Sustained vessel dilation induced by increased pulsatile perfusion of porcine carotid arteries in vitro

Arterial pulse pressure (PP) increases with exertional stress and ageing, and can modify vessel diameter in smaller vessels. To test if PP must exceed a certain range to influence vessel diameter, and determine if such effects are endothelium-dependent or intrinsic to vascular viscoelasticity, eight fresh excised porcine carotid artery segments were perfused with modified Krebs–Henseleit by a servo-controlled system generating physiological arterial pressure waveforms. In a separate group of vessels (n = 10), the endothelium was mechanically removed. Vessel external diameter was measured by video edge-detection. Vessels partially preconstricted with noradrenaline were perfused at 9 mL min^–1 mean flow, at mean pressure of 90 or 120 mmHg, and zero PP. PP alone was then increased to 40, 70, or 120 mmHg at 1 Hz cycling rate for 5 min, then returned to zero and vessel diameter measured immediately thereafter. The protocol was repeated after 10–20 min stabilization. Mean vessel diameter rose proportionally with PP only once PP exceeded 40 mmHg, with maximal increases of 6–9% at a PP of 120 mmHg. Similar responses were obtained in vessels with and without a functional endothelium, at both mean pressures. Thus, when exposed to higher than normal resting PP, conduit arteries dilate owing to the stress-relaxation response of their viscoelastic wall. This mechanism of PP-mediated vascular dilatation may contribute to enhanced organ perfusion when small resistance arteries are already dilated.     

Sustained vessel dilation induced by increased pulsatile perfusion of porcine carotid arteries in vitro.

Arterial pulse pressure (PP) increases with exertional stress and ageing, and can modify vessel diameter in smaller vessels. To test if PP must exceed a certain range to influence vessel diameter, and determine if such effects are endothelium-dependent or intrinsic to vascular viscoelasticity, eight fresh excised porcine carotid artery segments were perfused with modified Krebs-Henseleit by a servo-controlled system generating physiological arterial pressure waveforms. In a separate group of vessels (n = 10), the endothelium was mechanically removed. Vessel external diameter was measured by video edge-detection. Vessels partially preconstricted with noradrenaline were perfused at 9 mL min(-1) mean flow, at mean pressure of 90 or 120 mmHg, and zero PP. PP alone was then increased to 40, 70, or 120 mmHg at 1 Hz cycling rate for 5 min, then returned to zero and vessel diameter measured immediately thereafter. The protocol was repeated after 10-20 min stabilization. Mean vessel diameter rose proportionally with PP only once PP exceeded 40 mmHg, with maximal increases of 6-9% at a PP of 120 mmHg. Similar responses were obtained in vessels with and without a functional endothelium, at both mean pressures. Thus, when exposed to higher than normal resting PP, conduit arteries dilate owing to the stress-relaxation response of their viscoelastic wall. This mechanism of PP-mediated vascular dilatation may contribute to enhanced organ perfusion when small resistance arteries are already dilated.     

Diameters of arteries, veins, and airways in isolated dog lung

Triple resin casts were made of the pulmonary arteries, veins, and airways from six dog lungs. The airways were cast at a pressure of 25 cm resin in all six. In the first three, both vessels were cast at a pressure of 30 cm resin, and in the second three, arteries were at 10 cm resin and veins at 5 cm resin. Measurements were made of luminal airway diameters down to 1 mm and of the luminal diameters of the corresponding segments of the vascular trees. The relation of one to the other was shown by calculating the regression lines for the corresponding diameters. Intrapulmonary arteries and veins are of approximately equal diameter when cast at 30 cm resin, while the veins are 20% larger than the arteries when cast at 5 cm and 10 cm of resin, respectively. Both vessel diameters are 75% of bronchial at the higher pressure, while at the lower pressures arteries are 59%, and veins 71% of bronchial. In any individual, vessel diameters are a relatively constant proportion of airway diameter. This constant of proportionality varies considerably between dogs, its value ranging from 0.48 to 1.03. It is concluded that in any individual all three trees have similar diameter ratios--that is, the ratio between mean diameters of branches in successive orders.     

A New Biomechanical Perfusion System for <Emphasis Type="Italic">ex vivo</Emphasis> Study of Small Biological Intact Vessels

The vascular endothelium transduces physical stimuli within the circulation into physiological responses, which influence vascular remodelling and tissue homeostasis. Therefore, a new computerized biomechanical ex vivo perfusion system was developed, in which small intact vessels can be perfused under well-defined biomechanical forces. The system enables monitoring and regulation of vessel lumen diameter, shear stress, mean pressure, variable pulsatile pressure and flow profile, and diastolic reversal flow. Vessel lumen measuring technique is based on detection of the amount of flourescein over a vessel segment. A combination of flow resistances, on/off switches, and capacitances creates a wide range of pulsatile pressures and flow profiles. Accuracy of the diameter measurement was evaluated. The diameters of umbilical arteries were measured and compared with direct ultrasonographic measurement of the vessel diameter. As part of the validation the pulsatile pressure waveform was altered, e.g., in terms of pulse pressure, frequency, diastolic shape, and diastolic reversal flow. In a series of simulation experiments, the hemodynamic homeostasis functions of the system were successfully challenged by generating a wide range of vascular diameters in artificial and intact human vessels. We conclude that the system presented may serve as a methodological and technical platform when performing advanced hemodynamic stimulation protocols. Niklas Bergh and Mikael Ekman, Both authors contributed equally to the work     

Structure and function of small arteries

The small arteries (prearteriolar vessels with lumen diameter less than approximately 500 microns) contribute importantly to and participate actively in the regulation of the peripheral resistance. New techniques, building on the classic histological and hemodynamic techniques, have enabled detailed in vitro investigation of small arteries. At present, research in small arteries is in its infancy, and our understanding of the heterogeneity of small arteries within vascular beds, between vascular beds, and between species is extremely limited. This review attempts to describe the current status of the field. New techniques, based primarily on a wire myograph (where the vessels are mounted as ring preparations) and a pressure myograph (where vessels are cannulated and pressure-lumen relations are determined), have allowed in vitro investigations of small arteries. The more physiological arrangement of the pressure myograph allows, for example, investigation of the vasoconstrictor response to raised intravascular pressure (the Bayliss response), whereas the less-sophisticated wire myograph is similar to use and may be more useful in certain situations where particular mechanisms are being investigated. Both techniques allow simultaneous measurements of vessel tone and a variety of parameters (e.g., membrane potential and intracellular ion activities) and thus allow precise determination of the relation between small artery structure and function. The vessels appear to remain fully viable with regard to the contractility of their smooth muscle cells as well as to the function of their perivascular nerves and their endothelium. The evidence suggests that the monovalent transport mechanisms in the plasma membrane, in particular potassium channels, play an important role in the determination of the membrane potential in small arteries, although the relation is more complex than indicated by the Goldman equation. Confirmation of these findings requires, however, simultaneous determinations of ion transport and vascular tone under conditions where vessels are subjected to mechanical loading. The membrane potential, through its effect on potential-dependent calcium channels, plays an important role in the determination of vascular tone. With regard to calcium homeostasis, current knowledge is hampered by the lack of direct measurements of the relation between cytoplasmic calcium and vascular tone. The evidence, however, suggests that besides potential-dependent calcium channels, receptor-operated calcium channels are present in the plasma membrane, although this still requires confirmation. The role of the sarcoplasmic reticulum is not clarified.(ABSTRACT TRUNCATED AT 400 WORDS)     

Incorporating Autoregulatory Mechanisms of the Cardiovascular System in Three-Dimensional Finite Element Models of Arterial Blood Flow

The cardiovascular system is a closed-loop system in which billions of vessels interact with each other, and it enables the control of the systemic arterial pressure and varying organ flow through autoregulatory mechanisms. In this study, we describe the development of mathematical models of autoregulatory mechanisms for systemic arterial pressure and coronary flow and discuss the connection of these models to a hybrid numerical/analytic closed-loop model of the cardiovascular system. The closed-loop model consists of two lumped parameter heart models representing the left and right sides of the heart, a three-dimensional finite element model of the aorta with coronary arteries, three-element Windkessel models and lumped parameter coronary vascular models that represent the systemic circulation, and a three-element Windkessel model to approximate the pulmonary circulation. Using the connection between the systemic arterial pressure and coronary flow regulation systems, and the hybrid closed-loop model, we studied how the heart, coronary vascular beds, and arterial system respond to physiologic changes during light exercise and showed that these models can realistically simulate temporal behaviors of the heart, coronary vascular beds, and arterial system during exercise of healthy subjects. These models can be used to study temporal changes occurring in the heart, coronary vascular beds, and arterial system during cardiovascular intervention or changes in physiological states.     

Photoacoustic microscopy of blood pulse wave

Blood pulse wave velocity (PWV) is an important physiological parameter that characterizes vascular stiffness. In this letter, we present electrocardiogram-synchronized, photoacoustic microscopy for noninvasive quantification of the PWV in the peripheral vessels of living mice. Interestingly, blood pulse wave-induced fluctuations in blood flow speed were clearly observed in arteries and arterioles, but not in veins or venules. Simultaneously recorded electrocardiograms served as references to measure the travel time of the pulse wave between two cross sections of a chosen vessel and vessel segmentation analysis enabled accurate quantification of the travel distance. PWVs were quantified in ten vessel segments from two mice. Statistical analysis shows a linear correlation between the PWV and the vessel diameter which agrees with known physiology.     

Mechanical behavior of vascular smooth muscle in cylindrical segments of arteries in vitro

Vascular smooth muscle mechanics have been studied in vitro in cylindrical segments of dog carotid artery, human internal mammary artery, and human saphenous vein. Such cylindrical preparations maintain normal vessel geometry and also permit correlation of mechanical phenomena with transmural pressure. These studies show that the vascular muscle in cylindrical arteries develops a maximum active stress of 1.1×10⁵ N/m² for the whole wall, or 2.2–3.7×10⁵ N/m² for the volume of the wall occupied by vascular muscle. These values are similar to those reported for strip studies of vascular muscle and various preparations of skeletal muscle, but are two to five times that reported for cardiac papillary muscle preparations. In cylindrical preparations of arteries, maximum isometric active stress occurs at 150 mm Hg, whereas that in veins occurs at less than 15 mm Hg. Quick release experiments of cylindrical segments of vessels avoid the compliance of inactive tissue trapped beneath ligatures in strip studies. Quick release experiments in cylindrical segments of dog carotid artery reveal that at maximum isometric stress, the series elastic component (SEC) is extended 8–11%. Experiments employing temperature variations and degradative enzymes show that the SEC is located largely in elastin, with a lesser portion located in the contractile apparatus. At short-and long-muscle lengths, the active muscle develops decreased active stress and that developed at long lengths persists at all muscle lengths, even after shortening. This has been termed “attenuation” and appears to contribute to the static length-stress and pressure-diameter hysteresis exhibited by vessels. Excitation of vascular muscle in vessel segments held at constant pressure discloses that isobaric contraction decreases artery diameter a maximum of approximately 25%. This occurs at a dimension corresponding to approximately 100 mm Hg in the relaxed vessel. Isometrically and isobarically contracted vessels tend to fall along the same pressure-diameter coordinates, indicating equivalence of both modes of contraction. Distention of contracted vessels indicates that active vascular muscle markedly resists distention up to 150–250 mm Hg; at higher pressures the contracted vessel exhibits decreased stiffness as the contracted muscle yields. The vascular muscle, therefore, has a biphasic effect on circumferential elastic modulus relative to that of the relaxed vessel. Although controversial, evaluation of the effects of the active muscle on wall elastic modulus probably is most meaningful when the modulus is examined as a function of stress, or as a function of strain, where strain is computed with respect to a single initial dimension for both the relaxed and contracted vessel.     

Organization and structure of branches in the rat pulmonary arterial bed

Pulmonary arteries were fixed by perfusion under constant pressure and filled with rubber. The hardened rubber cast delineated the arterial bed, permitting dissection of axial vessels and all branches. Each segment was prepared for scanning electron microscopy and transmission electron microscopy. Branches arising at acute angles from the axial artery and the first two generations of its branches, regardless of diameter, had the same concentric muscle layer structure as parent vessels. Endothelial cells of the parent vessel were oriented into the ostia of these branches. Branches that came off the axial vessel or its branches at right angles had spiral muscle bundles and led to nonmuscular precapillary vessels. Right angle branches also had similar wall structure regardless of diameter. Near the ostia of right angle branches, endothelial cells of the parent vessels did not show orientation of their long axis into the branch lumens. It was concluded that branch arteries arising at acute angles are conduits which carry blood to distant parts of the lung while right angle branches are a histologically different group which distribute the blood to local capillary beds.     

Transmitter characteristics of cutaneous,renal and skeletal muscle small arteries in the rat

Aim: We studied transmitter characteristics of proximal and distal arteries supplying skin (saphenous artery and its medial tarsal branch), kidneys (terminal branches of renal artery and interlobar arteries) and skeletal muscle (proximal and distal sections of external sural artery). Methods: Artery segments were mounted in an isometric myograph and intramural nerves were activated by electrical field stimulation. Adrenergic and purinergic components of the neurogenic response were blocked using phenoxybenzamine and α,β‐methylene adenosine triphosphate (mATP), respectively. Results: Arteries from skin or kidney developed rapid and prominent neurogenic contractile responses, with half‐maximal amplitude reached within 5–15 s; responses in proximal vessels were greater than in distal vessels. Arteries from skeletal muscle responded to sympathetic stimulation with a moderate contraction developing over 1 min or more, the response of distal segments was greater than that of proximal segments. In skeletal muscle vessels the sympathetically evoked contraction was completely blocked by phenoxybenzamine, whereas in skin and renal vessels it was the combined effect of noradrenaline and adenosine triphosphate (ATP). Given alone, mATP did not change the magnitude of the response to nerve stimulation, but increased its latency and also potentiated the response to exogenous noradrenaline. In all vascular beds, distal vessels were more sensitive to noradrenaline and mATP. Conclusion: It thus appears that the noradrenaline/ATP ratio of the sympathetic vasoconstrictor response differs between vascular beds in a way that is consistent with known differences in the selective regulation of regional vascular resistance by the sympathetic nervous system.     

Transmitter characteristics of cutaneous,renal and skeletal muscle small arteries in the rat

AIM: We studied transmitter characteristics of proximal and distal arteries supplying skin (saphenous artery and its medial tarsal branch), kidneys (terminal branches of renal artery and interlobar arteries) and skeletal muscle (proximal and distal sections of external sural artery). METHODS: Artery segments were mounted in an isometric myograph and intramural nerves were activated by electrical field stimulation. Adrenergic and purinergic components of the neurogenic response were blocked using phenoxybenzamine and alpha,beta-methylene adenosine triphosphate (mATP), respectively. RESULTS: Arteries from skin or kidney developed rapid and prominent neurogenic contractile responses, with half-maximal amplitude reached within 5-15 s; responses in proximal vessels were greater than in distal vessels. Arteries from skeletal muscle responded to sympathetic stimulation with a moderate contraction developing over 1 min or more, the response of distal segments was greater than that of proximal segments. In skeletal muscle vessels the sympathetically evoked contraction was completely blocked by phenoxybenzamine, whereas in skin and renal vessels it was the combined effect of noradrenaline and adenosine triphosphate (ATP). Given alone, mATP did not change the magnitude of the response to nerve stimulation, but increased its latency and also potentiated the response to exogenous noradrenaline. In all vascular beds, distal vessels were more sensitive to noradrenaline and mATP. CONCLUSION: It thus appears that the noradrenaline/ATP ratio of the sympathetic vasoconstrictor response differs between vascular beds in a way that is consistent with known differences in the selective regulation of regional vascular resistance by the sympathetic nervous system.     

Oxygen consumption of pial arteries.

Pial arterioles and arteries, normally responsive to alterations in PaCO2, were obtained by microdissection from the parietal cortex of 53 anesthetized cats. The oxygen consumption of these vessels, determined with the Cartesian diver microrespirometer, was found to be size dependent. It increased progressively from vessels 60 mum in diameter to vessels 250 mum in diameter. In vessels 250--375 mum in diameter there was a progressive decrease in oxygen consumption with increasing vessel size. The oxygen consumption was not altered by increasing the oxygen concentration in the diver from 20% to 95%, or that of glucose from 1.1 to 2.0 mM. Planimetry of histological sections showed that the percentage of endothelium and smooth muscle increased as vessel diameter increased from 60 to 200 mum, and thereafter decreased with increasing vessel size. When these differences in the composition of the vessel wall were taken into account, there was still residual dependence of the oxygen consumption on vessel diameter. This may represent intrinsic differences in the metabolic rate of vascular smooth muscle in vessels of different size.     

Metabolic control of large-bore arterial resistance vessels,arterioles, and veins in cat skeletal muscle during exercise

The metabolic control of the vascular bed in cat gastrocnemius muscle during exercise was studied with a new technique (Björnberg et al. 1988) permitting continuous and simultaneous recordings of arteriolar and capillary pressures, and of resistances in the following consecutive vascular section: proximal arterial resistance vessels > 25 μm, arterioles < 25 μm, and on the venous side. The study thereby provided quantitative data for resistance and active intrinsic tone in these vascular segments at rest, during graded exercise vasodilatation, and in the post-exercise period. Slight activation of the metabolic control system by low-frequency somatomotor nerve stimulation (light exercise') caused inhibition of intrinsic tone and decreased vascular resistance selectively in the arteriolar section. At increasing workloads, arteriolar resistance was further decreased, but resistance and tone in the proximal arterial resistance vessels and the veins then became clearly reduced as well. This difference in effectiveness of the metabolic control system on the different segments of the vascular bed was expressed quantitatively in terms of a ‘metabolic vasodilator index’. Graded activation of the metabolic control system led to a marked segmental redistribution of intrinsic vascular tone, in turn resulting in an increased pressure drop across the proximal arterial vessels and the veins and a decreased pressure drop over the arterioles. The observed decrease in the pre- to post-capillary resistance ratio caused, at a constant arterial pressure of 100 mmHg, a graded increase in capillary pressure with increasing workloads, at maximum vasodilatation by an average value of 14 mmHg above the resting control value of 15.4 ± 0.6 mmHg. In the post-exercise period, recovery of vascular tone to control was more rapid in the proximal arterial resistance vessels and the veins than in the arteriolar segment.     

Simulation of steady cardiovascular flow in the presence of stenosis using a finite element method

Stenosis could affect one or more segments of the human cardiovascular system. It is a problem capable of causing grave effects. In the present study, the finite element method has been utilised to construct a computer simulation model for the human cardiovascular system in which one or more blood carrying elastic segments are affected by stenosis. Computational effects on the effects of stenosis in aorta arch, carotid, and coronary arteries on parameters of steady flow through the system are presented. It is found that when the total flow rate through the heart is maintained constant, the most notable effect is a very marked increase in pressure drop occurring over the length of the vessel affected with stenosis. Pressure drop in many other segments also increases but by a much smaller extent. On the other hand, when the pressure at the inlet of the ascending aorta and the outlet of the vena cava are maintained constant, the most marked effect is a decrease of flow rate through the stenosed vessel. Stenosis not only causes a pressure drop in the affected segments but it also changes pressures at points distal from the site of stenosis. It also causes a redistribution of flow through the cardiovascular system.     

Substance P-like immunoreactivity in nerves associated with the vascular system of guinea-pigs

Substance P-like immunoreactivity was localized by an indirect immunohistochemical technique in whole mounts and sections of blood vessels from the guinea-pig. There was a widespread association of nerve fibres that had substance P-like immunoreactivity with blood vessels, extending into all vascular beds. The relative densities of supply of different vessels were assessed visually and a rating scale used to compare them. Large elastic arteries close to the heart had dense networks of immunoreactive nerves associated with them. The density decreased as more peripheral beds were approached, except that there was a particularly dense network of nerves with arteries of the splanchnic beds. Arteries to myocardial, central nervous system, renal, reproductive and skeletal muscle beds all had substance P-immunoreactive nerves associated with them to varying extents. The venae cavae near the heart were densely supplied, but there were few fibres with their more peripheral extensions. Some large veins (e.g. pulmonary, hepatic portal and superior mesenteric) had a few fibres with them, but veins of peripheral vascular beds had very few or no immunoreactive nerve fibres. Substance P-like immunoreactivity in vascular nerves was markedly reduced in guinea-pigs that were injected with capsaicin but was unaffected by the injection of 6-hydroxydopamine. It is concluded that the vascular substance P-immunoreactive nerves are likely to be of sensory origin.     

The effect of vascular origin, oxygen, and tumour necrosis factor alpha on trophoblast invasion of maternal arteries in vitro

Extravillous trophoblasts (EVTs) invade and remodel uterine spiral arteries. Regulatory factors may include inherent vessel susceptibility, local oxygen levels and tumour necrosis factor alpha (TNFalpha). We have used an in vitro model to investigate interstitial and endovascular invasion of myometrial spiral arteries from pregnant and non-pregnant uteri and also omental arteries. To model endovascular invasion, fluorescent-labelled EVTs were perfused into the lumen of these dissected vessels. For interstitial invasion, labelled EVTs were layered on top. Cultures were either maintained in 17% or 3% oxygen, or cultured with TNFalpha. The invasion of arteries from pregnant women occurred via both routes at 17% oxygen, with endovascular invasion more efficient than interstitial. In omental arteries and spiral arteries from non-pregnant women, endovascular invasion was limited. Endovascular and interstitial invasion were lower in all arteries at 3% oxygen. Typically, endovascular events were clustered, with an associated disruption in the adjacent endothelium and smooth muscle. A role for TNFalpha in limiting invasion was also supported. In conclusion, priming of uterine arteries may be necessary prior to EVT invasion. Oxygen is a sensitive regulator within this physiological model and increased invasion at higher pO2 may explain the homing of EVT to maternal arteries rather than veins. Adequate vascular transformation may therefore rely on a balance between vascular receptivity, oxygen partial pressure, and exposure to inflammatory mediators.     

Pulsatile Perfusion Bioreactor System for Durability Testing and Compliance Estimation of Tissue Engineered Vascular Grafts

The aim of the study was to design, construct, and test a bioreactor for the conditioning of tissue-engineered vascular grafts under physiological pressure, flow, and environmental conditions and up to supra-physiological pulse frequencies (5 Hz) as the first step towards durability testing. The system also allows the calculation of the compliance of vascular grafts as an indicator of tissue development. The system relies on the combination of a pulse-free pump and a linear magnetic actuator applying pressure pulses with controllable profile and frequency. The compliance estimation is based on the accurate measurement of the vessel’s diameter by means of an optical micrometre. Software-based interface enables the control of a magnetic actuator and data acquisition to monitor the conditions of the system. Porcine carotid arteries were tested in the bioreactor for up to 4 weeks at different pulse frequencies. The tissue was analysed by means of histology and immunohistochemistry. Physiological pressures (~80 and 120 mmHg for diastolic and systolic phase, respectively) were generated in the system at frequencies between 1 and 5 Hz. The environmental conditions within the bioreactor were monitored and online determination of the compliance of the arteries was achieved under sterile conditions. Conditioning of the grafts resulted in the abundant production of ECM proteins. In conclusion, we developed a bioreactor for the conditioning of tissue engineered vascular grafts under controlled pressure conditions. The system is suitable to perform durability tests at supra-physiological pulse rates and physiological pressure levels under continuous monitoring of environmental variables (pH, pO₂, pCO₂, and temperature) and compliance.     

改进构建后的全生物化组织工程血管的组织结构与生物力学特性

目的改进体外构建的生物化组织工程血管(TEBV),研究其生物力学特性,获得能承载生理血流力学作用的血管替代物。方法用酶消化法制备猪颈总动脉脱细胞支架,加压灌注结合散点注射种植犬胸主动脉平滑肌细胞(VSMC),用自制的血管自动旋转流体培养系统培养3周,随后再用加压灌注法种植犬胸主动脉内皮细胞(EC),继续培养至4周,取材做HE染色。光镜和电镜观察VSMC及EC在支架内的生长情况。用力学测试仪器检测TEBV的应力-应变关系、拉伸弹性回复率以及最大断裂强度和长度。结果在血管自动旋转流体培养系统,VSMC种植3周在中膜层已经大量均匀分布,EC种植7天后已形成连续完整的EC单层;而应用单独的加压灌注法VSMC种植3周时仍不能均匀分布,EC种植1周后仍分布不均匀,未能形成连续的EC单层。TEBV培养至第4周,中膜层有大量VSMC生长,内膜层则形成连续的EC单层;透射电镜下可见VSMC、EC亚微结构与生理状态的细胞结构相似,可见缝隙连接等细胞连接方式,VSMC可产生新的胶原蛋白。扫描电镜可见EC在支架上生长良好,细胞轮廓清晰,形成连续的单层。力学特性检测结果显示:TEBV的粘弹性、拉伸弹性回复率以及最大断裂强度均接近生理血管。结论血管自动旋转流体培养系统在脱细胞血管支架上联合种植VSMC和EC,有利于种子细胞在支架腔面和管壁内均匀生长,改进了TEBV的组织结构。改进构建的TEBV生物力学特性接近生理血管,将有利于TEBV更好地承载血流动力学的作用。     

Galanin-positive nerves of trigeminal origin innervate rat cerebral vessels

Galanin (GAL)-positive nerve fibers in rat cerebral vessels were demonstrated by immunohistochemistry, and their origin in the trigeminal ganglia and pathway in the nasociliary nerve to the vessels was shown by retrograde tracer technique and nerve transection. Some fibers in the vertebrobasilar system appear to originate in extracranial sources. With the antiserum used only few GAL fibers could be seen in the vessels, mostly in the vertebrobasilar system. In neonatally sympathectomized animals a rich network could be visualized in most pial arteries - still particularly in the vertebrobasilar system - probably as a result of a diminished competition for nerve growth factor. No vasomotor effect of GAL could be detected in isolated segments of pial arteries, neither in normal nor in sympathectomized animals, which rules out a direct postsynaptic effect on vascular tone. GAL did not display prejunctional modulatory action on the adrenergic nerves present in the vascular preparations. A sensory function of GAL is discussed.