Cardiovascular responses produced by central injection of hydrogen peroxide in conscious rats
Cardiovascular responses produced by central injection of hydrogen peroxide in conscious rats
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DOI：
10.1016/j.brainresbull.2006.07.013
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发表时间：
2006-12-11
影响因子：
3.8
通讯作者：
Colombari, Eduardo
中科院分区：
文献类型：
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作者：
Cardoso, Leonardo Maximo;Colombari, Debora Simoes de Almeida;Colombari, Eduardo
活性氧簇(ROS)被证明可以调节神经元突触传递，并可能在心血管系统的自主神经控制中发挥作用。本研究观察了将过氧化氢(H_2O_2)单独或与抗氧化剂N-乙酰-L-半胱氨酸(N-乙酰-L-半胱氨酸)或过氧化氢酶联合注入第四脑室(第四脑室)对清醒大鼠平均动脉压和心率的影响。此外，还研究了自主神经系统对进入第4 V的H_2O_2引起的心血管反应的影响。实验动物为雄性Holtzman大鼠，体重280-320g，第4 V植入不锈钢套管，股动脉和股静脉分别植入聚乙烯心肌腱。在第4 V注射H_2O_2(0.5、1.0和1.5mU/0.2 mU L，n=6)，产生一过性(10min)剂量依赖性升压反应。1.0和1.5MU摩尔的H_2O_2也会产生持续时间较长的心动过缓(高剂量H_2O_2至少持续24小时)。预先在第4 V静脉注射N-乙酰-L半胱氨酸(250nmol/1mU L/鼠)阻断升压反应，并减弱第4 V静脉注射H_2O_2(1mU/0.5mU L/大鼠，n=7)引起的心率减慢。甲基溴阿托品(1.0 mg/kg，n=11)可阻断心动过缓，但不影响对H_2O_2的升压反应。盐酸哌唑嗪(1.0 mg/kg，n=6)静脉注射。消除升压反应，但不影响心动过缓。过氧化氢酶活性的增加(500uEA/1亩L/只大鼠注射到第4 V)也取消了对H_2O_2的升压反应和心动过缓反应。结果提示，ROS进入4V时增加，同时激活交感和副交感神经流出，引起升压和心动过缓反应。(C)2006 Elsevier Inc.保留所有权利。
Reactive oxygen species (ROS) have been shown to modulate neuronal synaptic transmission and may play a role on the autonomic control of the cardiovascular system. In this study we investigated the effects produced by hydrogen peroxide (H2O2) injected alone or combined with the anti-oxidant agent N-acetil-L-Cysteine (NAC) or catalase into the fourth brain ventricle (4th V) on mean arterial pressure and heart rate of conscious rats. Moreover the involvement of the autonomic nervous system on the cardiovascular responses to H2O2 into the 4th V was also investigated. Male Holtzman rats (280-320g) with a stainless steel cannula implanted into the 4th V and polyethylene carmulas inserted into the femoral artery and vein were used. Injections of H202 (0.5, 1.0 and 1.5 mu mol/0.2 mu L, n = 6) into the 4th V produced transient (for 10 min) dose-dependent pressor responses. The 1.0 and 1.5 mu mol doses of H2O2 also produced a long lasting bradycardia (at least 24 h with the high dose of H2O2). Prior injection of N-acetyl-L-cysteine (250 nmol/1 mu L/rat) into the 4th V blockade the pressor response and attenuated the bradycardic response to H2O2 (1 mu mol/0.5 mu L/rat, n = 7) into the 4th V. Intravenous (i.v.) atropine methyl bromide (1.0 mg/kg, n = 11) abolished the bradycardia but did not affect the pressor response to H2O2. Prazosin hydrochloride (1.0 mg/kg, n = 6) i.v. abolished the pressor response but did not affect the bradycardia. The increase in the catalase activity (500 UEA/1 mu L/rat injected into the 4th V) also abolished both, pressor and bradycardic responses to H2O2. The results suggest that increased ROS availability into 4th V simultaneously activate sympathetic and parasympathetic outflow inducing pressor and bradycardic responses. (c) 2006 Elsevier Inc. All rights reserved.