Relationship between sympathetic nervous activity and inflammatory response after subarachnoid hemorrhage in a perforating canine model.
The objective of the present study was to evaluate the correlation between sympathetic nerve activation and inflammatory response in the acute stage of subarachnoid hemorrhage (SAH) in a canine perforating model. SAH was induced by perforation of the basilar artery with the use of a microcatheter via the femoral artery in 20 mongrel dogs. Hemodynamic parameters and intracranial pressure were recorded, and blood sample for C3a, C5b-9, IL-6, IL-8 and noradrenaline kinetic determination were measured at 0, 5, 15, 30, 60, 120, and 180 min after SAH. Noradrenaline (pg/mL) increased abruptly from 104+/-59 to 2010+/-918 at 5 min after SAH. C3a and C5b-9 reached peak values at 15 min and IL-6 and IL-8 reached peak values at 30 min after SAH, respectively. The peak values of C3a and C5b-9 correlated positively with the peak value of noradrenaline (r=0.743 and r=0.753, respectively). The peak values of IL-6 and IL-8 also correlated positively with the peak values of noradrenaline (r=0.603 and r=0.681, respectively).These results suggest that a pronounced activation of the sympathetic nervous system and the inflammatory response occurs in acute stage of SAH. Significant association between the rate of spillover of norepinephrine to plasma and the plasma levels of inflammatory markers indicates that the two processes, sympathetic activation and immune response are quantitatively linked in early stage after SAH. The exact mechanisms underlying this phenomenon deserved further investigations.
Gao
Cheng
C
Department of Neurosurgery, The First Affiliated Hospital of Harbin Medical University, No.23, Youzheng Street, Nangang District, Harbin, Heilongjiang, 150001, China.
Liu
Xiangzhen
X
Shi
Huaizhang
H
Xu
Shancai
S
Ji
Zhiyong
Z
Wang
Chunlei
C
Wu
Pei
P
Liu
Zhen
Z
Zhao
Shiguang
S
D000818:Animals; D001488:Basilar Artery / Q000293:injuries / Q000473:pathology / Q000503:physiopathology; D015415:Biomarkers / Q000032:analysis / Q000378:metabolism; D002545:Brain Ischemia / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D002415:Cats; D003165:Complement System Proteins / Q000032:analysis / Q000378:metabolism; D004195:Disease Models, Animal; D004660:Encephalitis / Q000209:etiology / Q000503:physiopathology*; D005260:Female; D007378:Interleukins / Q000032:analysis / Q000378:metabolism; D002532:Intracranial Aneurysm / Q000150:complications / Q000209:etiology / Q000503:physiopathology*; D019586:Intracranial Hypertension / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D009638:Norepinephrine / Q000378:metabolism; D013345:Subarachnoid Hemorrhage / Q000150:complications / Q000209:etiology / Q000503:physiopathology*; D017779:Sympathetic Fibers, Postganglionic / Q000378:metabolism / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000378:metabolism / Q000503:physiopathology*; D015854:Up-Regulation / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology; D020301:Vasospasm, Intracranial / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology
D015415:Biomarkers; D007378:Interleukins; D003165:Complement System Proteins; D009638:Norepinephrine