局所麻醉ニ據ル起立截神術ニ關シテハ既ニ中央獸醫會雜誌第31輯第4卷(大正7年)ニ其30例ヲ報告セシモ爾來尚手術ノ機會アル毎ニ殊ニ外科手術實習ニ際シテ之ガ研究ヲ續ケ約60例ヲ得シガ故茲ニ再ビ舊法ノ改良點ヲ報告セントス
手術前動物ノ保定術部ノ消毒竝ニ使用藥品ニ關シテハ特ニ記載スルノ要ナキモ注射方法ニ就テハ多少改良セル所ナキニ非ラズ即チ從來ハ神經鞘内麻醉ヲ行ハズシテ常ニ神經幹ノ麻醉ハ皮上ヨリ之ヲ行ヒシモ斯ノ如キ方法ニテハ注射ガ神經幹ニ的中スルコト殆ド稀ニシテ常ニ神經ノ截斷時ニ著明ノ疼痛ヲ表スガ故截斷ノ目的ニ行フ神經幹ノ麻醉ハ皆鞘内麻醉ヲ行フコトトセリ即チ先ヅ最初皮膚皮下織筋肉腱膜等ノ麻醉ヲ行ヒ神經幹ニ向ツテハ注射ヲ行ハズシテ創ヲ造リ神經露出セバ茲ニ初メテ第2段ノ注射即チ神經鞘内麻醉ヲ行ヘリ鞘内麻醉ハ甚ダ容易ナルモノニシテ比較的多量ノ麻醉藥液ヲ注射シ得ルモノナリ但シ完全ナル神經幹ノ麻醉ヲ得ル迄ニハ數分間ヲ要スルモノトス
本法ニ據ル時ハ全注射ニ要スル藥液ノ量却テ尠ナク效果一層顯著ナリ

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Canine Distemper has already been recognized from a clinical point of view as an infectious disease before the era of bacteriology by Youatt (1830), Renner & Karle (1844), Weiss (1852), Hertwig (1853), Camille Leblanc (1857), Röll (1867), Venuta (1873) and others. Numerous records on its etiology have hitherto been reported.
It was Semmer who, in 1875, first demonstrated a bacterium as the causal agent of the disease. An organism similar to the above was also isolated by Friedberger in 1881. Since that time, many other strains of bacteria have been found in local lesions. Krajewski (1883) isolated diplococci from the tissues and the blood of an infected animal, Laoson (1882) bacilli and diplococci, Rabe (1883) diplococci and streptococci from the pustules, tears and nasal discharge, Mathis (1887) diplococci from the body fluid, pustules, tears and nasal discharge, Marcone and Meloni (1888) micrococci, Millais (1890) a bacillus as the primary and a micrococcus as the secondary causal agent from the lung lesions, Legrain and Jacquot (1890) a motile micrococcus from the pustules, Galli- Valerio an ovoid bacillus from the brain, spinal cord and lungs, Babes and Barzanesco (1895) a motile, Gram-negative, non-sporebearing bacillus from the blood, liver and lungs, Jensen (1896) a streptococcus, Babes and Starcovici (1897) a bacillus resembling the Bacillus typhosus, Taty and Jacquin (1898) a diplococcus from the central nervous system, Jess (1899) a small bipolar bacillus, 1.8-2.3μ in length, 0.6μ in breadth, from the tears, nasal discharge, blood, abdominal fluid and internal organs, Petropawski (1899) a bacillus, Monkton Copeman and Mallais (1900) a Gram-negative coccobacillus, Lignières and Phisalix (1900) a bacillus, Pasteurella canis, from the cardiac blood, and Wunsch heim (1905) a coccobacillus, Bacillus canicidus.
Contrary to those findings above mentioned, Carré (1905-1906) declared that the cause of the disease is an ultramicroscopic virus which passes through bacterial filters, and this opinion has been supported by Vallée, Bosc and McFadyean.
Kregenow, however, was of opinion different from Carré, and later Ferry (1910), McGowan (1910) and Leitch reported that they have proved independently a small, motile Gram-negative, non-sporebearing bacillus, 0.5-2.3μ in length, 0.4-0.5μ in breadth, as the primary causative agent, to which Ferry gave the name Bacillus bronchicanis, subsequently changing this Bacillus bronchisepticus.
Wunschheim, in 1913, described in his report that the disease is caused by the Bacillus paratyphosus B.
As will be seen from the facts referred to above, the cause of the disease is not yet determined. So it will be of interest to study the etiological significance of organisms isolated from various organs, especially from the lungs of the infected animal. For this purpose I have made, in the first place, some experiments upon the transmission of the virus into normal dogs and then upon the isolation of organisms from the lungs and other organs of the infected animal.
The results of these investigations are summarized as follows:
1) The disease could be transmitted into dogs by inoculating an emulsion prepared from the lungs of an infected dog. It is, however, highly probable that some other unknown factors should be required to produce the disease in experimental animals, for the artificial infection showed no constant transmission of this disease.
2) No evidence of infection was found in dogs which were inoculated with filtrate of the emulsion prepared from the affected lungs.
3) In 46 cases or about 85% of 54 affected lungs, a Br. type bacillus, similar to the Bacillus bronchisepticus, was found.
In 50% of these numbers, the bacillus was isolated in pure culture, while in 35% it was found in mixed culture with other organisms-streptococci in 19% and staphylococci in 11%.

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被働性過敏症ノ働性感作ニ及ボス影響,試驗注射ノ反復ニヨリテ生ジタル抗過敏症,抗過敏症ノ特殊性,遊離抗體ノ過敏症状發現ニ及ボス障碍,試驗管内及動物體内ニ於ケル過敏抗體ノ中和,抗過敏症もるもっとニ同種及異種動物免疫血清ヲ以テセル被働性感作,甲抗原ニ對シ抗過敏性ナルもるもっとニ乙抗原ヲ以テ免疫セルもるもっと血清ヲ以テセル被働性感作及もるもっとニ於ケル母體ヨリ仔體ヘノ過敏症抗體ノ移行ニ就テ試驗シ抗過敏症ノ性質ヲ説明セリ(尚詳細ハ獸疫調査所研究報告第7號ニ於テ報告スベシ)

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著者ハ健康〓馬90頭ニ就テ血液檢査ヲ行ヒ殊ニ白血球數ニ就テ詳細ナル觀察ヲ施シ年齡ニヨリテ變化シ行ク状況ヲ調ベ次ノ如キ結論ヲ與ヘタリ
白血球總數ハ5歳ノ時9400ニシテ6歳ノ時9100,7歳ノ時8800ト云フガ如ク漸次減少シ行キ8歳頃ヨリ以後概子變化ナク8500内外ノ數ヲ保ツ而シテ其内中性多核ハ5歳ノ時非常ニ尠ク3800ナルモ6歳トナル時ハ著シク増シテ4800トナリ其後數年間5000内外,13歳ヨリ5500,17歳ヨリ6000内外トナリ淋巴球ハ5歳ノ時非常ニ多ク5100ヲ示スモ6歳ノ時3600,7歳ノ時3200,8歳トナリテ遂ニ3000以下ニ減ジ,尚年齡ト共ニ僅ニ漸減シ19歳ノ頃2000トナルえおじん細胞ハ300-600ニシテ多少異動アルモ其眞相審ナラズ大單核移行型竝鹽基性細胞ハ概子30-50ヲ示セルモ元ヨリ檢出數尠キタメ俄ニ正確ナル批判ヲ加ヘ難シ
著者ハ其成績ニ鑑ミ各年齡ニ於ケル健康雜種〓馬ノ白血球數殊ニ中性多核及淋巴球ノ健常數ヲ左ノ如ク想定シ其異動ハ増減共ニ當該數ノ約1/5以内ヲ以テセリ

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In the veterinary circles carbon disulphide (CS₂) has long been known as an anthelminticum, chiefly used in the treatment of stomach disorders in the horse caused by the larvae of Gastrophilus equi, and of late it is highly recommended by many authors to employ this medicament as a specific for this parasitary disease.
In spite of having an effective anthelmintic property. the toxic action of CS₂ has not yet thoroughly been studied and in connection with this only a few experiments have hitherto been made.
In the books of toxicology by Kobert, Kunkel, Jaksch, etc., we find some descriptions about a number of cases of CS₂intoxication in men, most of them, however, being related to chronic intoxications occurred among workmen in match or rubber factories. Acute cases, in which men have taken CS₂ mistaking it for a drink, are also quoted in those books.
In the case of acute intoxication, according to the results obtained from the experiments with animals, paralysis of the respiratory system first appears, then that of the heart and finally general paralysis followed by coma. If it is the case of a slight intoxication, in which the animal is exposed to the CS2 gas for a short time, then it will easily be recovered under the supply of fresh air, but if exposed for a long time, the animal may die in one or two days, though once recovered. They report that an inhalation of air containing 5 volume % CS₂ gas is enough to kill experimental animals in a few minutes.
As to the subjective and objective symptoms which appear in men in the case of acute or chronic intoxication, they declare that the CS₂ content below 0.8mg in 1 litre of air is not dangerous.
I have made some CS₂ intoxication experiments with mice, guinea-pigs, and rabbits, etc.; from the results obtained I come to the following conclusions.
1) 1.5 volume per cent. CS₂ in the air can be considered as the minimal lethal dose, causing an acute intoxication in an experimental animal, and 3 volume per cent. CS₂ is enough to kill the animal within ten minutes; Thus the result of my experiments is coincident with that of the authors above mentioned, who stated that the air containing 5 volume per cent. CS₂ kills the animal within a few minutes. As already mentioned, if the CS₂ content in 1 litre of air is below 0.8mg, no disturbance will be recognized in the physiological functions of workers in a factory, though the air is stinking. 0.8mg in 1 litre is equal to 0.125 volume per cent. at 15°C and 760mm Hg, so this volume per cent. is less than 1/120 of the minimal lethal dose (1.5 vol. per cent.) obtained in the animal experiments.
2) The phrenic nerves of a rabbit which is in a state of apnoea, intoxicated by inhalation of a certain dose of CS₂, still react to an electric irritation in the same degree as before intoxication. This fact proves that the cause of intoxication death is the paralysis of the respiratory centre. The simultaneous disappearance of the movements of the alae of the nose and the accessory respiratory muscles, and of the movement of the diaphragma also proves that the inhalated CS₂ has given rise to the paralysis of the respiratory centre.
3) The respiration of an animal which breathes the air containing CS₂ at first accelerates, then becomes slow and finally stops. The blood pressure rises with the acceleration of respiration but it suddenly falls down at the stage of apnoea and a few minutes later palpitation of the heart stops.

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