According to the author's theory of excitation, the excitable system consists of the field of excitation and the active element, and the electric response of the system is elicited by the activation of the active element.
ENM is an electric circuit consising of two polarized layers as the field of excitation and a thyristor as the active element.
Electric responses of ENM are almost the same to those of the merve fiber.
Therefrom electric responses of ENM and those of the thyristor were compared obtaining the following results.
Strength-duration relation, relative refractory period, accommodation of stimulation, anode break-excitation, optimum frequency of AC stimulation etc. were observed on the system but not on the thyristor.
Overshoot, undershoot, etc. were observed on the course of action potential of ENM but not on the activation of the thyristor.
From these results it was known that those phenomena which were observed on the system but not on the active element were produced by modification of the activation of the active element through the field of excitation.

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It is thought that the morphogenesis of plasmatic arterionecrosis as the direct cause of hypertensive intracerebral hemorrhage is initiated by medial smooth muscle necrosis, and hypertension is believed to be the cause of medial smooth muscle cell necrosis.
Hypertension in rats with bilaterally constricted renal arteries can be normalized by removing the constricting clips from the renal arteries. Using this method, healing process of hypertensive medial smooth muscle cell necrosis in proximal and distal segments, especially in the former of the middle cerebral arteries was studied by light and electron microscopy.
After the removal of clips in hypertensive rats with severe systolic hypertension over 200 mm Hg, blood pressure dropped remarkably. In these rats, mortality and incidence of brain lesions such as softening, edema and bleeding decreased compared with the same aged hypertensive rats.
Electron microscopy showed that in the media of the proximal middle cerebral arteries, occurrence and progression of smooth muscle cell necrosis were suppressed and cell debris which had increased in the media of hypertensive rats diminished after the removal of clips. Basement membrane-like substances and collagen fibers were slightly increased in the medial extracellular space which decreased in width. The ratio of the total area of the media occupied by smooth muscle cells to the whole medial area became larger after the removal of clips as compared with that of hypertensive rats not only just before the removal of clips but also in the same experimental period.
On the other hand, autoradiographic study revealed that no ³H-thymidine was incorporated into the nuclei of medial smooth muscle cells at any time till 21 days after the removal of clips.
These facts indicate that total smooth muscle cell dimension in the media increased due to hypertrophy of the medial smooth muscle cells after the removal of clips.
Thickness of the media of the proximal segments of the middle cerebral arteries was measured by Suwa's method. There was on difference in the thickness of the media of the animals with the constricted renal arteries between before and 4 weeks after the removal of clips from the arteries. But the thickness of the media in these animals was thicker than that of normotensive rats.
Reaction products of intravenously injected horseradish peroxidase were seen in the vesicles of endothelial cells, but massive insudation of them by junctional transport into the subendothelial space was not observed before and after the removal of the clips. lt was the same in the untreated normotensive rats. So it can be said that increased vascular permeability did not play any role both in the occurrence and healing of the smooth muscle cell necrosis in this experimental study.
In conclusion, necrosis of the medial smooth muscle cells in th cerebral arteries, considered to be a trigger for the development of plasmatic arterionecrosis in hypertensive patients may be healed with hypertrophy of the remained medial muscle cells after normalization of high blood pressure.

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To clucidatc thc rcpairing process and the pathological significance of a minute endothelial injury in the development of atherosclerosis, endothelial desquamation areas of 0.84 × 0.l4mm (lesion A by 1 sec. current) and of 1.68 × 0.32mm (lesion B by 5 sec.) were induced by applying a weak electric current (200μA) to the endothelium in the middle portions of the rabbit common carotid arteries. And the endothelial repairing process and the effect of hypercholesterolemia on the process were studied by scanning electron microscopy and other pathomorphologic methods The following results were obtained :
1 At 30 minutes after the injury in both animal groups fed with a normal diet and a cholesterol-rich diet, white blood cells and platelets were seen adhereing to the denuded areas, and Evans blue injected intravenously was insudated into that areas. But large thrombus was not formed
2 In both groups, the denuded areas were rapidly repaired by migration of surrounding endothelial cells at 24 hours (lesion A) or 3 days (lesion B) after injury Regenerated endothelial cells were arranged radially around the center of the injured areas
3 In the group fed with the normal diet, the injured area did not proceed to any arteriosclerotic lesions by 9 weeks after the injury In the group fed with the cholesterol diet, on the contrary, marked atherosclerotic lesions were developed in the injured regions The insudation of Evans blue into the injured areas ceased coincidentally with reendothelialization in the group fed with the normal diet, but in the group fed with the cholesterol diet, the insudation continued for 9 weeks after the injury. Accordingly it was suggested that continued increased permeability in the injured endothelium was important in the development of atherosclerosis
4 In the group fed with the cholesterol diet, circulating blood mononuclear cells having a few lipid vacuoles were seen in the subendothelium before the migration of medial smooth muscle cells into the intima 24 hours after the injury Foam cells were generally seen in the superficial layer of the thickened intima, and smooth muscle cells with a few lipid vacuoles were found in the deep layer of the intima 3 weeks after the injury Accordingly it was considered that the intimal foam cells might be derived from both circulating mononuclear cells and medial smooth muscle cells
5 Three weeks after injury in the group fed with the cholesterol died, foam cells observed on the luminal surface might be released from the thickened intima into the arterial lumen through the newly opened interendothelial junctions or the portions of new endothelial cell loss
6 Neither minute endothelial desquamation nor cholesterol feeding alone induced arteriosclerotic lesions, but the combination of them caused marked atherosclerosis in the injured areas
The present study suggested that minute endothelial desquamation which was repaired in a short period of time under a normolipidemic condition, was an important factor in development of atherosclerosis under hypercholesterolemia

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Clinical and pathological study on changes of interlobular bile ducts in 44 patients with cholelithiasis were carried out, and 8 patients with obstructive jaundice by carcinoma, which were examined as control group.
Twenty-seven specimens revealed abnormal interlobular bile duct epithelium in 44 biopsy liver specimens from patients with cholelithiasis, in which cholecystolithiasis were 26 cases, choledocholithiasis were 16 cases, hepatolithiasis were 2 cases.
The epithelium was frequently infiltrated by neutrophils and lymphocytes, particularly neutrophils being predominant. The lumens of interlobular bile ducts were dilated, and cellular debris were often found in the lumen. Abnormal bile ducts had eosinophilic degenerative, swollen, vacuolized or flat epithelial cells with karyopyknosis or karyorrhexis, and partial destruction of the basement membrane. Also, PAS-positive and mucicarmine positive droplets and or granules were found in some interlobular bile duct epithelium.
In 5 patients, some of the interlobular bile ducts were disappeared on the serial sections.
Morphological changes of the interlobular bile ducts observed in cholelithiasis were similar to those observed in obstructive jaundice, however, the degree and incidence of various changes of the former were slighter than those of the latter.
On the other hand, in cases with abnormal interlobular bile ducts, fever and leukocytosis were often observed, but there was no significant difference between cases with abnormal interlobular bile ducts and cases without it. Al-Pase and serum total bilirubin of cases with abnormal interlobular bile ducts were higher than that of cases with normal interlobular bile ducts.
It seems that morphological changes of interlobular bile ducts in cholelithiasis result from inflammation and obstruction of the bile ducts.

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Effects of antipsychotics ; chlorpromazine (0.25-2^mg/kg s.c.), fluphenazine (0.025-0.1^mg /kg s.c.), haloperidol (0.013-0.05^mg/kg s.c.) and droperidol (0.013-0.1^mg/kg s.c.), tricyclic antidepressants ; imipramine (2.5-20^mg/kg i.p.) and amitriptyline (5-40^mg/kg i.p.), and anxiolitics and/or general depressants ; diazepam (0.25-2^mg/kg s.c.), chlordiazepoxide (2.5-20^mg/kg i.p.) and pentobarbital (2.5-20^mg/kg s.c.) given singly and combined with d-amphetamine (1^mg/kg s.c.) on rat's Sidmantype avoidance response (response-shock interval=30 sec, shock-shock interva 1=5 sec and 1session= 2 hr) were investigated.
All of these drugs except chlordiazepoxide suppressed the avoidance response with dose-dependent decreasing in the response (lever-pressing) rate and increasing in the shock rate. d-Ampheta mine 1^mg/kg s.c. increased the response rate to a 2.2-2.5 times higher level than that of the saline vehicle administered control, and decreased the shock rate. The effect of d-amphetamine was dose-dependently antagonized with the antipsychotics. Here, chlorpromazine 1.3^mg/kg, fluphenazine 0.06^mg/kg, haloperidol 0.03^mg/kg and droperidol 0.07^mg/kg were estimated to inhibit perfectly the effect of d-amphetamine 1^mg/kg. Imipramine, amitriptyline, diazepam, chlordiazepoxide and pentobarbital enhanced the response-increasing effect of d-amphetamine, in all doses except pentobarbital by more than 10^mg/kg. The doses which elicited the maximum increase in the response rate were imipramine 10^mg/kg, amitriptyline 10^mg/kg, diazepam 0.5^mg/kg, chlordiazepoxide 10^mg/kg and pentobarbital 5^mg/kg.
The present experiment demonstrated that d-amphetamine antagonized specifically with antipsychotics while not with antidepressants, anxiolitics and/or general depressants. These results suggest that the Sidman-type avoidance test in which drugs are given in combination with amphetamine is applicable to assess the pharmacological properties of psychotropic drugs in detail.

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ヒトの老化に伴って, 赤血球内の化学物質量に特異的な変化がみられるという報告はなかったが, 1974年に Purcell and Brozovic らは, 赤血球2, 3-diphosphoglycerate (2, 3-DPGと略す) 濃度が若年者に比して老年者では減少することを報告し, 注目されている.この2, 3-DPGは, ヘモグロビンの酸素親和性を低下させて, 組織での酸素放出を容易にして, 組織への酸素供給を増加させる生体にとって重要な役割をもっており, 生理的にも臨床的にも老年者にとって重要な意味をもっている.
今回われわれは健康老年者について, 2, 3-DPGテスト (Boehringer, Mannheim 社) を用いて, 赤血球2, 3-DPGを測定して, 青壮年者と比較検討する機会を持てたので, その成績を報告し, 考察を加える.

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