Atochin Dmitriy N, Chernysheva Galina A, Aliev Oleg I, Smolyakova Vera I, Osipenko Anton N, Logvinov Sergey V, Zhdankina Anna A, Plotnikova Tatiana M, Plotnikov Mark B
Cardiology Division, Department of Medicine, Cardiovascular Research Center, Harvard Medical School, Massachusetts General Hospital, 149 East, 13th street, 4th floor, Charlestown, MA 02129, USA.
Department of Pharmacology, Goldberg Research Institute of Pharmacology and Regenerative Medicine, Tomsk NRMC, 3 Lenin pr-t, 634028 Tomsk, Russia.
Brain Res Bull. 2017 Jun;132:213-221. doi: 10.1016/j.brainresbull.2017.06.005. Epub 2017 Jun 8.
We developed an improved three-vessel occlusion model of global cerebral ischemia in rats. This method consists in cessation of cerebral blood flow by accessing a. carotis communis sinistra through the ventral surface of the neck as well as tr. brachiocephalicus and a. subclavia sinistra through the first intercostal space, bypassing the pleural cavity and excluding pneumothorax. After the occlusion of the vessels that resulted in interruption of their blood flow, according to laser-Doppler flowmetry, there was a sharp decline in local cerebral blood flow in the visual cortex to 4±1% of the initial level. After restoring the level of local cerebral blood flow at the 5th minute, 10th minute, 20th minute and 24th hour of reperfusion, the levels of local cerebral blood flow were 51±7%, 41±5%, 35±8% and 54±9% of the initial level, respectively. Histo-quantitative analysis of changes in neurons of the hippocampus of rats showed that after ischemic injury, the numerical density of neurons in hippocampal zone CA1 in the observed 1mm region decreased by 29%, 22%, and 35%, respectively, compared to sham-operated animals (p<0.05). By the first day after global cerebral ischemia, the experimental group had shown a mean neurological deficit score equal to 7.5±1.0 and 7.9±0.7 points, followed by a decrease up to score 6.5±1.1 and 5.9±0.7 on the third day, 4.6±0.8 and 4.7±0.5 on the fifth day (on chloral hydrate and propofol anesthesia correspondently).
我们开发了一种改良的大鼠全脑缺血三血管闭塞模型。该方法包括通过颈部腹侧进入左颈总动脉以及通过第一肋间间隙进入头臂干和左锁骨下动脉来停止脑血流,绕过胸膜腔并排除气胸。在闭塞导致血流中断的血管后,根据激光多普勒血流仪检测,视皮层局部脑血流急剧下降至初始水平的4±1%。在再灌注的第5分钟、第10分钟、第20分钟和第24小时恢复局部脑血流水平后,局部脑血流水平分别为初始水平的51±7%、41±5%、35±8%和54±9%。对大鼠海马神经元变化的组织定量分析表明,与假手术动物相比,缺血损伤后,在观察的1mm区域内海马CA1区神经元的数值密度分别下降了29%、22%和35%(p<0.05)。在全脑缺血后的第一天,实验组的平均神经功能缺损评分分别为7.5±1.0和7.9±0.7分,随后在第三天降至6.5±1.1和5.9±0.7分,在第五天降至4.6±0.8和4.7±0.5分(分别对应水合氯醛和丙泊酚麻醉)。