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吗啡受体阻断剂纳洛酮(NAL,3mg/kg)可使失血性休克大鼠血压、脉压及呼吸率显著增加,并提高24h生存率。α受体阻断剂或肾上腺摘除可取消NAL对出血性休克的升压抗休克作用。利血平耗竭外周交感神经系统儿茶酚胺不能取消NAL的升压抗休克作用。利血平化后再切除肾上腺可取消NAL的升压抗休克作用。提示NAL主要通过肾上腺髓质使儿茶酚胺释放增加而引起血压升高。NAL不能使离体灌流肾上腺儿茶酚胺释放增加,说明NAL促进儿茶酚胺释放可能不是对髓质嗜铬细胞直接作用的结果。
Morphine receptor blocker naloxone (NAL, 3mg / kg) can significantly increase blood pressure, pulse pressure and respiration in hemorrhagic shock rats, and improve 24h survival rate. Alpha blockade or adrenalectomy abolishes the antihypertensive effect of NAL on hemorrhagic shock. Reserpine depletion of the peripheral sympathetic nervous system catecholamines can not cancel the anti-shock effect of NAL. Reserpine re-removal of the adrenal gland abolishes the antihypertensive effect of NAL. Tip NAL mainly through adrenal medulla so that catecholamine release caused by increased blood pressure. NAL did not increase excretion of adrenocortical catecholamines in vitro, suggesting that NAL-induced catecholamine release may not be a direct result of medullary chromaffin cells.