Park W S, Chang Y S, Ko S Y, Kang M J, Han J M, Lee M
Department of Pediatrics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Neurol Res. 1999 Jun;21(4):391-8. doi: 10.1080/01616412.1999.11740949.
This study was carried out to elucidate the pathophysiologic mechanism of cerebral hyperemia observed during the early phase of bacterial meningitis. We tested the hypothesis that microbial invasion through the blood-brain barrier is responsible for cerebral vasodilation and hyperemia in meningitis. Escherichia coli was given either intravenously (i.v.) or intracisternally (i.c.) to closely mimic the primary or secondary bacterial invasion occurring in meningitis and newborn piglets were grouped according to their invasion results (+ or -); 12 in the i.v. (+) group, 14 in the i.v. (-) group, 13 in the i.c. (+) group, 15 in the i.c. (-) group. The results were compared with eight animals in the control group. Near infrared spectroscopy (NIRS) was employed to monitor changes in total hemoglobin (HbT), oxygenated hemoglobin (HbO), deoxygenated hemoglobin (Hb), deduced hemoglobin (HbD), and oxidized cytochrome aa3 (Cyt aa3). HbT, as an index of cerebral blood volume, increased progressively in both i.v. (+) and i.v. (-) groups and became significantly different from control and baseline values at 2 h. Hb significantly increased only in i.v. (+) group. HbD, as an index of cerebral blood flow, decreased significantly in i.v. (+), i.v.(-) and i.c. (-) groups and this change was mitigated in i.c. (+) group, HbO was reduced in i.c. (-) group and this decrease was attenuated in i.c. (+) group. Increased Cyt aa3 was observed in all experimental groups after bacterial inoculation. Changes in ICP, blood pressure, cerebral perfusion pressure, blood or CSF glucose or lactate, CSF TNF-alpha level, or CSF leukocytes number were not associated with changes in NIRS findings. These findings suggest that primary or secondary bacterial invasion across the blood-brain barrier is primarily responsible for cerebral vasodilation and hyperemia observed during the early phase of bacterial meningitis.
本研究旨在阐明细菌性脑膜炎早期出现的脑充血的病理生理机制。我们检验了以下假设:通过血脑屏障的微生物入侵是脑膜炎时脑血管扩张和充血的原因。将大肠杆菌经静脉内(i.v.)或脑池内(i.c.)给予,以密切模拟脑膜炎中发生的原发性或继发性细菌入侵,并根据新生仔猪的入侵结果(+或-)进行分组;静脉内(+)组12只,静脉内(-)组14只,脑池内(+)组13只,脑池内(-)组15只。将结果与对照组的8只动物进行比较。采用近红外光谱(NIRS)监测总血红蛋白(HbT)、氧合血红蛋白(HbO)、脱氧血红蛋白(Hb)、衍生血红蛋白(HbD)和氧化细胞色素aa3(Cyt aa3)的变化。HbT作为脑血容量的指标,在静脉内(+)组和静脉内(-)组中均逐渐增加,并在2小时时与对照组和基线值有显著差异。仅静脉内(+)组的Hb显著增加。HbD作为脑血流量的指标,在静脉内(+)组、静脉内(-)组和脑池内(-)组中显著降低,而在脑池内(+)组中这种变化有所减轻,脑池内(-)组的HbO降低,而在脑池内(+)组中这种降低有所减弱。在细菌接种后,所有实验组均观察到Cyt aa3增加。颅内压、血压、脑灌注压、血液或脑脊液葡萄糖或乳酸、脑脊液肿瘤坏死因子-α水平或脑脊液白细胞数量的变化与NIRS结果的变化无关。这些发现表明,穿过血脑屏障的原发性或继发性细菌入侵是细菌性脑膜炎早期观察到的脑血管扩张和充血的主要原因。