LY171883 preserves mesenteric perfusion in porcine endotoxic shock.
LY171883 preserves mesenteric perfusion in porcine endotoxic shock.
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LY171883 在猪内毒素休克中保留肠系膜灌注。
DOI：
10.1016/0022-4804(90)90108-e
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Baum,T
中科院分区：
文献类型：
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作者：
Cohn,SM;Fink,MP;Lee,PC;Wang,H;Rothschild,HR;Deniz,YF;Baum,T
复苏后的正常内毒素猪的上级肠系膜动脉灌注（Q今）减少，肠粘膜内氢离子浓度[H+]增加。本研究验证了用特异性白三烯（LT）D4/E4受体拮抗剂LY 171883预处理可预防这些不良现象的假设。对戊巴比妥麻醉的猪（14-18 kg）进行仪器化，以允许测量Q tom（超声流量探头）和[H+]（眼压计）。根据动脉血和上级肠系膜静脉血的O2含量计算肠系膜O2输送量（O 2）和消耗量（V O 2）。在t=-20 min时，用LY 171883（10 mg/kg）或溶媒预处理各组（N= 6）猪。在t= 0 min时，在20 min内向猪输注脂多糖（LPS; 150 μg/kg），并用盐水（1.2 ml/kg min）复苏2 h。无论治疗组，平均动脉压和全身血管阻力指数在LPS输注后均显著降低。总体而言，心脏指数（CI）保持良好，但在t= 20、100和120 min时，对照组CI相对于t= 0 min值显著降低。LY 171883组的肠系膜Q值和O2值均保持正常，而对照组的这些参数均显著降低。对照组肠系膜V_（O2）一过性升高，但有显著性，LT受体拮抗剂可消除此现象。在对照组中，粘膜内[H+]增加了近三倍; LY 171883显著改善了这种不良反应。这些数据表明，在这种猪内毒素休克模型中，LT可能介导肠系膜Q值降低和粘膜内[H+]升高。
Superior mesenteric arterial perfusion (Q ̇) decreases and gut intramucosal hydrogen ion concentration,[H+], increases in resuscitated normodynamic endotoxic pigs. The present study tested the hypothesis that these adverse phenomena can be prevented by pretreatment with LY171883, a specific leukotriene (LT) D 4/E 4 receptor antagonist. Pentobarbital-anesthetized pigs (14–18 kg) were instrumented to permit measurement of Q ̇ (ultrasonic flow probe) and [H+](tonometer). Mesenteric O 2 delivery (ḊO 2) and consumption (V̇O 2) were calculated from the O 2 contents of arterial and superior mesenteric venous blood. At t=− 20 min, groups (N= 6) of pigs were pretreated with LY171883 (10 mg/kg) or vehicle. At t= 0 min, the pigs were infused over 20 min with lipopolysaccharide (LPS; 150 μg/kg) and resuscitated for 2 hr with saline (1.2 ml/kg min). Irrespective of treatment group, mean arterial pressure and systemic vascular resistance index decreased significantly after infusion of LPS. In general, cardiac index (CI) was well preserved, although in controls at t= 20, 100, and 120 min, CI decreased significantly with respect to the t= 0 min value. Normal mesenteric Q ̇ and ḊO 2 were maintained in the LY171883 group, whereas, in controls, these parameters decreased significantly. Mesenteric V̇O 2 increased transiently but significantly in controls; this phenomenon was abrograted by the LT receptor antagonist. In controls, intramucosal [H+] increased by almost threefold; this adverse effect was significantly ameliorated by LY171883. These data suggest that decreased mesenteric Q ̇ and increased intramucosal [H+] may be mediated by LT in this porcine endotoxic shock model.