Analysis of slipstream flow in two ruptured intracranial cerebral aneurysms.
Replicas of ruptured posterior communicating and basilar artery aneurysms were created from cadaveric specimens and then were placed in a circuit of pulsating non-Newtonian fluid. Individual fluid slipstreams were opacified with isobaric dyes, and images were recorded on film. The slipstreams entered the distal aneurysm neck with impact against the distal lateral wall of the aneurysm. They then swirled slowly in a reverse vortical pattern within the aneurysm sac. Fluid exited the aneurysm at the proximal neck. The flow pattern clearly shows the impact zone of entering slipstreams (the point of aneurysm rupture) and provides information pertaining to aneurysm growth and formation. (+info)
Diagnostic impact of cerebral transit time in the identification of microangiopathy in dementia: A transcranial ultrasound study.
BACKGROUND AND PURPOSE: The diagnosis and quantification of microangiopathy in dementia is difficult. The assessment of small-vessel disease requires expensive and sophisticated nuclear medicine techniques. This study was performed to identify microangiopathy related to the integrity of cerebral microcirculation by sonographic measurements (arteriovenous cerebral transit time [cTT]). METHODS: We performed transcranial color-coded duplex sonography in 40 patients with vascular dementia, 20 patients with Alzheimer's disease or Lewy body disease, and 25 age-matched controls. The clinical diagnosis was established by history of dementia and neuroimaging findings. Cognitive impairment was assessed by the Mini-Mental State Examination and Alzheimer's Disease Assessment Scale. cTT is defined as the time required by an ultrasound contrast agent to pass from a cerebral artery to a vein. This was measured by recording the power-Doppler intensity curves in the P2 segment of the posterior cerebral artery and the vein of Galen. Previous studies have shown a prolongation of cTT in patients with cerebral microangiopathy. RESULTS: cTT was substantially prolonged in patients with vascular dementia (5.8 seconds; 25th percentile 4.5; 75th percentile 7.5; U test, P<0.001) compared with controls (3.1 seconds; 2.3; 3.4) but not in patients with degenerative dementia (3.7 seconds; 3.7; 4.2). In patients with vascular dementia, cTT was significantly correlated with cognitive impairment. CONCLUSIONS: cTT may be useful tool to disclose small-vessel disease in demented patients. Examination is noninvasive and quickly performed. It may be also useful in follow-up examinations in patients undergoing therapy. (+info)
Oxidized low-density lipoprotein enhances myogenic tone in the rabbit posterior cerebral artery through the release of endothelin-1.
BACKGROUND AND PURPOSE: Cerebral arteries develop stretch-induced myogenic tone, which plays an important role in the regulation of blood flow to the brain. Although the effect of oxidized LDL (Ox-LDL) on many aspects of the vascular endothelial and smooth muscle cell function have been extensively investigated, its influence on myogenic activity has not been studied. METHODS: The effect of Ox-LDL on the myogenic tone that develops in the perfused rabbit posterior cerebral artery at intramural pressures between 40 and 90 mm Hg was examined. RESULTS: Ox-LDL (10 microg/mL) significantly enhanced myogenic tone by 21.4+/-6.1% to 28.5+/-1.8% at 60 to 90 mm Hg pressure (P<0.05) but had no influence on norepinephrine- (0.5 to 1 micromol/L) and KCl (20 mmol/L)-induced constriction. Ox-LDL was effective whether the artery was exposed to it from the intraluminal or the extraluminal surface. Lysophosphatidylcholine (10 micromol/L), a lipid component of Ox-LDL, had an equivalent potentiating effect. Native LDL (100 microg/mL) was inactive. The myogenic tone-potentiating effect of Ox-LDL was abolished by endothelium removal but was not influenced by the NO synthase inhibitor N(G)-nitro-L-nitro-arginine methyl ester (50 micromol/L). This effect was reversed by the endothelin-1 (ET-1) antagonist BQ-123 (1 micromol/L). This concentration blocked 1 to 3 nmol/L ET-1-induced constriction without altering constriction induced by 40 mmol/L KCl. The potentiating effect was suppressed by the specific protein kinase C inhibitor chelerythrine (1 micromol/L). CONCLUSIONS: Ox-LDL enhances myogenic tone through the release of ET-1 from the endothelium of the rabbit posterior cerebral artery. (+info)
Distal calcarine fusiform aneurysm: a case report and review of literature.
A 50 year old female who was operated for atrial septal defect 8 years back, presented with clinical features suggestive of subarachnoid haemorrhage (grade I, Hunt and Hess). CT scan of brain revealed haemorrhage in all the supratentorial basal cisterns, sylvian cistern and small haematoma in the left occipital lobe. Conventional CT and MR angiography revealed aneurysm in relation to distal part of the calcarine branch of the left posterior cerebral artery (PCA). Left occipital craniotomy in prone position followed by deep dissection in the occipital lobe showed fusiform aneurysm of the distal part of the calcarine branch. PCA aneurysms constitute only 0.2 to 1% of all intracranial aneurysms and among them distal PCA aneurysms are most rare, constituting only 1.3%. They too are mostly seen at the bifurcation of the PCA. The present case however, is unique in the sense that it has developed as a fusiform aneurysm in the distal part of the calcarine branch. To the best of our knowledge this is rare among the rarest. (+info)
Coupling of Ca(2+) to CREB activation and gene expression in intact cerebral arteries from mouse : roles of ryanodine receptors and voltage-dependent Ca(2+) channels.
Pathological changes of the vasculature are characterized by changes in Ca(2+) handling and alterations in gene expression. In neurons and other cell types, [Ca(2+)](i) often drives changes in gene expression. However, the relationship between Ca(2+) signaling and gene expression in vascular smooth muscle is not well understood. This study examines the ability of Ca(2+) influx through voltage-dependent, L-type Ca(2+) channels (VDCCs) and Ca(2+) release through ryanodine receptors (RyRs) to activate the transcription factor, cAMP-responsive element binding protein (CREB), and increase c-fos levels in intact cerebral arteries. Membrane depolarization increased the fraction of nuclei staining for phosphorylated CREB (P-CREB) and levels of c-fos mRNA in intact mouse cerebral arteries. Ryanodine, which inhibits RyRs, increased P-CREB staining and c-fos levels. Forskolin, an activator of adenylyl cyclase, and sodium nitroprusside, an NO donor, increased P-CREB and c-fos levels. Nisoldipine, an inhibitor of VDCCs, reversed the effects of depolarization and ryanodine on P-CREB and c-fos levels, but not the effects of forskolin or sodium nitroprusside. Inhibition of Ca(2+)/calmodulin-dependent protein kinase (CaM kinase) blocked increases in P-CREB and c-fos levels seen with membrane depolarization, suggesting that CaM kinase has an important role in the pathway leading from Ca(2+) influx to CREB-mediated changes in c-fos levels. Our data suggest that membrane depolarization increases [Ca(2+)](i) through activation of VDCCs, leading to increased P-CREB and c-fos, and that RyRs have a profound effect on this pathway by indirectly regulating Ca(2+) entry through VDCCs. These results provide the first evidence of Ca(2+) regulation of CREB and c-fos in arterial smooth muscle. (+info)
Hemodynamic changes around cerebral arteriovenous malformation before and after embolization measured with PET.
To estimate the changes in regional cerebral blood flow (rCBF) around cerebral arteriovenous malformation (AVM) before and after embolization, 6 patients with AVM were sequentially examined with positron emission tomography (PET). PET depicted the remodeling of rCBF in the ipsilateral hemisphere of AVM after embolization. Decrease of rCBF in the ipsilateral hemisphere was also detected in patients with focal symptoms before embolization, and improvement of clinical symptoms after embolization corresponded to disappearance of rCBF decrease. PET can detect hemodynamic changes after embolization, and has a possibility to estimate the effect of embolization in patients with AVM. (+info)
Radiation-induced cerebrovasculopathy of the distal middle cerebral artery and distal posterior cerebral artery--case report.
A 15-year-old girl underwent partial removal of a pituitary adenoma followed by local irradiation of the brain with a total of 70 Gy through two lateral opposing ports. Twenty years later, she experienced frequent transient ischemic attacks with left sensory disturbance. Cerebral angiography revealed stenoses of the right distal middle cerebral artery (MCA) and the right distal posterior cerebral artery without net-like vessels. There was a severe decrease of vasoreactivity in the right hemisphere. Right superficial temporal artery (STA)-MCA anastomosis was performed. Her neurological deficits were resolved and perfusion reserve capacity had markedly improved 6 months later. We recommend STA-MCA anastomosis in such cases. (+info)
Flow modulation of pressure-sensitive tone in rat pial arterioles: role of the endothelium.
BACKGROUND: Cerebral arteriolar tone is modulated in response to changes in transmural pressure and luminal flow. The effect of flow on the relation between pressure and diameter has not been fully evaluated in these vessels. This study was conducted to investigate this interaction and to determine the role of the endothelium in mediating it. METHODS: Rat pial arterioles from the territory of the posterior cerebral artery were mounted in a perfusion myograph. In some arterioles, the endothelium was removed by air perfusion. Diameters were recorded at pressures from 20 to 200 mmHg in the presence and absence of flow (10 microl/min). The response to flow (0-30 microl/min) was recorded at 60 and 120 mmHg. RESULTS: In the absence of flow, endothelium-intact arterioles demonstrated tone at distending pressures between 40 and 140 mmHg. In the presence of flow, tone did not develop until pressure exceeded 100 mmHg, and the vessels remained active at pressures up to 200 mmHg. Endothelium-denuded arterioles developed tone at the same pressure when perfused as when unperfused, but perfused vessels were able to maintain active tone at higher pressures. At 60 mmHg, flow caused dilation if the endothelium was intact and constriction if it had been removed. At 120 mmHg, flow caused constriction. Endothelium-dependent flow-relaxation was inhibited by N(G)-nitro-L-arginine methyl ester (10(-5) M) and abolished by indomethacin (10(-5) M). CONCLUSION: Flow inhibits the development of pial arteriolar tone at low intraluminal pressures through endothelium-dependent mechanisms. Conversely, perfusion extends the upper limit of the myogenically regulated pressure range through endothelium-independent activation of arteriolar smooth muscle contraction. (+info)