Endothelium-Dependent Relaxations and Concentrations: Their Physiology in the Cerebral Arteries and Pathology in Experimental Cerebral Vasospasm

1992 ◽  
pp. 37-49
Author(s):  
P. Kim
Keyword(s):  
Cerebral Vasospasm ◽  
Cerebral Arteries

Evaluation of Vasospasm after Subarachnoid Hemorrhage by Use of Multislice Computed Tomographic Angiography

Neurosurgery ◽  
2002 ◽  
Vol 51 (4) ◽  
pp. 939-943 ◽  
Author(s):  
Yasunari Otawara ◽  
Kuniaki Ogasawara ◽  
Akira Ogawa ◽  
Makoto Sasaki ◽  
Kei Takahashi
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Computed Tomographic Angiography ◽  
Computed Tomographic ◽  
Tomography System ◽  
Middle Cerebral Arteries ◽  
Multislice Images ◽  
Tomographic Angiography

Abstract OBJECTIVE Multislice computed tomographic angiography (CTA) can provide clearer vascular images, even of the peripheral arteries, than conventional CTA. Multislice CTA was compared with digital subtraction angiography (DSA) for the detection of cerebral vasospasm in patients with acute aneurysmal subarachnoid hemorrhage (SAH) to analyze whether multislice CTA can replace DSA in the detection of vasospasm after SAH. METHODS Within 72 hours after the onset of symptoms, multislice CTA and DSA were performed in 20 patients with SAH. Multislice CTA and DSA were repeated on Day 7 to assess cerebral vasospasm. Regions of interest were established in the proximal and distal segments of the anterior and middle cerebral arteries on both multislice CTA and DSA images, and the agreement between the severity of vasospasm on multislice CTA and DSA images was statistically compared. The multislice Aquilon computed tomography system (Toshiba, Inc., Tokyo, Japan) used the following parameters: 1 mm collimation and 3.5 mm per rotation table increment (pitch, 3.5). RESULTS The degree of vasospasm as revealed by multislice CTA correlated significantly with the degree of vasospasm revealed by DSA (P < 0.0001). The agreement between the severity of vasospasm on multislice images obtained via CTA and DSA in the overall, proximal, and distal segments of the cerebral arteries was 91.6, 90.8, and 92.3%, respectively. CONCLUSION Multislice CTA can detect angiographic vasospasm after SAH with accuracy equal to that of DSA.

scholarly journals Comparison of the Inhibitory Effects of Antithrombin III, α2-Macroglobulin, and Thrombin in Human Basilar Arteries: Relevance to Cerebral Vasospasm

1987 ◽  
Vol 7 (1) ◽  
pp. 68-73 ◽  
Author(s):  
Richard P. White
Keyword(s):  
Cerebral Vasospasm ◽  
Antithrombin Iii ◽  
Cerebral Arteries ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Vasorelaxant Effect ◽  
Basal Tone ◽  
At Iii ◽  
Basilar Arteries

Isolated human basilar arteries were used in this study to evaluate the inhibitory effect of antithrombin III (AT III), thrombin, and α2-macroglobulin (α2-M) on contractions elicited by K+, serotonin (5-HT), prostaglandin (PG) D2, PGF2α, and plasmin. α2-M (0.5–1.0 mg/ml) failed to affect the contractions produced by contractile agonists significantly but did notably reduce the basal tone of the arteries. Thrombin (1 and 10 U/ml) reduced basal tone and significantly inhibited the contractions elicited by K+, PGF2α, and plasmin. The relaxant effect of thrombin was abolished by procedures that destroy endothelium and by exposing the artery to thrombin for prolonged periods (tachyphylaxis). AT III (1–6 U/ml) reduced basal tone and significantly inhibited, in a concentration-dependent manner, the contractile responses to K+, 5-HT, PGD2, PGF2α, and plasmin. In sharp contrast to thrombin, AT III did not induce tachyphylaxis nor was its vasorelaxant effect significantly reduced by destruction of the endothelium. The results show AT III to be a potent and nonspecific inhibitor of human cerebral arteries and support the hypothesis that AT III may contribute to the delay of cerebral vasospasm seen in patients who experience aneurysmal hemorrhage.

scholarly journals Identification of Genes Differentially Expressed in Canine Vasospastic Cerebral Arteries after Subarachnoid Hemorrhage

1999 ◽  
Vol 19 (11) ◽  
pp. 1279-1288 ◽  
Author(s):  
Hideaki Onda ◽  
Hidetoshi Kasuya ◽  
Kintomo Takakura ◽  
Tomokatsu Hori ◽  
Tada-Atsu Imaizumi ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Cerebral Arteries ◽  
Differentially Expressed ◽  
Expression Array ◽  
Cdna Expression Array ◽  
Amyloid A ◽  
Serum Amyloid A Protein ◽  
Genes Encoding ◽  
Inducible Protein

To understand the molecular processes of continuous vasospasm of cerebral arteries after subarachnoid hemorrhage, mRNA differential display and screening of cDNA expression array were performed to identify genes that are differentially expressed in vasospastic arteries of canine two-hemorrhage models. The expression levels of 18 genes were found to be upregulated, and those of two genes to be down-regulated. Of these, 12 represent known genes or homologues of genes characterized previously, and the other eight genes are not related to any sequences in the databases. The known genes include five upregulated inflammation-related genes encoding monocyte chemotactic protein-1, cystatin B, inter-α-trypsin inhibitor family heavy chain-related protein, serum amyloid A protein, and glycoprotein 130, suggesting that inflammatory reaction may be involved in the development of cerebral vasospasm. The upregulation of three known genes encoding stress-related proteins of vascular endothelial growth factor, BiP protein, and growth-arrest and DNA-damage–inducible protein may be involved in possible cell survival in the damaged arteries. A full-length cDNA for the unknown clone DVS 27, whose expression was most highly upregulated, was isolated from the cerebral artery cDNA library by hybridization. Characterization of these genes should help to clarify the molecular mechanism of continuous cerebral vasospasm after subarachnoid hemorrhage.

Subarachnoid hemorrhage—induced upregulation of the 5-HT1B receptor in cerebral arteries in rats

2003 ◽  
Vol 99 (1) ◽  
pp. 115-120 ◽  
Author(s):  
Jacob Hansen-Schwartz ◽  
Natalie Løvland Hoel ◽  
Cang-Bao Xu ◽  
Niels-Aage Svendgaard ◽  
Lars Edvinsson
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Real Time ◽  
Cerebral Vasospasm ◽  
Cerebral Arteries ◽  
Specific Treatment ◽  
Content Type ◽  
Sequence Of Events ◽  
Arterial Blood ◽  
Receptor Phenotype ◽  
Fine Print

Object. Cerebral vasospasm following subarachnoid hemorrhage (SAH) leads to reduced blood flow in the brain. Inspired by organ culture—induced changes in the receptor phenotype of cerebral arteries, the authors investigated possible changes in the 5-hydroxytryptamine (HT) receptor phenotype after experimental SAH. Methods. Experimental SAH was induced in rats by using an autologous prechiasmatic injection of arterial blood. Two days later, the middle cerebral artery (MCA), posterior communicating artery (PCoA), and basilar artery (BA) were harvested and examined functionally with the aid of a sensitive in vitro pharmacological method and molecularly by performing quantitative real-time reverse transcription—polymerase chain reaction (PCR). In the MCA and BA the 5-HT1B receptor was upregulated, as determined through both functional and molecular analysis. In response to selective 5-HT1 receptor agonists both the negative logarithm of the 50% effective concentration was increased (one log unit in the MCA and one half unit in the BA), as was the agonist's potency (increased by 50% in the MCA and doubled in the BA). In addition, the authors found an approximately fourfold increase in the number of copies of messenger RNA coding for the 5-HT1B receptor as determined by quantitative real-time PCR. In the PCoA no upregulation of the 5-HT1B receptor was observed. Conclusions. Changes in the receptor phenotype in favor of contractile receptors may well represent the end stage in a sequence of events leading from SAH to the actual development of cerebral vasospasm. Insight into the mechanism of upregulation may provide new targets for developing specific treatment against cerebral vasospasm.

Reversal of delayed vasospasm by an inhibitor of the synthesis of 20-HETE

2005 ◽  
Vol 289 (5) ◽  
pp. H2203-H2211 ◽  
Author(s):  
Kazuhiko Takeuchi ◽  
Marija Renic ◽  
Quinn C. Bohman ◽  
David R. Harder ◽  
Noriyuki Miyata ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Vasospasm ◽  
Time Course ◽  
Cerebral Arteries ◽  
Cerebral Vasculature ◽  
Doppler Flowmetry ◽  
Delayed Cerebral Vasospasm ◽  
A Value ◽  
Intracisternal Injection ◽  
Basilar Arteries

This study characterized the time course of changes in cerebral blood flow (CBF) and vascular diameter in a dual-hemorrhage model of subarachnoid hemorrhage (SAH) in rats and examined whether acute blockade of the synthesis of 20-hydroxyeicosatetraenoic acid (20-HETE) with N-(3-chloro-4-morpholin-4-yl)phenyl- N′-hydroxyimido formamide (TS-011) can reverse delayed vasospasm in this model. Rats received an intracisternal injection of blood (0.4 ml) on day 0 and a second injection 2 days later. CBF was sequentially measured using laser-Doppler flowmetry, and the diameters of the cerebral arteries were determined after filling the cerebral vasculature with a casting compound. CBF fell to 67% of control after the first intracisternal injection of blood but returned to a value near control 24 h later. CBF again fell to 63% of control after a second intracisternal injection of blood and remained 30% below control for 5 days. The fall in CBF after the second intracisternal injection of blood was associated with a sustained 30% reduction in the diameters of the middle cerebral, posterior communicating, and basilar arteries. Acute blockade of the synthesis of 20-HETE with TS-011 (0.1 mg/kg iv), 5 days after the second SAH, increased the diameters of the cerebral arteries, and CBF returned to control. These results indicate that the rats develop delayed vasospasm after induction of the dual-hemorrhage model of SAH and that blockade of the synthesis of 20-HETE fully reverses cerebral vasospasm in this model. They also implicate 20-HETE in the development and maintenance of delayed cerebral vasospasm.

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 Morphological changes of intracranial pressure quantifies vasodilatory effect of verapamil to treat cerebral vasospasm

2020 ◽  
Vol 12 (8) ◽  
pp. 802-808 ◽  
Author(s):  
Xiuyun Liu ◽  
Jeffrey R Vitt ◽  
Steven W Hetts ◽  
Koa Gudelunas ◽  
Nhi Ho ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Cerebral Vasospasm ◽  
Morphological Changes ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Delayed Cerebral Ischemia ◽  
Continuous Assessment ◽  
Cerebral Vasoconstriction ◽  
Before And After ◽  
Cerebral Vasodilation

IntroductionAfter aneurysmal subarachnoid hemorrhage (SAH), both proximal and distal cerebral vasospasm can contribute to the development of delayed cerebral ischemia. Intra-arterial (IA) vasodilators are a mainstay of treatment for distal arterial vasospasm, but no methods of assessing the efficacy of interventions in real time have been established.ObjectiveTo introduce a new method for continuous intraprocedural assessment of endovascular treatment for cerebral vasospasm.MethodsThe premise of our approach was that distal cerebral arterial changes induce a consistent pattern in the morphological changes of intracranial pressure (ICP) pulse. This premise was demonstrated using a published algorithm in previous papers. In this study, we applied the algorithm to calculate the likelihood of cerebral vasodilation (VDI) and cerebral vasoconstriction (VCI) from intraprocedural ICP signals that are synchronized with injection of the IA vasodilator, verapamil. Cerebral blood flow velocities (CBFVs) on bilateral cerebral arteries were studied before and after IA therapy.Results192 recordings of patients with SAH were reviewed, and 27 recordings had high-quality ICP waveforms. The VCI was significantly lower after the first verapamil injection (0.47±0.017) than VCI at baseline (0.49±0.020, p<0.001). A larger dose of injected verapamil resulted in a larger and longer VDI increase. CBFV of the middle cerebral artery increases across the days before the injection of verapamil and decreases after IA therapy.ConclusionThis study provides preliminary validation of an algorithm for continuous assessment of distal cerebral arterial changes in response to IA vasodilator infusion in patients with vasospasm and aneurysmal SAH.

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