Neurogenic hyperacute ascites in mice.
Neurogenic hyperacute ascites in mice.
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小鼠神经源性超急性腹水。
DOI：
10.1042/cs0710327
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Theodore,J
中科院分区：
文献类型：
--
作者：
Nelson,DP;Robin,ED;Wong,RJ;Morin,ME;Bensch,KG;Murphy,BJ;Theodore,J
1.对四组小鼠进行受控致命性头部创伤，然后评估是否存在腹水(神经源性超急性腹水，NHA)。这些动物几乎是瞬间死亡，没有持续疼痛或痛苦的证据。对一组动物的腹水量进行了测定。两组创伤患者接受了β阻滞剂心得安和α阻滞剂酚妥拉明的预治疗。第五组为非创伤组，用乙醚吸入处死作为对照组。另外两组未受创伤的小鼠在乙醚吸入处死前给予α肾上腺素能激动剂甲氧胺盐酸盐或β激动剂甲磺酸异乙基酯，然后评估是否有腹水。在未经治疗的创伤小鼠和未治疗的对照动物中，87-100%的小鼠有渗出性腹水。酚妥拉明预处理对腹水发生率无影响。与单纯创伤相比，心得安治疗可显著降低腹水发生率(P<；0.001)。给予异乙基乙胺(β激动剂)可使100%的受试动物出现腹水。甲氧胺(α激动剂)给药未引起腹水。描述了一种以前未描述的急性脑创伤的后果(NHA)，它似乎是由中枢起源的β交感神经活动介导的。NHA可被β受体阻断剂抑制，并可被β激动剂所模拟。
1. Four groups of mice were subjected to controlled fatal head trauma and then evaluated for the presence of ascites (neurogenic hyperacute ascites, NHA). The animals died virtually instantaneously and without evidence of maintained pain or suffering. The volume of ascites was determined in one group of animals. Two of the traumatized groups were pretreated, one with the β-blocker propranolol and the other with the α-blocker phentolamine. A fifth, non-traumatized, group which was killed with ether inhalation served as a control group. Two more groups of non-traumatized mice were administered either the α-adrenergic agonist methoxamine hydrochloride or the β-agonist isoethrane mesylate before killing by ether inhalation, and then evaluated for ascites.2. Transudative ascitic fluid was found in 87–100% of untreated traumatized mice and in no control animals. Pretreatment with phentolamine had no effect on the prevalence of ascites. Pretreatment with propranolol produced a significant decrease in the prevalence of ascites compared with trauma alone (P< 0.001). Isoethrane (β-agonist) administration caused ascites in 100% of the treated animals. Methoxamine (α-agonist) administration did not cause ascites.3. A previously undescribed consequence of acute brain trauma is described (NHA) which appears to be mediated by β-sympathetic activity of central origin. NHA is inhibited by β-blockade and can be simulated with β-agonist administration.