Nitric Oxide Related Pathophysiological Changes Following Subarachnoid Haemorrhage

2011 ◽  
pp. 105-109 ◽  
Author(s):  
Mohammed Sabri ◽  
Jinglu Ai ◽  
R. Loch Macdonald
Keyword(s):  
Nitric Oxide ◽  
Subarachnoid Haemorrhage

scholarly journals The Role of Nitric Oxide in Resolution of Vasospasam Corresponding with Cerebral Vasospasms after Subarachnoid Haemorrhage: Animal Model

2008 ◽  
Vol 8 (2) ◽  
pp. 177-182
Author(s):  
Kemal Dizdarević
Keyword(s):  
Nitric Oxide ◽  
Animal Model ◽  
Subarachnoid Haemorrhage ◽  
Cerebral Vasospasm ◽  
Subarachnoid Space ◽  
Arterial Wall ◽  
Cerebral Arteries ◽  
Control Group ◽  
Blood Products

Intracranial aneurysmal rupture is the common cause of spontaneous subarachnoid haemorrhage (SAH). This haemorrhage is typically diffuse and located in extracerebral subarachnoid space in which main cerebral arterial branches are situated. The intimate and long-term contact of arterial wall and blood products in the closed space causes the cerebral vasospasm as a serious and frequent complication of SAH. It is connected with significant morbidity and mortality due to developing of focal cerebral ischaemia and subsequently cerebral infarction. The aim of our experimental research was to create the animal model of vasospasm using the femoral artery due to examination of reduced basic dilator activity cause in arterial wall after SAH. The important characteristic of major cerebral arteries is their localization in the closed subarachnoid space which enables their to have long-term contact with blood products after haemorrhage. Thirty six femoral arteries (FA) of eighteen female rats weighing about 300 g were used. In vivo, femoral arteries are microsurgically prepared in both inguinal regions in all rats. Eighteen arteries were encompassed by polytetrafluoroethylene (PTFE) material forming closed tube and autologous blood was injected in the tube around the arterial wall. Additional eighteen arteries, as a control group, were also put in PTFE tube but without exposing to the blood. All rats are left to live for eight days. Afterwards, rats were sacrificed and their arteries were in vitro examined including an isometric tension measurement and histological changes analysis. The tension was measured during application of vasoconstrictors and vasodilatators (nitric oxide, NO). FA exposed to periadventitial blood exhibit hyper reactivity to constrictors (KCl, phenylephrine, acetylcholine) compared to control group. It was also found that NO donor (sodium nitroprusside) diminished arterial spasm induced by blood and vasoconstrictors. In conclusion, FA can be used as a model for vasospasm correlating with cerebral vasospasm after SAH and therefore this model can be utilized in future experiments assessing cerebral vasospasm. The reduced basic dilator activity of spastic femoral artery is caused by an absence of gaseous messenger NO next to the arteries but not by diminished response vasculature to NO. Absence of NO after SAH probably causes the reduced basic dilator activity of cerebral arteries as well. The guanylate-cyclase level in the arterial wall is consequently reduced after SAH primary due to absence of NO but not due to direct reduction of enzyme activities caused by process of blood degradation inside of subarachnoid space.

scholarly journals Ratio of Nitric Oxide Metabolite Levels in Cerebrospinal Fluid and Serum, and Their Correlation with Severity and Outcome in Patients with Subarachnoid Haemorrhage

2021 ◽  
Vol 28 (6) ◽  
pp. 42-54
Author(s):  
Kho Giat Seng ◽  
Regunath Kandasamy ◽  
Mohamad Adam Bujang ◽  
Mummedy Swammy ◽  
Muzaimi Mustapha ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cerebrospinal Fluid ◽  
Subarachnoid Haemorrhage

scholarly journals Vasospasm in Cerebral Inflammation

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Michael Eisenhut
Keyword(s):  
Nitric Oxide ◽  
Brain Injury ◽  
Bacterial Meningitis ◽  
Subarachnoid Haemorrhage ◽  
Interleukin 1 ◽  
Cerebral Arteries ◽  
Neurological Deficits ◽  
Double Blind ◽  
Calcium Dependent ◽  
Cerebral Inflammation

All forms of cerebral inflammation as found in bacterial meningitis, cerebral malaria, brain injury, and subarachnoid haemorrhage have been associated with vasospasm of cerebral arteries and arterioles. Vasospasm has been associated with permanent neurological deficits and death in subarachnoid haemorrhage and bacterial meningitis. Increased levels of interleukin-1 may be involved in vasospasm through calcium dependent and independent activation of the myosin light chain kinase and release of the vasoconstrictor endothelin-1. Another key factor in the pathogenesis of cerebral arterial vasospasm may be the reduced bioavailability of the vasodilator nitric oxide. Therapeutic trials in vasospasm related to inflammation in subarachnoid haemorrhage in humans showed a reduction of vasospasm through calcium antagonists, endothelin receptor antagonists, statins, and plasminogen activators. Combination of therapeutic modalities addressing calcium dependent and independent vasospasm, the underlying inflammation, and depletion of nitric oxide simultaneously merit further study in all conditions with cerebral inflammation in double blind randomised placebo controlled trials. Auxiliary treatment with these agents may be able to reduce ischemic brain injury associated with neurological deficits and increased mortality.

Role of nitric oxide in the CBF autoregulation during acute stage after subarachnoid haemorrhage in rat pial artery

2003 ◽  
Vol 17 (5) ◽  
pp. 563-573 ◽  
Author(s):  
Hyun Gee Cho ◽  
Hwa Kyoung Shin ◽  
Yung Woo Shin ◽  
Jeong Hyun Lee ◽  
Ki Whan Hong
Keyword(s):  
Nitric Oxide ◽  
Subarachnoid Haemorrhage ◽  
Acute Stage ◽  
Pial Artery

Nitric oxide in subarachnoid haemorrhage and its therapeutics implications

2006 ◽  
Vol 148 (6) ◽  
pp. 605-613 ◽  
Author(s):  
D. Hänggi ◽  
H.-J. Steiger
Keyword(s):  
Nitric Oxide ◽  
Subarachnoid Haemorrhage
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