Maeda M, Nakai M, Krieger A J, Sapru H N
Department of Systems Physiology, University of Occupational and Environmental Health, Kitakyushu, Japan.
Acta Neurochir Suppl (Wien). 1994;60:171-3. doi: 10.1007/978-3-7091-9334-1_46.
Acute brain swelling is well known to be acute vasodilatation of cerebral vessels and sometimes results from brain injury. One of the causes of acute brain swelling may be disturbance of central control mechanisms of cerebral vessels. However, the presence of acute spinal cord swelling is little noticed. We present here a possibility that acute spinal cord swelling may be occur following the dysfunction of the cardiovascular center of the medulla. In urethane-anesthetized, paralyzed and artificially ventilated rats, the neurons in the rostral ventrolateral pressor area (VLPA), origin of the sympathetic nerve activities in the brain stem, were chemically stimulated by microinjection of L-glutamate and the spinal cord blood flow (SCBF) was determined using labeled microspheres. The SCBFs of cervical, thoracic, and lumbar cord decreased significantly from 27 +/- 3 (mean +/- S.E.M.) to 20 +/- 2 (p < 0.01), from 22 +/- 1 to 17 +/- 2 (p < 0.05), and from 41 +/- 5 to 26 +/- 3 (p < 0.05) ml.min-1.(100 g)-1, respectively (n = 12). The spinal cord vascular resistances (SCVRs) of cervical, thoracic, and lumbar cord increased significantly from 3.7 +/- 0.4 to 5.0 +/- 0.6 (p < 0.05), from 4.2 +/- 0.2 to 5.9 +/- 0.7 (p < 0.05), and from 2.5 +/- 0.2 to 3.8 +/- 0.4 (p < 0.05) mmHg per [ml.min-1.(100 g)-1], respectively (n = 12). These results suggest that the neurons within the VLPA may play a role in the control of spinal cord circulation. There is a possibility that the dysfunction of the VLPA may cause acute spinal cord swelling.
急性脑肿胀是众所周知的脑血管急性扩张，有时由脑损伤引起。急性脑肿胀的原因之一可能是脑血管中枢控制机制紊乱。然而，急性脊髓肿胀的存在却很少受到关注。我们在此提出一种可能性，即急性脊髓肿胀可能在延髓心血管中枢功能障碍后发生。在氨基甲酸乙酯麻醉、麻痹并人工通气的大鼠中，通过微量注射L - 谷氨酸化学刺激延髓头端腹外侧升压区（VLPA）中的神经元，该区域是脑干交感神经活动的起源，并使用标记微球测定脊髓血流量（SCBF）。颈髓、胸髓和腰髓的SCBF分别从27±3（均值±标准误）显著降至20±2（p < 0.01）、从22±1降至17±2（p < 0.05）和从41±5降至26±3（p < 0.05）ml·min⁻¹·(100 g)⁻¹（n = 12）。颈髓、胸髓和腰髓的脊髓血管阻力（SCVR）分别从3.7±0.4显著增加至5.0±0.6（p < 0.05）、从4.2±0.2增加至5.9±0.7（p < 0.05）和从2.5±0.2增加至3.8±0.4（p < 0.05）mmHg/[ml·min⁻¹·(100 g)⁻¹]（n = 12）。这些结果表明，VLPA内的神经元可能在脊髓循环控制中发挥作用。VLPA功能障碍有可能导致急性脊髓肿胀。
