Nagoya Journal of Medical Science

In order to clarify the mechanism of hyperlipemia during pancreatic dis- orders, investigations on changes of serum lipids, measurements of lipoprotein and number of chylomicra after oral administration of fat (safflower oil or olive oil) and studies on post-heparin lipoprotein lipase were done on patients with chronic pancreatitis and on dogs with experimental pancreatic disorders. The results obtained were as follows. (1) β/α Lipoprotein indices and β-lipoprotein levels were increased in pancreatitis. (2) There was an impaired removal of chylomicra from plasma in pancreatitis. (3) Post-heparin lipoprotein lipase activities in the dogs with pancreatic disorders were significantly lower than those in the normal controls. (4) No inhibitor on lipoprotein lipase activity was detected in plasma in the dogs with pancreatitis. The possible relationships of these phenomena to the mechanism of lipid metabolism in pancreatic disorders have been discussed. It was concluded that the decreased delivery of the lipoprotein lipase into the circulation was one of the possible causes of hyperlipemia in pancreatic disorders.

In certain Beryllium refining factory, the author experienced 192 cases of various acute beryllium diseases, on which clinical pictures including environ- mental factors, beryllium patch test and clinical courses were investigated. Among them, 11 cases of acute beryllium pneumonitis were mainly studied, be- cause of its specific clinical manifestations.
In this clinical study, a hypersensitivity phenomenon to beryllium seemed to play an important role in development of the disease.
To investigate this subject, experimental studies were performed in guinea pigs and mice. Guinea pigs were pretreated with minute doses of beryllium for certain period, and in those animals beryllium patch test and intracutaneous test were performed comparing with control animals. Mice were also pretreated with beryllium in the same way, to which beryllium was administrated intraperitoneally, and intraperitoneal cellular reaction was observed.
Based on the clinical and experimental findings, it may be concluded that a hypersensitivity phenomenon to beryllium plays an important role as one of the etiologic factors in the acute beryllium disease.

Twenty-three patients of pulseless disease were described with clinical and histopathological findings. Twenty-two cases whose ages range 16 to 41 were female and one was male. In nineteen of twenty-three cases surgical treatments were performed: removal of carotid body in 7, excision with Tetron graft in 4, by-pass prosthesis with Tetron in 5 and autogenous vein graft in 2 cases. Biopsies were taken in 13 cases, and the histological features were classified into 4 types: adventitis type in 8 cases. tuberculoid granuloma type in one case, giant cell arteritis type and diffuse productive inflammation type in two cases.
The main lesions were limitted to the media and the adventitia, and the intimal changes seemed to be secondary reaction, and the vasa vasorum may be primary sites of involvement of pulseless disease. The lesion of the elastic fibres seems to play an important role in the pathogenesis.
In order to clarify the exact etiologic relationship of primary elasticopathy to granulomatous reaction with elasticophagic giant cell, elastase suspension was infused in the common carotid artery of the rabbits intravascularly (37 cases) and extravascularly (21 cases), and elastolysis of the arterial wall was made, thereby, the elastogranulomous reaction and multinucleare giant cells phagocytosing the fragments of disintegrated internal elastic lamina were recognized in 2 cases (Figs. 15 and 16 ).
From the results of these experiments, it is clear that a causal relation exists between degenerating elastic fibres and granulomatous tissue reaction accompany· ing giant cell formation in vivo, and elastase has an elastolytic activity in vivo, and the fragments of the elastic fibres act as foreign bodies. The following conditions are necessary for the occurrence of elasticophagic giant cells: a specific destruction of the elastic fibres to provoke giant cells, for example, hard and slightly soluble fragments of the internal elastic lamina, and a mesenchymal activation brought about by some factors, one of which was typhoid-paratyphoid vaccination in this experiment.
The change in early stage of the elastic fibre by elastase was not observed in vivo, but at the incubation before elastolysis, metachromasia of the elastica became negative and no initial increase of the metachromatic reaction was ob- served. A newly formed elastic fibre was presented in early stage in the intimal thickening, but the regeneration of disintegrated elastic fibre was not seen in the media.
The effect of estrogen intensified metachromatic reaction of A.M.P. in the arterial walls, but it could not prevent the elastolytic action by elastase.
For the present, although exact etiology of pulseless disease is still unexplained, from clinical and exper imental results, the elasticopathy associated with anti-elastin auto-immune mechanism or allergy following infection may be important in the pathogenesis of pulseless disease.

This study is a part of the work which has been done in purpose of investigating the effects of a long term exposure to a lowered barometric pressure in the 1965-1966 Nagoya university scientific and mountaineering expedition to the Andes. Changes in breath holding time, P_o2 and P_co2, of the expired air at the breaking point and alveolar P_o2 and P_co2, pulmonary ventilation and respiratory frequency were measured in the 14 male subjects during the 22 days of sojourn at an altitude of 4200 m. Breath holding time and P_co2 of the expired air at the breaking point and alveolar P_co2 became increasingly lower during the two weeks of sojourn. After the 2nd week the breath holding time, P_co2 level at the break- ing point reached the minimum while the alveolar P_co2 continued to fall. Pulmonary ventilation and respiratory frequency as well as the alveolar P_co2 increased and reached a ceiling during the third week of sojourn. Those rather quick changes during the first two weeks would indicate an increased sensitivity of the respiratory center to CO₂ stimulus, but the discrepancy between the change in breathh olding time and that in alveolar P_co2 after the third week of sojourn was difficult to be interpreted in this paper.

EKG and heart rate engaging in mountaineering as well as at rest were re- corded by the telemetry on three subjects of the 1965-1966 Nagoya university scientific and mountaineering expedition to the Andes at altitudes of 4200 to 7000 m (near the summit of Mt. Aconcagua, Argentina). Resting heart rate, 51-61 beats/min at sea level rose to 99-108 beats/min by a quick transition to an altitude (4200 m above sea level), but it became increasingly less during the course of high altitude acclimatization and reached 70-84 beats/min. Daily variation of the resting heart rate, within 12-14 beats/min at sea level, rose to 25-35 beats/ min at an altitude of 5000 m. Heart rate reached 130 beats/ min in subject N., 136 beats/min in subject I. and 163 beats/min in subject 0. during engaging in mountaineering at the altitude of 4200-5000 m. The ceiling level of the heart rate seems to be 145 beats/min for the three sujects, and 163 beats/min of subject O. which is 20-25 beats/min above the ceiling level will be explained by another unknown mechanism. Heart rate of subject I. did not exceed 145 beats/ min even in mountaineering at an altitude of 7000 m. Heart rate fell markedly during sleep at 6200 m in all subjects. In subject 0., !t decreased to the resting heart rate at sea level and with such a marked fall in hesrt rate the subject could not perform strenuous mountaineering next day. Resting EKG of the subject was normal at 4200 m after altitude acclimatization, and as far as the heart r ate was within the ceiling level, there was observed no abnormal events in EKG. With increased heart rate to above 140 beats/min, depression of ST segment, ectopic beats and marked arrhythmia were observed in subject 0.