Pre-arrest baseline measurements.

Recent studies suggested intrathecal vasodilator administration as a therapy to mitigate post-ischemic cerebral hypoperfusion following cardiac arrest. We examined the effects of two commonly used intrathecal vasodilators, sodium nitroprusside (SNP) and nicardipine, on cerebral pial microcirculation, cortical tissue oxygen tension (PctO2), and electrocortical activity in the early post-resuscitation period using a porcine model of cardiac arrest. Thirty pigs were resuscitated after 14 min of untreated cardiac arrest. At 30 min after resuscitation from cardiac arrest, 30 pigs randomly received 4 mg of SNP, 4 mg of nicardipine, or saline placebo via subdural intracranial catheters and were observed for 5 h. Group effect and group-time interaction were assessed using linear mixed-effects models. The mean arterial pressure was lower in the nicardipine group (coefficient [95% confidence interval {CI}], -15.824 [-24.082 to -7.566]) and higher in the SNP group (coefficient [95%CI], 11.232 [2.974–19.490]) compared to the saline group. The percentage of pial arteriole diameter relative to the pre-arrest baseline value (coefficient [95% CI], 48.970 [13.884–84.057]), microvascular flow index (coefficient [95% CI], 0.296 [0.071–0.521]), and PctO2 (coefficient [95% CI], 26.926 [12.404–41.449]) were higher in the SNP group but not in the nicardipine group compared to the saline group. Amplitude-integrated electroencephalography amplitude recovery was faster in the SNP group (coefficient [95% CI], 1.149 [0.468–1.829]) but not in the nicardipine group compared to the saline group. In conclusion, intrathecal SNP but not nicardipine was effective in treating post-ischemic cerebral hypoperfusion after cardiac arrest.近期研究表明，鞘内血管扩张剂（intrathecal vasodilator）给药可作为治疗心搏骤停（cardiac arrest）后缺血性脑低灌注（post-ischemic cerebral hypoperfusion）的手段。本研究采用心搏骤停猪模型（porcine model of cardiac arrest），探究两种常用鞘内血管扩张剂——硝普钠（sodium nitroprusside, SNP）与尼卡地平（nicardipine）——对复苏早期软脑膜微循环（cerebral pial microcirculation）、皮层组织氧分压（cortical tissue oxygen tension, PctO2）及脑电活动（electrocortical activity）的影响。30头家猪经14分钟未干预的心搏骤停后接受复苏。在心搏骤停复苏后30分钟时，30头实验动物通过硬膜下颅内导管随机接受4mg硝普钠、4mg尼卡地平或生理盐水安慰剂，并被连续观察5小时。研究采用线性混合效应模型（linear mixed-effects models）评估组间效应及组-时间交互作用。与生理盐水对照组相比，尼卡地平组平均动脉压（mean arterial pressure）更低（系数[95%置信区间{CI}]：-15.824 [-24.082至-7.566]），而硝普钠组平均动脉压更高（系数[95%CI]：11.232 [2.974–19.490]）。与生理盐水对照组相比，硝普钠组软脑膜小动脉直径相较于心搏骤停前基线值的百分比（系数[95%置信区间{CI}]：48.970 [13.884–84.057]）、微血管血流指数（系数[95%置信区间{CI}]：0.296 [0.071–0.521]）及皮层组织氧分压（系数[95%置信区间{CI}]：26.926 [12.404–41.449]）均显著升高，而尼卡地平组未出现此类变化。与生理盐水对照组相比，硝普钠组的振幅整合脑电图（amplitude-integrated electroencephalography）振幅恢复速度更快（系数[95%置信区间{CI}]：1.149 [0.468–1.829]），而尼卡地平组未观察到该改善。综上，鞘内给予硝普钠而非尼卡地平，可有效改善心搏骤停后的缺血性脑低灌注。