Dean Caron
Department of Anesthesiology/151, Medical College of Wisconsin and the Zablocki Department of Veterans Affairs Medical Center, Milwaukee, WI 53295, USA.
Neurosci Lett. 2004 Jan 2;354(1):79-83. doi: 10.1016/j.neulet.2003.09.054.
In response to hemorrhage in the anesthetized rat, an initial renal sympathoexcitation is followed by profound sympathoinhibition and hypotension with increasing blood loss. Microinjection of the gamma-aminobutyric acid(A) agonist muscimol to block neurotransmission through the sympathoinhibitory region of the ventrolateral periaqueductal gray matter (vlPAG) did not alter resting sympathetic nerve activity or blood pressure. However, the response to hemorrhage was converted to a maintained renal sympathoexcitation with a delayed and attenuated accompanying hypotension. These data indicate that neurons in the vlPAG mediate the sympathetic and cardiovascular responses to severe hemorrhage.
在麻醉大鼠中，对出血的反应是，最初出现肾交感神经兴奋，随后随着失血量增加，出现深度交感神经抑制和低血压。向腹外侧导水管周围灰质（vlPAG）的交感抑制区域微量注射γ-氨基丁酸（A）激动剂蝇蕈醇以阻断神经传递，并未改变静息交感神经活动或血压。然而，对出血的反应转变为持续的肾交感神经兴奋，并伴有延迟和减弱的低血压。这些数据表明，vlPAG中的神经元介导了对严重出血的交感神经和心血管反应。
