N(G)-nitro-L-arginine methyl ester, but not methylene blue, attenuates anaphylactic hypotension in anesthetized mice.
N(G)-nitro-L-arginine methyl ester, but not methylene blue, attenuates anaphylactic hypotension in anesthetized mice.
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DOI：
10.1254/jphs.fp0070169
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发表时间：
2007
影响因子：
3.5
通讯作者：
H. Takano;Wei Liu;Zhan-sheng Zhao;S. Cui;Wei Zhang;T. Shibamoto
中科院分区：
文献类型：
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作者：
H. Takano;Wei Liu;Zhan-sheng Zhao;S. Cui;Wei Zhang;T. Shibamoto
为了阐明NO在小鼠过敏性低血压中的作用，在麻醉的BALB/c小鼠中测定了一氧化氮（NO）合酶抑制剂N（G）-硝基-L-精氨酸甲酯（L-NAME）对抗原诱导的低血压和门脉高压的影响。直接并同时测量体循环动脉压（Psa）、中心静脉压（Pcv）和门静脉压（Ppv）。首先用卵清蛋白致敏小鼠，然后注射抗原降低Psa，升高Ppv。用L-NAME（1 mg/kg）预处理可减弱这种抗原诱导的全身性低血压，但不能增加Ppv。用亚甲蓝（3.0 mg/kg）或1H-[1，2，4]恶二唑[4，3-a]喹喔啉-1-酮（10 mg/kg）观察可溶性鸟苷酸环化酶抑制剂对过敏性低血压的影响。两者均不调节任何抗原诱导的变化。此外，亚甲蓝没有改善由化合物48/80（4.5mg/kg）诱导的全身性低血压，化合物48/80是一种肥大细胞去甲肾上腺素，其可以产生非免疫性过敏样反应。这些数据表明，在麻醉的BALB/c小鼠中，L-NAME可减轻过敏性低血压，而不影响门静脉高压。L-NAME的这种有益作用似乎不依赖于可溶性鸟苷酸环化酶途径。
To clarify the role of NO in mouse anaphylactic hypotension, effects of a nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), on antigen-induced hypotension and portal hypertension were determined in anesthetized BALB/c mice. Systemic arterial pressure (Psa), central venous pressure (Pcv), and portal venous pressure (Ppv) were directly and simultaneously measured. Mice were first sensitized with ovalbumin, and then the injection of antigen was used to decrease Psa and increase Ppv. Pretreatment with L-NAME (1 mg/kg) attenuated this antigen-induced systemic hypotension, but not the increase in Ppv. The effect of inhibitors of soluble guanylate cyclase on anaphylactic hypotension were studied with either methylene blue (3.0 mg/kg) or 1H-[1,2,4]oxadiazole[4,3-a]quinoxalin-1-one (10 mg/kg). Neither modulated any antigen-induced changes. Furthermore, methylene blue did not improve systemic hypotension induced by Compound 48/80 (4.5 mg/kg), a mast cell degranulator, which can produce non-immunological anaphylactoid reactions. These data show in anesthetized BALB/c mice that L-NAME attenuated anaphylactic hypotension without affecting portal hypertension. This beneficial effect of L-NAME appears not to depend on the soluble guanylate cyclase pathway.