The leucocyte migration inhibition test (LMT) using the agarose plate method introduced by Clausen is simple and highly reproducible.
Using thyroglobulin, mitochondria and thyroid microsomal fractions as antigens, LMT was performed on ten patients with insulin dependent diabetics, twenty patients with insulin independent diabetics, eleven patients with Graves' diseases, ten patients with chronic thyroiditis and ten healthy controls.
The migration index was expressed as a percentage of migration and calculated from the following formula.
Migration index (M I) =average areas of migration in test suspension/average areas of migration in control suspension×100
Using a thyroid microsomal fraction, the mean migration index for the insulin dependent diabetics (93.2±11.6) was significantly lower than in the normal subjects (104.3±10.9) (0.025<p<0.05).
Using thyroglobulin as an antigen for the insulin dependent diabetics and insulin independent diabetics, the mean migration indices (±SD) were 93.7±10.8 and 102.8±10.6 respectively.
The corresponding values for the control group were 100.6±7.3.
Using a mitochondria, MI values for insulin dependent and independent diabetics were 97.7±5.5 and 99.6±12.6 respectively, while MI value for the control group was 103.9±13.6.
The mean migration indices obtained with the mitochondria and thyroglobulin were not significantly depressed when the diabetic groups were compared with the normal subjects.

抄録全体を表示

The galactose tolerance tests were performed using the recently developed galactose-dehydrogenase technique in normal, hepatic and diabetic cases. The results obtained were compared with glucose tolerance tests, and in particular the changes of carbohydrate metabolites were investigated.
In all cases, no significant changes of plasma IRI during galactose loading tests were found with both oral and intravenous administration. Furthermore, a correlation between ΔIRI and Δgalactose was not statistically recognized.
The correlation between ΔIRI and Δglucose was significant in normal subjects in oral glucose tolerance tests, but not significant in galactose tolerance tests. However, no correlation was observed in the groups of diseases in both oral glucose and galactose tolerance tests.
In the relationship between ΔIRI and ΔNEFA, slightly positive correlation was found in normal subjects during oral glucose loading, whereas a tendency of negative correlation was found in them during oral galactose loading. This tendency was particularly remarkable in patients with liver diseases whose blood galactose levels were retarded.
The decrease in blood NEFA levels during oral galactose loading were compared with the glucose tolerance tests. The decrease of NEFA following oral galactose loading reached a maximum level after 1 hour. On the other hand, the decrease following glucose loading was still maintained after 2 hours, and was more remarkably compared to galactose loading. It was thought that the initial decrease in blood NEFA levels between 30 and 60 minutes after loading was induced by the direct action of galactose or glucose, and the continuous decrease up to 2 hours after glucose loading was caused by insulin release.

抄録全体を表示

It is well-known that thyroidal ¹³¹I-uptake is not suppressed by the T₃-suppression test in Graves' disease. However, it has not been elucidated whether serum TSH is suppressed or not. As the basal level of TSH in Graves' disease is generally very low, a comparision of TSH levels before and after the T₃-suppression test is difficult. An investigation was made of changes in serum T₃, T₄, TSH before and after the T₃-suppression test in patients treated for Graves' disease (Group I.....non suppressed patients whose TSH decreased after the suppression test, Group II.....suppressed patients, Group III.....non suppressed patients in whom a TSH decrease after the suppression test was not confirmed). After daily administration of 75γ of T₃ for 8 days, serum TSH was significantly reduced from 16.5±2.7μU/ml (mean±SE) to 0.6±0.3/μU/ml in Group I, whereas thyroidal ¹³¹I-uptake was not suppressed (26.4±3.7% before; 26.6±3.4% after). Immediately after the suppression test serum T₄ did not show a significant decrease in non-suppressed patients (Group I, III), but in suppressed patients (Group II) serum T₄ was significantly reduced from 8.6±0.3μg/dl to 6.7±0.5μg/dl.
The conclusions were as follows :
1. The non-suppressibility of ¹³¹I-uptake may be due to thyroidal autonomy or the existence of thyroid stimulators other than TSH.
2. In general, during recovery from Graves' disease the secretion of pituitary TSH occurs earlier than the suppression of the thyroidal gland.
3. It is suggested, that to evaluate the T₃ suppression test, reduction of serum T₄ is a more useful indicator than changes in 24-hr thyroidal ¹³¹I-uptake.

抄録全体を表示

There have been many reports, using pancreatic specific glucagon-antibody “K30”. Since some clearly stated that after pancreatectomy, plasma pancreatic glucagon levels increased, it has become a major problem whether, in the normal state, the gastrointestinal glucagon which react the pancreatic specific glucagon antibody is determined, or whether there is any physiological activity of the extrapancreatic glucagon on the blood sugar metabolism.
The present study was designed to detect any increase in the gastrointestinal glucagon which react the pancreatic specific glucagon antibody in the normal state, and also to examine the function of the extrapancreatic glucagon on the blood sugar metabolism.
Twenty healthy dogs, weighing from 10 to 12kg, were used. These dogs were operated on under Ketalar anesthesia. After insertion of polyethlene catheters into the femoral and axillar veins, tracheal catheters were intubated. Under additional Ravonal anesthesia, gastroenterectomy of these dogs was performed, resecting from the end of the esophagus to the end of the ampulla of the rectum with a midline abdominal incision. The pancreases of all the dogs were preserved almost intact. The bleeding volumes and packed cell volumes (PCV) were measured during this operation at ten minute intervals. At the end of this operation, which took one hour and a half, PCV decreased from 43% to 32% in each dog. The five control dogs were exsanguinated at 32% of PCV for one and a half hours and only laparotomy was performed as a sham-operation under Ketalar anesthesia.
1) Immediately after surgery, Arginine was administered at the rate of 130mg/kg/min for 15 minutes to the five gastroenterectomized dogs and to the five dogs who had under-gone the Sham operation. Plasma glucagon immunoreactivity (GI) (measured using pancreatic specific glucagon-antibody “K30” (Unger, Texas)) rose from a mean baseline value of 115 ± 9pg/ml up to a mean peak value of 200 ± 9pg/ml at 10 minutes in the gastroenterectomized dogs, and also, in the control dogs, GI rose from a mean baseline value of 158 ± 16 pg/ml to a mean peak value of 300 ±25pg/ml at 15 minutes. Total GLI (measured using non-specific glucagon-antibody “K4023” (Novo, Denmark)) increased from a mean baseline value of 130 ±14pg/ml to a mean peak value of 220 ±18pg/ml at 15 minutes in the gastroenterectomized. dogs, and also, in the control dogs, total GLI increased from a mean baseline value of 330 ±13pg/ml to a mean peak value of 705 ±62pg/ml at 10 minutes. IRI (measured by the two-antibody method) rose from a mean baseline value of 13 ±2μU/ml to a mean peak value of 46 ±812U/ml at 15 minutes in the gastroenterectomized dogs, and also, in the control dogs, IRI rose from a mean baseline value of 16 ±4/.2U/ml to a mean peak value of 32 ±3μU/ml. Blood sugar levels (BS) (measured by the glucose oxidase method) decreased from 152±2mg/dl to a mean trough value of 127 ±4mg/dl at 15 minutes in the gastroenterectomized dogs, but showed little change in the control dogs.
2) At 2 hours after surgery, Arginine was administered at the same rate and the same volume as that at just after surgery to the five gastroenterectomized dogs and the five control dogs. There was no remarkable difference between the responses of GI, total GLI, IRI and BS to that at 2 hours after surgery and those responses at just after surgery.
GI responses in arginine experiments showed significantly lower values at any point in the gastroenterectomized dogs than those in the control dogs (with the Student's t-test P<0.05). There was no significant difference between the response of GI and that of total GLI in the arginine experiments in the gastroenterectomized dogs at any point. Also IRI response showed no significant difference between the gastroenterectomized dogs and the control dogs.

抄録全体を表示

成熟雌ラットにおいて周期的LH分泌調節に重要な役割りを果す性ステロイドフィードバックの中枢神経機序について, 数実験を綜合して検討した.実験結果は次の通りである.
1) 正常性周期の各時期に弓状核単一発火活動を促進する内側視束前野電気刺激の有効最小電流 (閾値) をウレタン麻酔下急性実験で求めた.更に去勢雌ラットを用いてEstradiol Benzoate (EB) の単独または連続投与動物及びProgesterone (PROG) の単独又はEB処理後投与動物において同閾値をみた.正常性周期において, 閾値は発情前期に最低, 非発情第1期に最高となる周期的変化を示した.去勢動物は高い閾値を示したがEB投与により閾値は発情前期のレベル迄低下した.PROGは閾値をほとんど変化させなかった.
2) 内側底部の中隔一視束前野領域をステンレス電極の直流通電によって刺激してその結果誘発されるLH分泌をRIA法で定量し, 刺激に対するこの神経領域のLH分泌反応性をネンブタール処置発情前期ラット (正常雌) と新生児期アンドロジェン処理によって周期的排卵機能を失った連続発情ラット (雄性雌) とで比較した.刺激によってLHを分泌させた部位は正常雌では視索上核, 内側視束前野から背側及び腹側対角帯核 (内側底部中隔野) と広く分布し, 当該部位内でのLH反応性は等価であった.雄性雌でも視索上核を除いた同一部位の刺激でLH分泌を起し, 同強度の刺激によるLH分泌反応は正常雌と量的, 時間経過共に同等であった.
3) 去勢雌ラットにEBを投与し, その3日後に更にEBまたはPROGを投与した時に見られるLH分泌へのエストロジェンまたはプロジェステロンの正・負饋還に対する内側或いは外側中隔野の選択的電気的破壊或いは前交連上端における広範囲神経束切断の影響をRIA法を用いて検索した.その結果エストロジェンの負饋還及びプロジェステロンの正饋還は中隔野破壊或いは神経束切断の影響を受けなかったが, エストロジェン正饋還は分界条が完全に切断された場合には完全に抑制された.またエストロジェン正饋還は中隔野破壊によって量的・時間経過共に強い影響を受けた.
LH分泌調節中枢神経系の最終共通路をなすと考えられる内側底部中隔・内側視束前野-内側底部視床下部系の神経興奮性はエストロジェン血中濃度変化に応じて周期的に変動し, 発情前期午後に最も高い興奮性を示す.この系の興奮性変動が発情前期critical periodにおけるneural surgeに深く関与している.しかし内側底部中隔・視束前野刺激によるLH分泌反応性が新生児期アンドロジェンによって影響を受けておらず, またLH分泌に対するエストロジェン正饋還が中隔部の神経連絡切断, 殊に分界条切断で強く抑制されている.この事実はLH分泌が最終共通路をなす二重調節機能の自動的調節によるのでなく, より開放的な調節系によって調節されており, 視床下部外因子特に内側扁桃核一分界条系がエストロジェン正饋還を受けて性分化の発現と周期的LH分泌調節機序に必須の役割りを果している事を示唆している.

抄録全体を表示