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低血压和血管紧张素升压反应丧失是由于中枢神经系统损伤和严重出血所致。

HYPOTENSION AND LOSS OF PRESSOR RESPONSE TO ANGIOTONIN AS THE RESULT OF TRAUMA TO THE CENTRAL NERVOUS SYSTEM AND SEVERE HEMORRHAGE.

机构信息

Lilly Laboratory for Clinical Research, Indianapolis City Hospital, Indianapolis.

出版信息

J Exp Med. 1943 Jul 1;78(1):41-58. doi: 10.1084/jem.78.1.41.

DOI:10.1084/jem.78.1.41
PMID:19871308
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2135365/
Abstract
  1. Angiotonin refractoriness and hypotension follow upon injury to the central nervous system in dogs and cats. Refractoriness does not develop when the nervous system is quickly and expertly destroyed or the activity of the nervous system depressed by widespread injection into it of a local anesthetic. The syndrome develops in the absence of the kidneys and the suprarenal glands. 2. Glycine, methyl isothiourea, and rest are the only agents studied which tend to restore responsiveness, and the first two of these have only an irregular and temporary effect. 3. There is a marked degree of specificity in the syndrome since undiminished pressor responses to adrenalin, tyramine, methyl isothiourea are observed during complete angiotonin refractoriness. 4. Despite the prolonged hypotension, change in the amount of plasma proteins and in the hematocrit readings is not striking. 5. Parallelism seems to exist between the fall in blood pressure after trauma to the nervous system and development of angiotonin refractoriness. After the syndrome has developed, elevation of the blood pressure by the injection of gum acacia solution or whole blood does not restore the responsiveness to angiotonin. 6. Angiotonin refractoriness and hypotension also develop after marked hemorrhage. Suprarenalectomy or nephrectomy does not prevent its appearance.
摘要
  1. 犬猫中枢神经系统损伤后会出现血管紧张素无反应性和低血压。如果神经系统迅速而熟练地被破坏,或者通过广泛注射局部麻醉剂来抑制神经系统的活动,就不会产生无反应性。该综合征在没有肾脏和肾上腺的情况下发生。

  2. 甘氨酸、甲基异硫脲和休息是唯一被研究过的有恢复反应倾向的药物,前两种药物只有不规则和暂时的效果。

  3. 该综合征具有明显的特异性,因为在完全的血管紧张素无反应性期间,肾上腺素、酪胺和甲基异硫脲仍能引起明显的加压反应。

  4. 尽管存在长时间的低血压,但血浆蛋白量和红细胞压积读数的变化并不明显。

  5. 似乎在神经系统创伤后血压下降与血管紧张素无反应性的发展之间存在平行关系。该综合征发展后,通过注射树胶阿拉伯溶液或全血升高血压并不能恢复对血管紧张素的反应性。

  6. 明显出血后也会出现血管紧张素无反应性和低血压。肾上腺切除术或肾切除术并不能阻止其发生。

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1
HYPOTENSION AND LOSS OF PRESSOR RESPONSE TO ANGIOTONIN AS THE RESULT OF TRAUMA TO THE CENTRAL NERVOUS SYSTEM AND SEVERE HEMORRHAGE.低血压和血管紧张素升压反应丧失是由于中枢神经系统损伤和严重出血所致。
J Exp Med. 1943 Jul 1;78(1):41-58. doi: 10.1084/jem.78.1.41.
2
THE SITE OF ANGIOTONIN DESTRUCTION.血管紧张素破坏部位。
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J Exp Med. 1940 Jan 1;71(1):29-42. doi: 10.1084/jem.71.1.29.
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On the mechanism of L-dopa-induced postural hypotension in the cat.关于猫中左旋多巴诱发体位性低血压的机制
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J Exp Med. 1940 Mar 31;71(4):495-519. doi: 10.1084/jem.71.4.495.
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THE ETIOLOGY OF HYPERTENSION DUE TO COMPLETE RENAL ISCHEMIA.因完全性肾缺血导致的高血压的病因。
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The relation of angiotonin and 1-norepinephrine to essential hypertension as determinded by the reaction of the nailfold capillary bed.通过甲襞毛细血管床反应确定血管紧张素和1-去甲肾上腺素与原发性高血压的关系。
J Exp Med. 1956 Apr 1;103(4):477-86. doi: 10.1084/jem.103.4.477.

引用本文的文献

1
THE SITE OF ANGIOTONIN DESTRUCTION.血管紧张素破坏部位。
J Exp Med. 1946 Apr 30;83(5):425-39.

本文引用的文献

1
ANGIOTONIN-ACTIVATOR, RENIN- AND ANGIOTONIN-INHIBITOR, AND THE MECHANISM OF ANGIOTONIN TACHYPHYLAXIS IN NORMAL, HYPERTENSIVE, AND NEPHRECTOMIZED ANIMALS.血管紧张素激活酶、肾素和血管紧张素抑制剂,以及正常、高血压和肾切除动物中血管紧张素快速脱敏的机制。
J Exp Med. 1940 Mar 31;71(4):495-519. doi: 10.1084/jem.71.4.495.
2
A CRYSTALLINE PRESSOR SUBSTANCE (ANGIOTONIN) RESULTING FROM THE REACTION BETWEEN RENIN AND RENIN-ACTIVATOR.一种由肾素和肾素激活物反应生成的晶态加压物质(血管紧张素)。
J Exp Med. 1940 Jan 1;71(1):29-42. doi: 10.1084/jem.71.1.29.
3
ON THE NATURE OF THE PRESSOR ACTION OF RENIN.肾素加压作用的本质。
J Exp Med. 1939 Oct 31;70(5):521-42. doi: 10.1084/jem.70.5.521.