Wh. Ng et al., Nitric oxide and subarachnoid hemorrhage: Elevated levels in cerebrospinalfluid and their implications, NEUROSURGER, 49(3), 2001, pp. 622-626
OBJECTIVE: Nitric oxide (NO) plays an important role in the pathogenesis of
neuronal injury after brain ischemia, and decreased levels of NO have been
implicated in the pathogenesis of vasospasm after subarachnoid hemorrhage
(SAH). In this study, we measured the ventricular cerebrospinal fluid (CSF)
NO levels in patients with SAH and correlated the levels with clinical gra
de and middle cerebral artery velocities measured with transcranial Doppler
ultrasound.
METHODS: All patients with spontaneous SAH documented on computed tomograph
y and with an external ventricular drain inserted within 24 hours of hemorr
hage were included in the study. A total of 16 patients were studied betwee
n August 1999 and August 2000. CSF was collected serially at the time of su
rgery and subsequently at daily intervals. it was collected during the time
that the external ventricular drain remained patent and in situ. NO levels
were measured by photometric analysis by using a nitrite/nitrate assay kit
(Cayman Chemical, Ann Arbor, MI).
RESULTS: The peak NO level in patients with SAH ranged from 9.96 to 168.16
mu mol, with a median of 36.93 mu mol. The levels were significantly elevat
ed as compared with the control group (5.16 mu mol, P < 0.05). The median N
O level in patients with poor-grade SAH was 67.14 <mu>mol as compared with
27.42 mu mol in patients with good-grade hemorrhage (P < 0.05). No correlat
ion was seen between CSF NO levels and middle cerebral artery velocities. T
he median NO level was 33.2 <mu>mol in patients with a poor outcome as comp
ared with 30.25 mu mol in patients with a good outcome (P > 0.05).
CONCLUSION: This study showed that NO levels are elevated after spontaneous
SAH, and the degree of elevation is higher in patients with poor-grade SAH
.