Splanchnic PGI2 release and "no reflow" following intestinal reperfusion.
Splanchnic PGI2 release and "no reflow" following intestinal reperfusion.
复制标题
肠道再灌注后内脏 PGI2 释放且“无回流”。
DOI：
10.1006/jsre.1995.1088
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Myers,SI
中科院分区：
文献类型：
--
作者：
Turnage,RH;Kadesky,KM;Bartula,L;Guice,KS;Oldham,KT;Myers,SI
本研究探讨了肠再灌注（IR）期间内脏血流量减少与血管舒张性前列腺素PGI 2释放受损相关的假设。Sprague-Dawley大鼠肠系膜上级动脉（SMA）闭塞120分钟，再灌注60分钟。SMA血流通过跨音速血流探针和放射性标记微球（141 Ce和103 Ru）测量。假手术动物作为对照（SHAM）。通过测定IR和SHAM动物门静脉（PV）和下腔静脉（IVC）内血栓素B2（TxB 2，TxA 2的稳定代谢物）、6-酮-PGF 1a（6-keto，PCI 2的稳定代谢物）和PGE 2定量内脏类花生酸释放。跨音速血流探针测量IR动物的SMA血流<基线的10%和SHAM的27%（IR和SHAM分别为8 ± 2%和29 ± 3%，P < 0.05）。微球组肠血流量为（0.33 ± 0.12）ml/min/g，IR组为（1.34 ± 0.13）ml/min/g，SHAM组为（1.34 ± 0.13）ml/min/g（P < 0.05）。IR诱导的内脏类花生酸释放的最大变化发生在6-酮。缺血后，PV中6-酮水平是SHAM的2倍（P < 0.05）。再灌注后5分钟，PV 6-keto水平是对照组的22倍（P < 0.05），是IVC的4倍（P < 0.05）。再灌注60分钟时，6-酮的水平降低到IVC中的水平。这些数据支持这一假设，即内脏血流量严重减少严重IR。此外，虽然内脏PGI 2释放增加，其释放既不持续，也不足以补偿与这种损伤模型相关的血流量减少。
This study examines the hypothesis that reduced splanchnic blood flow during intestinal reperfusion (IR) is associated with impaired release of the vasodilatory prostanoid PGI2. Sprague-Dawley rats underwent occlusion of the superior mesenteric artery (SMA) for 120 min and reperfusion for up to 60 min. SMA blood flow was measured by transonic flow probe and radiolabeled microspheres (141Ce and103Ru). Sham-operated animals served as controls (SHAM). Splanchnic eicosanoid release was quantitated by measuring thromboxane B2(TxB2, stable metabolite of TxA2), 6-keto-PGF1a(6-keto, stable metabolite of PCI2), and PGE2within the portal vein (PV) and inferior vena cava (IVC) of animals sustaining IR and SHAM. SMA flow in IR animals was <10% of baseline and 27% of SHAM when measured by transonic flow probe (8 ± 2% and 29 ± 3%, IR and SHAM, respectively, P < 0.05). Similar results were obtained when intestinal blood flow was measured with microspheres (0.33 ± 0.12 vs 1.34 ± 0.13 ml/min/g, IR vs SHAM, P < 0.05). The greatest change in IR-induced splanchnic eicosanoid release occurred with 6-keto. Following ischemia, 6-keto levels in the PV were twice those of SHAM (P < 0.05). Five minutes after reperfusion, PV 6-keto levels were 22 times those of controls (P < 0.05) and 4 times greater than those of the IVC (P < 0.05). By 60 min of reperfusion, levels of 6-keto were reduced to those in the IVC. These data support the hypothesis that splanchnic blood flow is critically reduced by severe IR. Furthermore, although splanchnic PGI2release is increased, its release is neither sustained nor adequate to compensate for the reduced blood flow associated with this injury model.