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在内毒素给药后,对用阿司匹林预处理的猫进行肠系膜血管收缩实验。

Mesenteric vasoconstriction after endotoxin administration in cats pretreated with aspirin.

作者信息

Greenway C V, Murthy V S

出版信息

Br J Pharmacol. 1971 Oct;43(2):259-69.

Abstract
  1. Study of the delayed responses to lethal doses of endotoxin in cats is complicated by acute pulmonary vasoconstriction which results in hypotension, cardiac failure and pulmonary oedema. This acute response is abolished if the animal is pretreated with aspirin (10-100 mg/kg). In these cats, pretreated with aspirin, arterial pressure and right atrial pressure remain unchanged in the first 2 h after administration of endotoxin. Later, arterial pressure falls and the animals die but no haemorrhagic lung lesions are visible.2. These results confirm our previous conclusion that the delayed lethal response to endotoxin is an independent action and not a secondary consequence of the acute response. The mechanism of the action of aspirin is discussed and it is suggested that it prevents the release by endotoxin of vasoactive substances, possibly from platelets.3. In cats pretreated with aspirin, administration of endotoxin results in a marked mesenteric vasoconstriction. Although arterial pressure does not decrease significantly, superior mesenteric arterial flow decreases to 20% of control in the first hour after endotoxin and remains at this low level until the animal dies. Mesenteric ischaemia may contribute to the cat's death.4. The mesenteric vasoconstriction is not reduced by prior administration of phenoxybenzamine and is only slightly reduced after phenoxybenzamine, hypophysectomy and nephrectomy. It is concluded that catecholamines, vasopressin and angiotensin play at most a minor role in the mechanism of this vasoconstriction and that other unknown factors are predominant.
摘要
  1. 猫对内毒素致死剂量的延迟反应研究因急性肺血管收缩而变得复杂,这种收缩会导致低血压、心力衰竭和肺水肿。如果动物预先用阿司匹林(10 - 100毫克/千克)处理,这种急性反应就会被消除。在这些预先用阿司匹林处理的猫中,给予内毒素后的最初2小时内,动脉压和右心房压保持不变。随后,动脉压下降,动物死亡,但未见出血性肺部病变。

  2. 这些结果证实了我们之前的结论,即内毒素的延迟致死反应是一种独立作用,而非急性反应的继发后果。文中讨论了阿司匹林的作用机制,并提出它可能阻止内毒素从血小板等释放血管活性物质。

  3. 在预先用阿司匹林处理的猫中,给予内毒素会导致明显的肠系膜血管收缩。尽管动脉压没有显著下降,但内毒素给药后的第一小时内,肠系膜上动脉血流量降至对照值的20%,并一直维持在这个低水平直至动物死亡。肠系膜缺血可能是导致猫死亡的原因之一。

  4. 预先给予苯氧苄胺并不能减轻肠系膜血管收缩,在苯氧苄胺、垂体切除和肾切除后,这种收缩仅略有减轻。由此得出结论,儿茶酚胺、血管加压素和血管紧张素在这种血管收缩机制中至多起次要作用,其他未知因素起主要作用。

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本文引用的文献

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Inhibition of Anaphylactic Shock by Acetylsalicylic Acid.乙酰水杨酸对过敏性休克的抑制作用。
Science. 1948 Oct 29;108(2809):478-9. doi: 10.1126/science.108.2809.478.
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Intestinal is chemic shock and the protective role of the liver.
Am J Physiol. 1959 Aug;197:281-5. doi: 10.1152/ajplegacy.1959.197.2.281.
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Role of histamine in endotoxin shock.组胺在内毒素休克中的作用。
Proc Soc Exp Biol Med. 1960 Jul;104:379-81. doi: 10.3181/00379727-104-25843.
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TRIGGER MECHANISM OF ENDOTOXIN SHOCK.内毒素休克的触发机制
Am J Physiol. 1964 May;206:944-6. doi: 10.1152/ajplegacy.1964.206.5.944.
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HEPATIC REGULATION OF SODIUM AND WATER IN ASCITES.腹水形成过程中肝脏对钠和水的调节
JAMA. 1964 Jan 11;187:117-8. doi: 10.1001/jama.1964.03060150041009.
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Serotonin release by bacterial endotoxin.细菌内毒素释放血清素。
Proc Soc Exp Biol Med. 1961 Dec;108:774-6. doi: 10.3181/00379727-108-27063.

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