Independency of myocardial stunning of endothelial stunning?
Independency of myocardial stunning of endothelial stunning?
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DOI：
10.1007/s00395-007-0657-0
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发表时间：
2007-07-01
影响因子：
9.5
通讯作者：
Schipke, Jochen D.
中科院分区：
文献类型：
--
作者：
Garcia, Solange C.;Pomblum, Valdeci;Schipke, Jochen D.
背景与目的血管内皮细胞在调节血管张力中起着重要作用。冠状动脉内皮细胞功能障碍的原因是复杂的，可能涉及到缺血/再灌注损伤。我们调查了血管内皮细胞、平滑肌和心肌功能障碍是否是独立现象。方法在不间断缺血的情况下，快速切取兔心脏，连接到改良的朗宁多夫装置上，用含有牛红细胞的改良Krebs-Henseleit液灌流。常氧对照心脏(n=16)灌流125min。缺血后心脏(n=15)灌流45min，全心缺血20min，再灌流60min。将常氧和缺血后的心脏分为三组，分别给予0.9%氯化钠(安慰剂)、3-吗啉磺胺(SIN-1；100mM)或P物质(SP；5 NM)。结果SIN-1作用后，常氧心脏的CBF最大增加63%，SP作用后最大增加62%。再灌流60min后，两组缺血后心脏均恢复至95%LVEPmax。在缺血后的心脏，SIN-1仍使CBF增加58%，而内皮依赖性血管运动受损：SP仅使CBF增加9%。总结与结论特殊的治疗方案允许区分心肌顿抑和血管顿抑。结果表明，虽然心肌功能已经恢复，但内皮细胞的损伤比平滑肌细胞更严重，而且这种损伤持续到心肌顿抑之外。因此，当心功能障碍已经解决时，内皮依赖性功能障碍仍然会损害血管的扩张。
Background and objective Vascular endothelial cells play an important role in the control of vascular tone. The reasons for coronary endothelial dysfunction are complex and may involve ischemia/reperfusion injury. We investigated whether endothelial, smooth muscle, and myocardial dysfunction are independent phenomena. Methods Rabbit hearts were rapidly excised without intermittent ischemia, connected to a modified Langendorff apparatus, and perfused with a modified Krebs-Henseleit solution containing bovine erythrocytes. Normoxic control hearts (n = 16) were perfused for 125 min. Postischemic hearts (n = 15) were perfused for 45 min, submitted to global ischemia (20 min) and reperfused (60 min). Both the normoxic and the postischemic hearts were divided into three groups that received either 0.9% NaCl (placebo), or 3-morpholinosydnonimine (SIN-1; 100 mu M),or substance P (SP; 5 nM). Results After SIN-1, CBF in the normoxic hearts was increased by maximum 63% and after SP by 62%. 60 min after the onset of reperfusion, the postischemic hearts of both groups had recovered to 95% LVPmax. In the postischemic hearts, SIN-1 increased CBF still by 58%, while the endothelium-dependent vasomotion was impaired: SP improved CBF by only 9%. Summary and conclusions The particular protocol permitted differentiation between myocardial and vascular stunning. The results show that, while myocardial function has already recovered, endothelial cells are more severely impaired than smooth muscle cells, and that this injury persists beyond myocardial stunning. Thus, endothelial-dependent dysfunction can still impair vasodilatation while ventricular dysfunction has already resolved.