Zochodne D W, Ho L T
Department of Medicine, Queen's University, Kingston, Ont., Canada.
Brain Res. 1990 Dec 3;535(1):43-8. doi: 10.1016/0006-8993(90)91822-x.
In severe peripheral nerve ischemia in the rat, serial nerve blood flow (NBF) measurements have identified evidence of 'no reflow', a mechanism of continued fiber damage during reperfusion. It has been postulated that 'no reflow' also occurs in nerve compression due to direct mechanical or ischemic (if compression is prolonged) injury of microvessels, resulting in continuing nerve fiber damage. To address this question, we measured endoneurial blood flow (NBF), oxygen tension and pH at the site of an acute nerve crush injury. In further sets of experiments, NBF and endoneurial oxygen tension were examined before and after prolonged epochs of crush. NBF and MR (microvascular resistance) were not appreciably different than values obtained in control animals without intervening brief nerve crush. NBF was slightly higher and MR slightly lower 2 h after injury, but the difference was not statistically significant. No evidence of significant endoneurial hypoxia or acidosis was observed. Similarly, after more prolonged crush there was no significant oligemia or hypoxia. The studies provide no evidence that 'no reflow' occurs in crush injury even if the injury is maintained for a period of time known to induce 'no reflow' with severe ischemia. We suggest that nerve damage in crush, and possibly compression, more likely arises from direct mechanical injury of fibers.
在大鼠严重的周围神经缺血模型中，通过连续测量神经血流量（NBF）发现了“无复流”现象，这是一种在再灌注期间导致纤维持续损伤的机制。据推测，在神经受压时，由于微血管受到直接机械性损伤或缺血性损伤（如果压迫时间延长），“无复流”现象也会发生，进而导致神经纤维持续损伤。为了解决这个问题，我们测量了急性神经挤压伤部位的神经内膜血流量（NBF）、氧分压和pH值。在进一步的实验中，我们检测了长时间挤压前后的NBF和神经内膜氧分压。与未经过短暂神经挤压的对照动物相比，NBF和微血管阻力（MR）没有明显差异。损伤后2小时，NBF略高，MR略低，但差异无统计学意义。未观察到明显的神经内膜缺氧或酸中毒迹象。同样，在更长时间的挤压后，也没有明显的血液减少或缺氧现象。这些研究没有提供证据表明即使挤压损伤持续一段时间（已知该时间会在严重缺血时诱导“无复流”），挤压伤中也会出现“无复流”现象。我们认为，挤压伤以及可能的压迫伤导致的神经损伤更可能是由纤维的直接机械损伤引起的。
