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本工作在戊巴比妥钠麻醉的家兔上进行。采用夹闭肠系膜上动脉产生内毒素的方法建立中毒性休克的实验模型。用放射免疫分析法测定了休克前后脑区、脑脊液以及血浆中脑啡肽的变化并观察了脑室或静脉注射纳络酮的抗休克效应。结果①中毒性休克时,脑内的亮脑啡肽含量升高。其中下丘脑、延脑、桥脑显着升高,中脑无明显改变,丘脑、纹状体有所下降。脑脊液中亮脑啡肽含量明显增加。血浆中亮脑啡肽水平明显增高,但外周静脉血与肾静脉血中无显著差别。②侧脑室或静脉注射鸦片受体阻断剂纳络酮,均可使休克动物的血压回升。脑室注射的升压数值略大,维持升压时间也较长。实验结果提示:脑啡肽参与中毒性休克过程。阻断鸦片样物质的作用,可能是治疗中毒性低血压休克的一个途径。
This work was performed on rabbits anesthetized with pentobarbital sodium. An experimental model of toxic shock was established by clipping the superior mesenteric artery to produce endotoxin. Radioimmunoassay was used to determine the changes of enkephalins in brain regions, cerebrospinal fluid and plasma before and after shock and to observe the anti-shock effects of intraventricular or intravenous naloxone. Results ① toxic shock, brain enkelin enkephalin content increased. Including hypothalamus, medulla oblongata, pons, brain significantly increased, no significant change in the midbrain, thalamus, striatum decreased. Cerebrospinal fluid enkephalin increased significantly. Brilliant enkephalin levels in plasma were significantly higher, but there was no significant difference between peripheral venous blood and renal venous blood. ② lateral ventricle or intravenous injection of opiate receptor blocker naloxone, can shock the blood pressure of animals. Ventricular injection of the boost slightly larger value to maintain a longer boost time. Experimental results suggest that enkephalin is involved in toxic shock. Blocking the opioid effect may be a way to treat toxic hypotensive shock.