Kuroiwa T, Bonnekoh P, Hossmann K A
Max-Planck-Institute for Neurological Research, Department for Experimental Neurology, Cologne, F.R.G.
J Neurol Sci. 1990 Jul;97(2-3):251-9. doi: 10.1016/0022-510x(90)90223-a.
The threshold of carotid artery back pressure for the development of neuronal injury in the hippocampus was determined in gerbils following bilateral carotid artery occlusion of 5 or 10 min. Arterial back pressure was measured during ischemia at the left carotid bifurcation distal to the vascular occlusion, and neuronal injury evaluated one week after ischemia by counting the number of surviving neurons in the left hippocampal CA1 sector. With an arterial back pressure below 5 mm Hg, the mean density of surviving neurons decreased from 199 +/- 16/mm (mean +/- SD) to less than 21/mm both after 5 and 10 min ischemia (P less than 0.05). With a back pressure of between 5 and 15 mm Hg, neuronal density was 117 +/- 77/mm (not significantly different from control) after 5 min, and 24 +/- 18/mm (P less than 0.05) after 10 min ischemia. Above 15 mm Hg neither 5 nor 10 min ischemia produced significant neuronal damage. Thus, at threshold arterial back pressure, induction of neuronal injury in the hippocampus depends on the duration of ischemia, indicating progressive impairment of microcirculation with longer periods of ischemia.
在沙土鼠双侧颈动脉闭塞5或10分钟后，测定海马神经元损伤发生时的颈动脉背压阈值。在缺血期间，于血管闭塞远端的左颈动脉分叉处测量动脉背压，并在缺血一周后通过计数左海马CA1区存活神经元的数量评估神经元损伤情况。当动脉背压低于5 mmHg时，5分钟和10分钟缺血后存活神经元的平均密度均从199±16/mm（平均值±标准差）降至低于21/mm（P<0.05）。当背压在5至15 mmHg之间时，5分钟缺血后神经元密度为117±77/mm（与对照组无显著差异），10分钟缺血后为24±18/mm（P<0.05）。高于15 mmHg时，5分钟和10分钟缺血均未产生明显的神经元损伤。因此，在阈值动脉背压下，海马神经元损伤的诱导取决于缺血持续时间，表明随着缺血时间延长，微循环逐渐受损。
