Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic.
Physiol Res. 2011;60(6):975-9. doi: 10.33549/physiolres.932281.
Neurogenic pulmonary edema (NPE), which is induced by acute spinal cord compression (SCC) under the mild (1.5 %) isoflurane anesthesia, is highly dependent on baroreflex-mediated bradycardia because a deeper (3 %) isoflurane anesthesia or atropine pretreatment completely abolished bradycardia occurrence and NPE development in rats subjected to SCC. The aim of the present study was to evaluate whether hypertension-associated impairment of baroreflex sensitivity might exert some protection against NPE development in hypertensive animals. We therefore studied SCC-induced NPE development in two forms of experimental hypertension - spontaneously hypertensive rats (SHR) and salt hypertensive Dahl rats, which were reported to have reduced baroreflex sensitivity. SCC elicited NPE in both hypertensive models irrespective of their baroreflex sensitivity. It is evident that a moderate impairment of baroreflex sensitivity, which was demonstrated in salt hypertensive Dahl rats, does not exert sufficient protective effects against NPE development.
神经源性肺水肿（NPE）是由轻度（1.5%）异氟醚麻醉下的急性脊髓压迫（SCC）引起的，它高度依赖于压力反射介导的心动过缓，因为更深的（3%）异氟醚麻醉或阿托品预处理完全消除了 SCC 大鼠的心动过缓和 NPE 发展。本研究的目的是评估高血压相关的压力反射敏感性损害是否会对高血压动物的 NPE 发展产生一些保护作用。因此，我们研究了两种实验性高血压 - 自发性高血压大鼠（SHR）和盐性高血压 Dahl 大鼠中 SCC 诱导的 NPE 发展，据报道这两种高血压动物的压力反射敏感性降低。SCC 在这两种高血压模型中均引起了 NPE，而与它们的压力反射敏感性无关。显然，盐性高血压 Dahl 大鼠中表现出的中等程度的压力反射敏感性损害不能对 NPE 的发展产生足够的保护作用。
