Moser Miriam, Schwarz Yannik, Herta Johannes, Plöchl Walter, Reinprecht Andrea, Zeitlinger Markus, Brugger Jonas, Ramazanova Dariga, Rössler Karl, Hosmann Arthur
Departments of Neurosurgery.
Department of Anesthesia, General Intensive Care Medicine and Pain Management.
J Neurosurg Anesthesiol. 2024 Oct 1;36(4):317-325. doi: 10.1097/ANA.0000000000000928. Epub 2023 Jul 27.
Nimodipine is routinely administered to aneurysmal subarachnoid hemorrhage patients to improve functional outcomes. Nimodipine can induce marked systemic hypotension, which might impair cerebral perfusion and brain metabolism.
Twenty-seven aneurysmal subarachnoid hemorrhage patients having multimodality neuromonitoring and oral nimodipine treatment as standard of care were included in this retrospective study. Alterations in mean arterial blood pressure (MAP), cerebral perfusion pressure (CPP), brain tissue oxygen tension (pbtO 2 ), and brain metabolism (cerebral microdialysis), were investigated up to 120 minutes after oral administration of nimodipine (60 mg or 30 mg), using mixed linear models.
Three thousand four hundred twenty-five oral nimodipine administrations were investigated (126±59 administrations/patient). After 60 mg of oral nimodipine, there was an immediate statistically significant (but clinically irrelevant) drop in MAP (relative change, 0.97; P <0.001) and CPP (relative change: 0.97; P <0.001) compared with baseline, which lasted for the whole 120 minutes observation period ( P <0.001). Subsequently, pbtO 2 significantly decreased 50 minutes after administration ( P =0.04) for the rest of the observation period; the maximum decrease was -0.6 mmHg after 100 minutes ( P <0.001). None of the investigated cerebral metabolites (glucose, lactate, pyruvate, lactate/pyruvate ratio, glutamate, glycerol) changed after 60 mg nimodipine. Compared with 60 mg nimodipine, 30 mg induced a lower reduction in MAP (relative change, 1.01; P =0.02) and CPP (relative change, 1.01; P =0.03) but had similar effects on pbtO 2 and cerebral metabolism ( P >0.05).
Oral nimodipine reduced MAP, which translated into a reduction in cerebral perfusion and oxygenation. However, these changes are unlikely to be clinically relevant, as the absolute changes were minimal and did not impact cerebral metabolism.
尼莫地平通常用于动脉瘤性蛛网膜下腔出血患者，以改善功能预后。尼莫地平可引起显著的全身性低血压，这可能会损害脑灌注和脑代谢。
本回顾性研究纳入了27例接受多模态神经监测并以口服尼莫地平治疗作为标准治疗的动脉瘤性蛛网膜下腔出血患者。使用混合线性模型，在口服尼莫地平（60毫克或30毫克）后长达120分钟内，研究平均动脉压（MAP）、脑灌注压（CPP）、脑组织氧分压（pbtO₂）和脑代谢（脑微透析）的变化。
共研究了3425次口服尼莫地平给药情况（每位患者126±59次给药）。口服60毫克尼莫地平后，与基线相比，MAP（相对变化，0.97；P<0.001）和CPP（相对变化：0.97；P<0.001）立即出现具有统计学意义（但临床意义不大）的下降，且在整个120分钟观察期内持续存在（P<0.001）。随后，给药50分钟后pbtO₂在观察期剩余时间内显著下降（P=0.04）；100分钟后最大下降幅度为-0.6毫米汞柱（P<0.001）。60毫克尼莫地平给药后，所研究的脑代谢物（葡萄糖、乳酸、丙酮酸、乳酸/丙酮酸比值、谷氨酸、甘油）均未发生变化。与60毫克尼莫地平相比，30毫克引起的MAP（相对变化，1.01；P=0.02）和CPP（相对变化，1.01；P=0.03）下降幅度较小，但对pbtO₂和脑代谢的影响相似（P>0.05）。
口服尼莫地平降低了MAP，这导致脑灌注和氧合减少。然而，这些变化在临床上可能并不相关，因为绝对变化很小且未影响脑代谢。
