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窒息产生的肾上腺分泌物

DOI:
10.1152/ajplegacy.1926.76.3.538
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发表时间:
1926
影响因子:
--
通讯作者:
E. A. Molinelli
E. A. Molinelli
中科院分区:
--
文献类型:
--
作者:
B. Houssay;E. A. Molinelli

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嗜铬细胞反应和肾上腺素含量。关闭气管或呼吸一氧化碳(照明性气体)造成的窒息会降低狗、兔、公鸡和猴子肾上腺的嗜铬细胞反应强度和肾上腺素含量(Kahn,1912;Borberg,1913)。结果是通过比较窒息前和窒息后取出的肾上腺得出的结果。KoDama在关闭气管窒息的猫和狗的研究中发现,肾上腺中的肾上腺素含量比通常在正常动物中发现的要少。一些研究人员简单地测量了肾上腺血液中的肾上腺素浓度。Canon和Hoskins(1911)通过股静脉将导管插入下腔静脉,直到腰部-肾上腺静脉的水平。窒息后获得的血液抑制了兔离体肠的收缩,而来自股静脉的血液仍然不活跃。这种影响是由于肾上腺分泌,因为一旦肾上腺被取出,就不会观察到它,除非窒息是极端的。Czubalski(1913)还发现,窒息后抽取的狗的去纤血可以抑制收缩并松弛离体肠。Gley和Ququiaud(1917)测量血压升高效应的报告称,窒息狗肾上腺血液中的肾上腺素浓度增加了两到三倍,但没有重视这一事实,认为这是窒息导致血压上升的原因。Volhard和Hulse(1923)研究了三只弯曲的狗,即使在窒息后,也无法在从股静脉或心脏提取的滴定血液(特伦德伦堡存活青蛙法)中发现肾上腺素。循环和血液的使用足以解释这些负面的结果。
Chromaphil reaction and epinephrin content. Asphyxia produced by closing the trachea or breathing carbon monoxide (illuminating gas) diminishes the intensity of the chromaphil reaction and the epinephrin content of the adrenals in dogs, rabbits, cocks and monkeys (Kahn, 1912; Borberg, 1913). The results were obtained by comparing one adrenal taken out before asphyxia with the other taken out after asphyxia. Kodama, working with cats and dogs asphyxiated by closing the trachea, found a smaller epinephrin content in the adrenals than is usually found in normal animals.Direct estimation of adrenal secretion. Some investigators have simply measured the epinephrin concentration of adrenal blood. Cannon and Hoskins (1911) introduced a catheter through the femoral vein into the vena cava up to the level of the lumbo-adrenal veins. Blood so obtained after asphyxia inhibited the contractions of the isolated intestine of rabbits, while blood from the femoral vein remained inactive. This effect is due to adrenal secretion as it is not observed once the adrenals have been taken out, unless asphyxia is extreme. Czubalski (1913) also found that the defibrinated blood of dogs drawn after asphyxia inhibits the contractions and relaxes the isolated intestine. Gley and Quinquaud (1917) measuring the blood-pressure-raising effect reported an increase of two to three times the epinephrin concentration of adrenal blood in asphyxiated dogs, but attach no importance to this fact as a cause of the rise in blood pressure produced by asphyxia. Volhard and Hulse (1923) studied three curarized dogs and could not find epinephrin in titrated blood (Trendelenburg’s surviving-frog method) taken from the femoral vein or the heart, even after asphyxia. Curarization and the use of blood from the general circulation suffice to explain these negative results.