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本工作应用家兔作急性实验发现:(1)脑室注射50微克β-內啡肽,可使血压下降12.2±2.0毫米汞柱。此效应可被脑室注射鸦片受体阻断纳络酮所拮抗。(2)在出血性和中毒性休克时,脑内鸦片样物质的活性显著升高。其中以脑干部位升高得更为明显。(3)脑室注射80微克纳络酮可以部分桔抗出血性和中毒性休克的低血压效应,延长中毒性休克动物的存活时间。(4)脑室注射100微克的5-羟色胺可以逆转纳络酮的抗休克作用,使休克低血压效应加剧。这些实验结果提示:中枢鸦片样物质在休克发生过程中具有重要作用。阻断鸦片样物质的作用,可能是防治休克低血压效应的一个途径。
The work of rabbits for acute experiments found that: (1) intraventricular injection of 50 micrograms of β-endorphin, blood pressure can drop 12.2 ± 2.0 mm Hg. This effect can be antagonized by intracerebroventricular injection of opiate receptors to block naloxone. (2) In hemorrhagic and toxic shock, brain opioid activity was significantly increased. Among them, the brain stem increased more obviously. (3) Intraventricular injection of 80 micrograms of naloxone can partially inhibit the hypotensive effect of hemorrhagic and toxic shock and prolong the survival time of toxic shock animals. (4) Intraventricular injection of 100 micrograms of serotonin can reverse the anti-shock effect of naloxone, exacerbating the hypotensive effect of shock. These experimental results suggest that the central opioid plays an important role in the process of shock. Blocking the effects of opioids may be a way to combat the hypotensive effects of shock.