate effect of age on intrinsic regulatory mechanism which was proposed to be present between bronchial trees and bronchial vascular system. Changes in bronchial muscular reactivity and bronchial vascular tone to the administration of serotonin, acetylcholine and adrenaline in small doses were tested simultaneously by the method described in previous reports and the result was compared between the young and the old group. Serotonin and acetylcholine caused bronchial arterial dilatation as well as bronchoconstriction, while adrenaline injected directly into bronchial artery resulted in bronchial arterial constriction and bronchodilation. The young and the old group showed essentially same mode of reaction to each drug and changes in bronchial vascular system in relation to variable bronchial muscular tone were not significantly different. The reversed reaction in air ways and bronchial arteries to the administration of these drugs might be reasonably explained by the proposed intrinsic regulatory mechanism between two systems, which would enhance bronchial arterial dilatation to allow increase of flow in accordance with bronchial constriction. The effect of age on this mechanism, as disclosed in the present investigation, seemed to be insignificant. Physiological and morphological changes of the air ways in the old group were certainly far beyond the extent that could be expected from concomitant changes in bronchial vascular system. This result has suggested the assumption that chronic irritation of air ways due to continious exposure to external environment should play more important role than physiological aging in establishing such a remarkable changes in the air way.
In order to determine the effect of the coronary stenosis on the cardiac hypertrophy, a clinical and pathological correlation was made on 418 consecutive autopsy cases. A high incidence of cardiac hypertrophy was demonstrated in the cases with severe hypertension in which the average of the annual systolic pressure was 180mmHg or higher, or the average of the annual diastolic pressure was 100mmHg or higher. A cardiac hypertrophy was frequently present in the cases with large ischemic myocardial lesions. However, the correlation between the severity of the coronary stenosis and cardiac hypertrophy was not obvious when the cases with large myocardial lesions were excluded, except in those with severe hypertension. In the presence of severe hypertension, a cardiac hypertrophy was more frequent in the cases with severe coronary stenosis. When neither associated with hypertension nor large myocardial lesions, a cardiac hypertrophy was rather infrequent even in the presence of severe coronary stenosis. Although a possibility cannot be excluded that an association of severe coronary stenosis may enhance the development of cardiac hypertrophy in the presence of severe hypertension, it is not very likely that a severe coronary stenosis per se is an important stimulus to the development of cardiac hypertrophy.
The very low density lipoproteins (VLDL) comprise a wide morphologic spectrum of particle sizes, so it is useful to investigate the influence of diet on them. VLDL increased in human subjects when plasma triglyceride (TG) was raised by high carbohydrate diet. When plasma TG concentration rose, the TG to protein ratio (TG/P) in VLDL increased in all cases and the ncrements were greater in the cases of hypertriglyceridemia. This means that the large sized lipoproteins are mainly produced when VLDL is increased by carbohydrate rich diet and suggests that over production is a cause of hypertriglyceridemia. On the contrary, VLDL and TG/P fell when plasma TG was lowered by high fat diet. The decrements were greater in normal subjects than hypertriglyceridemic ones. This shows that, when VLDL decrease, it tends to be small one and this tendency is less marked in hypertriglyceridemic subjects and suggests impaired removal of TG in them. In comparison of increment to decrement, the increment exceeded the decrement in hypertriglyceridemic subjects, though in normal ones the decrement is greater than the increment. Fatty acid composition of VLDL was studied by increasing or decreasing it. The increments and decrements of myristic, palmitic, palmitoleic and stearic acid were marked in all subjects, when VLDL increased and decreased. This shows that the fatty acids which can be synthesized, have an important role in change of VLDL by diet.
One hundred fifty-one patients were subjected to the study, who survived more than one month after the onset of acute ischemic stroke. Death occurred in 37 patients (25%) during the three years of observation, the frequency of which was much greater than an expected death rate of 7 per cent in the general population adjusted for age and sex. Higher mortality was found in the patients to have findings as follows; disturbance of consciousness, mental disturbance, moderate to severe abnormality in electroencephalogram, albuminuria, increased blood urea nitrogen, decreased cranial blood flow and stenosis of cerebral arteries disclosed by angiography. Further cerebrovascular episodes occurred in 20 per cent of the patients during the three years; 5 per cent in the first, 11 per cent in the second and 4 per cent in the third year. The recurrence seemed more frequent in the patients to have following findings; slight or no residual disability in patients aged 60 and over, certain abnormalities in electrocardiogram such as abnormally tall R, depressed ST-segment and inverted T wave, and partial occlusion of the cerebral arteries in the carotid system. There was no occurrence in 16 patients to have a complete arterial occlusion on angiogram.
O 240 cases with the cerebro-vascular diseases, 22 cases with the occlusion of the middle cerebral artery at its origin or at its big branches, were found by the carotid angiography. The patients could be divided into the 4 groups according to the onset, clinical feature, neurological findings and prognosis. Group 1: 6 cases. In most of them severe unconsciousness and motor-disturbances were observed. It is difficult to make the differential diagnosis between this group and the patients with cerebral hemorrhage at the bedside. Group 2: 8 cases. Their chief complaints were ataxia, agnosia, Gerstmann's syndrome and aphasia. Hemiplegia and disturbance of consciousness were not found in most cases. Group 3: 3 cases. Chief complaint of this group was the hemiplegia with facial palsy which was almost similar to the so-called hemiparesis of capsular type. Group 4: 5 cases. It was transient for the patients to have symptomes, for example, hemiparesis, dysarthria, and sensory disturbance. Some of them had the attack recurrently, and others did not so. Cerebral circulation was measured according to the modified N2O method. CBF of group 1, 2, 3, 4 was 34.6±6.8, 38.7±4.4, 37.5±0.9, 52.0±8.8, respectively (ml/100g brain/min). Blood supply to the brain was kept sufficiently in group 4 and not so well in group 1. Collateral circulation observed by the serial angiography developed very well in group 4, moderately in group 2, 3 and scarcely in group 1. In a series of this study, it seems likely that those who had the well-developed collateral circulation showed mild clinical symptomes and good blood supply to the brain.