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机构地区:[1]泰山医学院生理学教研室,泰安271000 [2]上海医科大学生理学教研室,上海200032
出 处:《中国应用生理学杂志》1993年第3期251-254,共4页Chinese Journal of Applied Physiology
摘 要:重度急性失血(30%总量)可使麻醉家兔防御性升压反应明显降低(P<0.05)。吸入低氧(含10%~14%氧气)混合气1~2min可使防御升压反应轻度增加(P<0.05)。持续低氧10~20min则使防御升压反应明显降低(P<0.01)。失血状态下侧脑室注射纳洛酮50~80μg/100μl,可使基础血压和防御升压反应明显升高(P<0.01)。提示重度失血时,防御升压反应明显降低可能与中枢缺氧及失血时脑内阿片样物质的释放抑制心血管中枢有关。The defence pressor response induced by stimulation of periaqueductal grey (PAG) decreased significantly following severe blood loss (30% of total blood volume) (P< 0.05). Inhalation of a gas mixture of low O2 (containing 10%-14% O2) over a period of 10-20 min produced a significant decrease in the defence pressor response (P< 0.01), but at the first 1-2 min of inhalation, the defence pressor response showed a slight increase (P> 0.05). Under the condition of blood loss, intracerebroventricular administration of naloxone (50-80μg/ 100μl) resulted in an obvious increase in both defence pressor response and basal blood pressure (P<0.01). It is suggested that the decrease in defence pressor response following severe blood loss might result from the inhibitory effects of central hypoxia as well as the release of endogenous opiate-like substance on the defence cardiovascular center after severe bleeding.
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