An In Vitro Patient-Specific Biological Model of the Cerebral Artery Reproduced with a Membranous Configuration for Simulating Endovascular Intervention

2005 ◽  
Vol 17 (3) ◽  
pp. 327-334 ◽  
Author(s):  
Seiichi Ikeda ◽  
◽  
Fumihito Arai ◽  
Toshio Fukuda ◽  
Makoto Negoro ◽  
...  

We propose an in vitro patient-specific anatomical model of the human cerebral artery and its simulation of endovascular intervention, a potent treatment modality for cerebrovascular diseases. Our proposed model reproduces the 3-dimensional vasculature lumen, using computed tomography (CT) and magnetic resonance (MR) fluoroscopic information, within a thin artery-like membranous configuration having material properties close to arterial tissue. This cerebral arterial model reproduces an exceedingly realistic surgical feel, dynamic vascular deformation and, other important aspects involving endovascular intervention, realizing a highly realistic surgical simulation. We also propose another vasculature model that reproduces the subarachnoid space around the cerebral arteries. This version simulates endovascular intervention realistically. The model is compatible with current major imaging modalities such as CT, MR, and transcranial Doppler (TDC), and should provide effective platforms for applications, such as diagnosis, surgical planning, medical training, hemodynamic analysis and medical system development and evaluation, especially surgical robots.

2008 ◽  
Vol 20 (3) ◽  
pp. 441-448 ◽  
Author(s):  
Seiichi Ikeda ◽  
◽  
Carlos Tercero Villagran ◽  
Toshio Fukuda ◽  
Yuta Okada ◽  
...  

Endovascular intervention using interventional radiology (IVR) is most commonly used in cerebralvascular treatment. Medical imaging such as digital subtraction angiography (DSA) and vascular mapping make vasculature and catheters easier to read from fluoroscopy during endovascular intervention. We propose simulating IVR using augmented reality, reproducing fluoroscopic images and a patient-specific blood vessel model without X-ray imaging. The advantages of the patient-specific vascular model reproducing the human vasculature lumen with 13 μm resolution include 1) a realistic “feel,” 2) excellent tool behavior simulation during intervention, and 3) surgical training alternative to physician training in-vitro. Simulated fluoroscopic images are created in two steps: First, the blood vessel model refraction index is matched to surrounding glycerin solution to conceal the vascular model, making the silicone vasculature appear human as seen in endovascular intervention. Second, an augmented reality (AR) environment is created using image subtraction and overlap, making model-based endovascular simulation more understandable for catheter use and fluoroscopy use and reading.


1994 ◽  
Vol 266 (3) ◽  
pp. H1027-H1033 ◽  
Author(s):  
M. A. Hajdu ◽  
G. L. Baumbach

The goal of this study was to investigate factors that contribute to reductions in internal diameter of large and small cerebral arteries during chronic hypertension. We measured diameter of second- and third-order branches of the posterior cerebral artery in vitro during maximal dilation with EDTA in 6-mo-old stroke-prone spontaneously hypertensive rats (SHRSP, n = 7) and Wistar-Kyoto rats (WKY, n = 7). Cross-sectional area of the vessel wall, measured histologically, was not significantly different at 70 mmHg in SHRSP and WKY in large or small branches of posterior cerebral artery. In large branches of posterior cerebral artery, external and internal diameters were significantly less at 70 mmHg in SHRSP than in WKY, whereas external and internal diameters converged at 0 mmHg in the two groups of rats. In small branches, on the other hand, external and internal diameters were significantly less at all levels of intravascular pressure in SHRSP than in WKY. The stress-strain relation in posterior cerebral artery of SHRSP was shifted to the left in large branches and to the right in small branches, which indicates that distensibility was reduced in large cerebral arteries of SHRSP and increased in small cerebral arteries. These findings suggest that different mechanisms are responsible for impairment of maximal dilator capacity in large and small cerebral arteries of SHRSP: reduced distensibility in large arteries and remodeling with reduced external diameter in small arteries. Furthermore the findings provide additional support for the concept that hypertrophy may not be a primary factor in impaired maximal dilation.


2002 ◽  
Vol 283 (6) ◽  
pp. H2217-H2225 ◽  
Author(s):  
Masanori Ishiguro ◽  
Corey B. Puryear ◽  
Erica Bisson ◽  
Christine M. Saundry ◽  
David J. Nathan ◽  
...  

Cerebral artery vasospasm is a major cause of death and disability in patients experiencing subarachnoid hemorrhage (SAH). Currently, little is known regarding the impact of SAH on small diameter (100–200 μm) cerebral arteries, which play an important role in the autoregulation of cerebral blood flow. With the use of a rabbit SAH model and in vitro video microscopy, cerebral artery diameter was measured in response to elevations in intravascular pressure. Cerebral arteries from SAH animals constricted more (∼twofold) to pressure within the physiological range of 60–100 mmHg compared with control or sham-operated animals. Pressure-induced constriction (myogenic tone) was also enhanced in arteries from control animals organ cultured in the presence of oxyhemoglobin, an effect independent of the vascular endothelium or nitric oxide synthesis. Finally, arteries from both control and SAH animals dilated as intravascular pressure was elevated above 140 mmHg. This study provides evidence for a role of oxyhemoglobin in impaired autoregulation (i.e., enhanced myogenic tone) in small diameter cerebral arteries during SAH. Furthermore, therapeutic strategies that improve clinical outcome in SAH patients (e.g., supraphysiological intravascular pressure) are effective in dilating small diameter cerebral arteries isolated from SAH animals.


Cephalalgia ◽  
2012 ◽  
Vol 33 (3) ◽  
pp. 152-159 ◽  
Author(s):  
Gustaf Grände ◽  
Elisabeth Nilsson ◽  
Lars Edvinsson

Background Dilatation of cranial vessels has been proposed as a part of the cascade that initiates an episode of migraine. This is based on the observation that intravenous administration of several substances with vasodilator properties can trigger migraine-like symptoms in migraineurs. Methods We used in vitro myography of human cerebral arteries and in vitro pressurized arteriography of rat middle cerebral artery (MCA) to evaluate the vasomotor responses of cerebral arteries to increasing concentrations of vasoactive substances used to elicit migraine-like attacks. Results All substances except carbachol induced a strong vasodilatory response when applied to the abluminal side of a rat MCA but negligible response when applied to the luminal side. Luminal carbachol gave a strong dilatory response but a weak response at the abluminal side. The prostaglandins PGE2 and epoprostenol constricted the rat MCA while human cerebral arteries relaxed. The pEC50 of carbachol, histamine, epoprostenol, VIP and sildenafil differed significantly between cerebral arteries from man and rat. The differences in pEC50 for SNP, αCGRP, PACAP-27 and PACAP-38 were not significant between the species. PGE2 had no noticeable effect on human arteries in vitro. Conclusion All tested substances with the exception of VIP and carbachol have been found to elicit migraine-like attacks in migraineurs. Since these two agents have vasodilatory effects in humans, it suggests that vasodilatation is not the only reason for eliciting a migraine-like attack in migraineurs. In addition, there are significant species differences that show the importance of performing experiments in human vessels.


1982 ◽  
Vol 2 (4) ◽  
pp. 439-450 ◽  
Author(s):  
Tony Jer-Fu Lee ◽  
L. R. Kinkead ◽  
S. Sarwinski

This study examines, using an in vitro tissue bath technique, the nature of the transmitter mechanism(s) in the pig cerebral artery. Of the arteries with intact endothelium, about 25% relaxed on application of acetylcholine (ACh) at low concentration (3 × 10−7 to 3 × 10−6 M) and constricted at concentrations exceeding 10−5 M. The remaining arterial preparations either constricted (61%) or exhibited no response (14%) at any concentration of ACh tested (3 × 10−7 to 3 × 10−3 M). On the other hand, none of the arteries without endothelium relaxed at any concentration of ACh tested (3 × 10−7 to 3 × 10−3 M); of these, 90% constricted and 10% exhibited no response. These results show that ACh-induced cerebral vasodilation is dependent on endothelial cells and the direct action of ACh on the vascular smooth muscle cells is constriction. Contrary to findings in the large cerebral arteries of the cat and several other species, about 90% of the pig cerebral arteries, with or without endothelium, dilated upon application of norepinephrine (NE) at low concentration (10−7 to 3 × 10−5 M) and constricted at concentrations exceeding 3 × 10−5 M. The NE dose–response relationships were not different in arteries with and without endothelial cells, indicating that the NE-induced vasodilation was independent of the endothelial cells. The relaxation and constriction were blocked by the respective β- and α-receptor antagonists, suggesting that both responses resulted from direct stimulation by NE of β and α receptors on the smooth muscle cells. Transmural nerve stimulation (TNS) consistently induced vasodilation of the arteries whether or not the endothelial cells were present. The vasodilation was abolished by tetrodotoxin (TTX) and cold storage denervation. The TNS-induced vasodilation was not smaller in arteries without endothelium than in those with endothelium. This suggests that TNS-induced vasodilation was independent of the endothelial cells. When examined histochemically, the pig cerebral artery exhibited rich catecholamine fluorescence. Biochemical assays indicate that NE is the primary catecholamine. However, the TNS-induced vasodilation was not affected by atropine, guanethidine, or propranolol, nor prevented by reserpine. It is suggested that an as yet unidentified transmitter is responsible for the TNS-induced vasodilation. Results of this study suggest that the nerve-released ACh is a potential vasoconstrictor transmitter and that NE is a potential vasodilator transmitter in the large cerebral artery of the pig. The neurogenic control of the pig cerebral circulation may be different from that of other species, including humans.


1995 ◽  
Vol 7 (5) ◽  
pp. 1389
Author(s):  
MD Schreiber ◽  
JA Madden ◽  
RF Covert ◽  
MB Hershenson ◽  
LJ Torgerson

Drugs, such as cocaine, which may alter monoamine neurotransmitter responsiveness, could adversely affect the regulation of cerebral vasculature. Cocaine exhibits at least two mechanisms that may alter vascular responsiveness: synaptic uptake inhibition, which may augment response to stimulation, and Na+ channel inhibition, which may attenuate response. To help elicit the concentration-dependent effects of cocaine, the effects of cocaine on monoamine neurotransmitter responsiveness were studied in vitro on fetal sheep cerebral arteries (120 days gestation). The changes in diameter of segments of cannulated, pressurized fetal sheep cerebral artery were measured with a videomicroscaler system. Cumulative concentration-response curves (10(-10) to 10(-4)M) were generated for two monoamines, norepinephrine and serotonin, alone and in the presence of cocaine (10(-5) or 10(-4)M). Cocaine caused concentration-dependent alteration of response. At 10(-4)M, cocaine attenuated mean maximal norepinephrine-induced vasoconstriction 46.2% (P < 0.05). At 10(-5)M, cocaine increased sensitivity to norepinephrine (log EC50 decreased -6.63 +/- 0.09 to -7.11 +/- 0.03) and to serotonin (log EC50 decreased -7.24 +/- 0.04 to -7.81 +/- 0.09) (P < 0.05). The higher concentration of cocaine (10(-4)M) did not significantly decrease log EC50 norepinephrine. Cocaine (10(-4)M) also attenuated the response to single doses of norepinephrine (10(-6)M) and serotonin (10(-6)M) by 26.5% and 40.0%, respectively (P < or = 0.05). It is concluded that cocaine has concentration-dependent effects on vasoconstriction of the fetal sheep cerebral artery in vitro. This cocaine-induced alteration of cerebral vascular responsiveness to monoamines may be important in the regulation of fetal cerebral blood flow.


1989 ◽  
Vol 9 (6) ◽  
pp. 743-747 ◽  
Author(s):  
I. Jansen ◽  
B. Fallgren ◽  
L. Edvinsson

Vascular endothelium has been found to produce a strong and potent vasoconstrictor peptide, endothelin. In this study, we have examined basic mechanisms underlying the contractile response of cerebral vessels to endothelin using in vitro pharmacology and electrophysiology. It was found that endothelin produced strong concentration-dependent contractions of circular segments of the feline middle cerebral artery. The response was slow in onset and long lasting. The vessels showed a remarkably strong tachyphylactic reaction upon repeated exposure to endothelin. The contractile effect of endothelin was not modified by the α-adrenoceptor antagonist phen-tolamine (10−6 M) or the 5-hydroxytryptamine antagonist ketanserin (10−6 M). Mechanical removal of the endothelium decreased potassium contractions while the maximum response to endothelin was only slightly reduced. There was no change in sensitivity of the cerebral artery to endothelin. The addition of a calcium antagonist (10−6 M diltiazem or 3 × 10−8 M nimodipine) or removal of extracellular calcium from the buffer solution did not change the sensitivity of the artery to endothelin but the maximum response to endothelin was reduced by between 40 and 60% by these procedures. The resting membrane potential of the cat middle cerebral artery was –62.8 ± 3.5 mV. There was no significant depolarization in conjunction with cumulative administration of endothelin in concentrations below 1 × 10−9 M. However, bursts of excitatory junction potentials were occasionally seen in response to high concentrations of endothelin (5 × 10−9 M). The findings suggest that the contractile response to endothelin of cat cerebral arteries involved influx of extracellular calcium through voltage-sensitive calcium channels and is in part mediated via a voltage-insensitive mechanism. Further work is necessary to define the intracellular actions of endothelin.


2000 ◽  
Vol 279 (2) ◽  
pp. H511-H519 ◽  
Author(s):  
Greg G. Geary ◽  
Diana N. Krause ◽  
Sue P. Duckles

Gender and estrogen status are known to influence the incidence and severity of cerebrovascular disease. The vasoprotective effects of estrogen are thought to include both nitric oxide-dependent and independent mechanisms. Therefore, using small, resistance-sized arteries pressurized in vitro, the present study determined the effect of gender and estrogen status on myogenic reactivity of mouse cerebral arteries. Luminal diameter was measured in middle cerebral artery segments from males and from females that were either untreated, ovariectomized (OVX), or OVX with estrogen replacement (OVX + EST). The maximal passive diameters of arteries from all four groups were similar. In response to increases in transmural pressure, diameters of arteries from males and OVX females were smaller compared with diameters of arteries from either untreated or OVX + EST females. In the presence of N G-nitro-l-arginine methyl ester, artery diameters decreased in all groups, but diameters remained significantly smaller in arteries from males and OVX females compared with untreated and OVX + EST females. After endothelium removal or when inhibition of nitric oxide synthase and cyclooxygenase were combined, differences in diameters of arteries from OVX and OVX + EST were abolished. These data suggest that chronic estrogen treatment modulates myogenic reactivity of mouse cerebral arteries through both endothelium-derived cyclooxygenase- and nitric oxide synthase-dependent mechanisms.


2020 ◽  
pp. neurintsurg-2020-015990
Author(s):  
Vitor Nagai Yamaki ◽  
Nicole Mariantonia Cancelliere ◽  
Patrick Nicholson ◽  
Marta Rodrigues ◽  
Ivan Radovanovic ◽  
...  

BackgroundWith the recent advent of advanced technologies in the field, treatment of neurovascular diseases using endovascular techniques is rapidly evolving. Here we describe our experience with pre-surgical simulation using the Biomodex EVIAS patient-specific 3D-printed models to plan aneurysm treatment using endovascular robotics and novel flow diverter devices.MethodsPre-procedural rehearsals with 3D-printed patient-specific models of eight cases harboring brain aneurysms were performed before the first in-human experiences. To assess the reliability of the experimental model, the characteristics of the aneurysms were compared between the patient and 3D models. The rehearsals were used to define the patient treatment plan, including technique, device sizing, and operative working projections.ResultsThe study included eight patients with their respective EVIAS 3D aneurysm models. Pre-operative simulation was performed for the first in-human robotic-assisted neurovascular interventions (n=2) and new generation flow-diverter stents (n=6). Aneurysms were located in both the anterior (n=5) and posterior (n=3) circulation and were on average 11.0±6.5 mm in size. We found reliable reproduction of the aneurysm features and similar dimensions of the parent vessel anatomy between the 3D models and patient anatomy. Information learned from pre-surgical in vitro simulation are described in detail, including an improved patient treatment plan, which contributed to successful first in-world procedures with no intraprocedural complications.ConclusionsPre-procedural rehearsal using patient-specific 3D models provides precise procedure planning, which can potentially lead to greater operator confidence, decreased radiation dose and improvements in patient safety, particularly in first in-human experiences.


Sign in / Sign up

Export Citation Format

Share Document