Hypotension following acute hypovolaemia depends on the caudal midline medulla
Hypotension following acute hypovolaemia depends on the caudal midline medulla
复制标题
急性低血容量后的低血压取决于尾部中线延髓
DOI：
10.1097/00001756-199806010-00032
复制
发表时间：
1998
期刊：
影响因子：
1.7
通讯作者：
R. Bandler
中科院分区：
文献类型：
--
作者：
L. Henderson;K. Keay;R. Bandler
急性低血容量症可引起突然的、危及生命的低血压和心动过缓。低血压也可以通过尾侧中线延髓（CMM）的兴奋引起。本研究探讨了CMM降压区对急性低血容量引起的低血压的可能作用。灭活的CMM，无论是木质素或氯化钴没有改变静息动脉压。然而，木质素注射液阻止了动脉压的下降，氯化钴注射液延迟了发作，并显着减弱了低血容量诱发的低血压的大小。这些研究结果表明，CMM是失血后触发低血压的关键区域，并且介导心血管对急性低血容量症等挑战的反应的大脑区域与调节静息动脉压的区域不同。
ACUTE hypovolaemia evokes abrupt, life-threatening hypotension and bradycardia. Hypotension can be evoked also by excitation of the caudal midline medulla (CMM). This study investigated the possible contribution of the CMM depressor area to hypotension evoked by acute hypovolaemia. Inactivation of the CMM, with either lignocaine or cobalt chloride did not alter resting arterial pressure. However lignocaine injections blocked the fall in arterial pressure, and cobalt chloride injections delayed the onset and significantly attenuated the size of hypovolaemic-evoked hypotension. These findings suggest that the CMM is a key region triggering hypo-tension after blood loss, and that the brain areas mediating cardiovascular response to challenges such as acute hypovolaemia are not the same areas that regulate resting arterial pressure.