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首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Involvement of phospholipase A(2) pathway for the Indian red scorpion venom-induced augmentation of cardiopulmonary reflexes elicited by phenyldiguanide.
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Involvement of phospholipase A(2) pathway for the Indian red scorpion venom-induced augmentation of cardiopulmonary reflexes elicited by phenyldiguanide.

机译:磷脂酶A(2)通路参与印度红蝎毒引起的苯二胍诱发的心肺反射增强。

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摘要

The present study was conducted to examine the role of phospholipase A(2) and prostaglandins in Indian red scorpion (Mesobuthus tamulus; MBT) venom-induced augmentation of cardiopulmonary reflexes elicited by phenyldiguanide (PDG). Trachea, femoral artery and jugular vein were cannulated in urethane anesthetized adult albino rats. The effect of jugular venous injection of PDG on ECG, BP and respiratory activity were recorded. Injection of PDG (10mug/kg) evoked tachypnea/apnea, bradycardia and hypotension lasting for 60s. After injecting MBT venom (100mug/kg) for 30min, the PDG evoked reflex responses were augmented by two times and increased the pulmonary water content in envenomed animals, significantly. The venom-induced augmentation of PDG reflex and the increase in pulmonary water content were blocked in animals pretreated with B(2) kinin receptor antagonist (Hoe 140; 2.32mug/kg). These responses induced by venom were also blocked by a phospholipase A(2) antagonist (PACOCF(3); 1mg/kg) and a prostaglandin synthase inhibitor (indomethacin; 10mg/kg). The observations indicate that the venom-induced responses (augmentation of PDG reflex response and increased pulmonary water content) involve PLA(2)-prostaglandin pathway that is triggered by B(2) kinin receptors to sensitize the receptors located on the vagal C-fibres.
机译:进行本研究以检查磷脂酶A(2)和前列腺素在印度红蝎(Mesobuthus tamulus; MBT)毒液诱导的苯二胍(PDG)引起的心肺反射增强中的作用。在经尿烷麻醉的成年白化病大鼠中插管气管,股动脉和颈静脉。记录颈静脉注射PDG对ECG,BP和呼吸活动的影响。注射PDG(10mug / kg)引起呼吸急促/呼吸暂停,心动过缓和低血压持续60s。注射MBT毒液(100mug / kg)30分钟后,PDG引起的反射反应增加了两倍,并显着增加了被毒动物的肺水含量。在用B(2)激肽受体拮抗剂(Hoe 140; 2.32mug / kg)预处理的动物中,阻止了毒液诱导的PDG反射增强和肺水含量增加。这些由毒液诱导的反应也被磷脂酶A(2)拮抗剂(PACOCF(3); 1mg / kg)和前列腺素合酶抑制剂(吲哚美辛; 10mg / kg)阻断。观察结果表明,毒液诱导的反应(增强PDG反射反应和增加肺水含量)涉及由B(2)激肽受体触发的PLA(2)-前列腺素途径,以使位于迷走性C纤维上的受体敏感。

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