失血性休克后中性粒细胞对内脏血流的调节
Neutrophil regulation of splanchnic blood flow after hemorrhagic shock.
作者信息
Turnage R H, Kadesky K M, Rogers T, Hernandez R, Bartula L, Myers S I
机构信息
Department of Surgery, University of Texas Southwestern Medical School at Dallas 76235, USA.
出版信息
Ann Surg. 1995 Jul;222(1):66-72. doi: 10.1097/00000658-199507000-00011.
OBJECTIVE
This study examines the hypothesis that neutrophils impair splanchnic blood flow during resuscitation from hemorrhage by inhibiting the release of the compensatory vasodilator PGI2 from the bowel.
SUMMARY BACKGROUND DATA
Resuscitation from hemorrhagic shock is associated with neutrophil infiltration into the intestine, reduced splanchnic perfusion, and reduced release of PGI2 from the intestine.
METHODS
Sprague-Dawley rats received either vinblastine (VIN) to deplete circulating neutrophils or normal saline (NS). These animals then underwent either hemorrhage and resuscitation (SK + R) or sham operation (SHAM). Superior mesenteric artery flow and splanchnic 6-keto PGF1a (metabolite of PGI2) release were measured.
RESULTS
Superior mesenteric artery blood flow was significantly greater in VIN-treated animals sustaining SK + R than in those treated with NS (p < 0.05). Neutrophil depletion preserved 6-keto PGF1a release after SK + R, whereas 6-keto PGF1a release in the NS-treated, SK + R group was significantly reduced (p < 0.05).
CONCLUSION
These data are compatible with the hypothesis that neutrophils may influence splanchnic perfusion after SK + R by inhibiting splanchnic PGI2 release.
目的
本研究检验了这样一个假设，即中性粒细胞在出血复苏过程中通过抑制肠道代偿性血管舒张剂前列环素（PGI2）的释放来损害内脏血流。
总结背景数据
失血性休克复苏与中性粒细胞浸润到肠道、内脏灌注减少以及肠道PGI2释放减少有关。
方法
将Sprague-Dawley大鼠分为两组，一组接受长春碱（VIN）以消耗循环中的中性粒细胞，另一组接受生理盐水（NS）。然后这些动物分别接受出血和复苏（SK + R）或假手术（SHAM）。测量肠系膜上动脉血流和内脏6-酮-前列腺素F1α（PGI2的代谢产物）的释放。
结果
接受VIN治疗且经历SK + R的动物的肠系膜上动脉血流显著高于接受NS治疗的动物（p < 0.05）。中性粒细胞耗竭使SK + R后6-酮-前列腺素F1α的释放得以保留，而接受NS治疗的SK + R组中6-酮-前列腺素F1α的释放显著减少（p < 0.05）。
结论
这些数据与以下假设相符，即中性粒细胞可能通过抑制内脏PGI2释放来影响SK + R后的内脏灌注。
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