Vasodilating prostaglandin E1 does not reproduce interleukin-1beta-induced oxygen metabolism abnormalities in rabbits.

Vasodilating prostaglandin E1 does not reproduce interleukin-1beta-induced oxygen metabolism abnormalities in rabbits.
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血管舒张前列腺素 E1 不会在兔子中重现白细胞介素 1β 诱导的氧代谢异常。

DOI:
10.1002/ams2.84
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发表时间:
2015
影响因子:
1.6
通讯作者:
Yasuyuki Kuwagata
Yasuyuki Kuwagata
中科院分区:
--
文献类型:
--
作者:
Shigenari Matsuyama;Koichi Hayakawa;Kazuhito Sakuramoto;Muroya Takashi;Yasushi Nakamori;Hitoshi Ikegawa;Takeshi Shimazu;Yasuyuki Kuwagata

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背景我们已有报道,重组人白介素1β通过引起血管扩张前列腺素(S)的过度产生而导致循环休克,同时通过引起氧消耗(VO2)对氧输送(DO2)的异常依赖而损害氧代谢。方法16只兔随机分为3组,每组10只,分别给予10 μg/kg IL-1β(IL-1β组,n= 5)、1 μg/kg/min PGE 1(PGE1组,n= 6)或生理盐水(n= 5)。所有兔均采用心脏分步充气的方法,将气囊置入心包囊内,以降低氧饱和度。结果IL-1、β和PGE1均使平均动脉压下降约25%,心脏指数无明显变化。与对照组(yβ0.05x + 8.7)相比,IL-1 + 组(y = 0.13x + 6.4)的非供应依赖线斜率显著增加(y = 0.01x + 10.0),而PGE1组(yβ0.01x + 10.0)的供应非依赖性线斜率明显增加(y = 0.05x + 8.7)。结论PGE1引起的单纯血管扩张和降压不足以解释IL-1β引起的氧代谢异常。
BackgroundWe have reported that administration of recombinant human interleukin (IL)‐1β induced circulatory shock in rabbits by causing overproduction of vasodilating prostaglandin(s) and simultaneously impaired oxygen metabolism by causing an abnormal dependence of oxygen consumption (VO2) on oxygen delivery (DO2). The present study was carried out to compare the effect of administration of exogenous PGE1with that of IL‐1β on oxygen metabolism.MethodsSixteen rabbits were assigned to one of three groups and given a single injection of 10 μg/kg IL‐1β (IL‐1β group,n= 5), continuous infusion of 1 μg/kg/min PGE1(PGE1group,n= 6), or saline (control group,n= 5). All rabbits were subjected to stepwise cardiac tamponade to decrease DO2by inflating a balloon placed into the pericardial sac. The VO2/DO2relation was analyzed by the dual‐line method.ResultsBoth IL‐1β and PGE1decreased the baseline value of mean arterial pressure by approximately 25% without inducing significant alteration of the cardiac index. With respect to the VO2/DO2relation, the slope of the supply‐independent line was significantly increased in the IL‐1β group (y = 0.13x + 6.4), but not in the PGE1group (y = 0.01x + 10.0) compared to that in the control group (y = 0.05x + 8.7).ConclusionThese results indicate that simple vasodilation and hypotension induced by administration of PGE1are insufficient to account for the abnormal oxygen metabolism induced by IL‐1β.