Rat Common Carotid Artery Research Articles

Simulated microgravity induces an inflammatory response in the common carotid artery of rats.

Post-spaceflight orthostatic intolerance is one of the most important adverse effects after exposure to space microgravity, and there are still no effective countermeasures. It has been considered that arterial remodeling may play an important role in the occurrence of post-spaceflight orthostatic intolerance, but the cellular mechanisms remain unknown. In this study, we investigated whether an inflammatory response exists in the common carotid artery of rats exposed to simulated microgravity. For this, Sprague-Dawley rats were subjected to 4 weeks of hindlimb unweighting to simulate microgravity. The expression levels of the adhesion molecules E-selectin and vascular cell adhesion molecule-1 (VCAM-1), and the cytokine monocyte chemoattractant protein-1 (MCP-1) in the common carotid artery of simulated microgravity rats were evaluated by immunohistochemical staining, quantitative RT-PCR, and Western blot analyses. The recruitment of monocytes in the common carotid artery of rats exposed to simulated microgravity was investigated by en face immunofluorescence staining and monocyte binding assays. Our results provided convincing evidence that there is an inflammatory response in the common carotid artery of rats exposed to simulated microgravity. Our work suggests that the inflammatory response may be a novel cellular mechanism that is responsible for the arterial remodeling that occurs during exposure to microgravity.

In Vivo Observation of the Hypo-echoic “Black Hole” Phenomenon in Rat Arterial Bloodstream: A Preliminary Study

The “black hole,” a hypo-echoic hole at the center of the bloodstream surrounded by a hyper-echoic zone in cross-sectional views, has been observed in ultrasound backscattering measurements of blood with red blood cell aggregation in in vitro studies. We investigated whether the phenomenon occurs in the in vivo arterial bloodstream of rats using a high-frequency ultrasound imaging system. Longitudinal and cross-sectional ultrasound images of the rat common carotid artery (CCA) and abdominal aorta were obtained using a 40-MHz ultrasound system. A high-frame-rate retrospective imaging mode was employed to precisely examine the dynamic changes in blood echogenicity in the arteries. When the imaging was performed with non-invasive scanning, blood echogenicity was very low in the CCA as compared with the surrounding tissues, exhibiting no hypo-echoic zone at the center of the vessel. Invasive imaging of the CCA by incising the skin and subcutaneous tissues at the imaging area provided clearer and brighter blood echo images, showing the “black hole” phenomenon near the center of the vessel in longitudinal view. The “black hole” was also observed in the abdominal aorta under direct imaging after laparotomy. The aortic “black hole” was clearly observed in both longitudinal and cross-sectional views. Although the “black hole” was always observed near the center of the arteries during the diastolic phase, it dissipated or was off-center along with the asymmetric arterial wall dilation at systole. In conclusion, we report the first in vivo observation of the hypo-echoic “black hole” caused by the radial variation of red blood cell aggregation in arterial bloodstream.

Mucin Covalently Bonded to Microfibers Improves the Patency of Vascular Grafts

Due to high incidence of vascular bypass procedures, an unmet need for suitable vessel replacements exists, especially for small-diameter (<6 mm) vascular grafts. Here, we developed a novel, bilayered, synthetic vascular graft of 1-mm diameter that consisted of a microfibrous luminal layer and a nanofibrous outer layer, which was tailored to possess the same mechanical property as native arteries. We then chemically modified the scaffold with mucin, a glycoprotein lubricant on the surface of epithelial tissues, by either passive adsorption or covalent bonding using the di-amino-poly(ethylene glycol) linker to microfibers. Under static and physiological flow conditions, conjugated mucin was more stable than adsorbed mucin on the surfaces. Mucin could slightly inhibit blood clotting, and mucin coating suppressed platelet adhesion on microfibrous scaffolds. In the rat common carotid artery anastomosis model, grafts with conjugated mucin, but not adsorbed mucin, exhibited excellent patency and higher cell infiltration into the graft walls. Mucin, which can be easily obtained from autologous sources, offers a novel method for improving the hemocompatibility and surface lubrication of vascular grafts and many other implants.

Correction

HomeCirculationVol. 128, No. 11Correction Free AccessCorrectionPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessCorrectionPDF/EPUBCorrection Originally published10 Sep 2013https://doi.org/10.1161/CIR.0b013e3182a8c0d6Circulation. 2013;128:e174This article corrects the followingInfusion of Light Chains From Patients With Cardiac Amyloidosis Causes Diastolic Dysfunction in Isolated Mouse HeartsAdventitial Cells Do Not Contribute to Neointimal Mass After Balloon Angioplasty of the Rat Common Carotid ArteryIn the articles by De Leon et al, “Adventitial Cells Do Not Contribute to Neointimal Mass After Balloon Angioplasty of the Rat Common Carotid Artery” (Circulation. 2001;104:1591–1593) and Liao et al, “Infusion of Light Chains From Patients With Cardiac Amyloidosis Causes Diastolic Dysfunction in Isolated Mouse Hearts” (Circulation. 2001;104:1594–1597), which published in the October 2, 2001 issue of the journal, the DOIs were missing for both articles. The DOIs are as follows:De Leon et al, “Adventitial Cells Do Not Contribute to Neointimal Mass After Balloon Angioplasty of the Rat Common Carotid Artery” (Circulation. 2001;104:1591–1593)DOI: 10.1161/01.cir.0000433836.90987.c6Liao et al, “Infusion of Light Chains From Patients With Cardiac Amyloidosis Causes Diastolic Dysfunction in Isolated Mouse Hearts” (Circulation. 2001;104:1594–1597)DOI: 10.1161/01.cir.0000433837.98610.85The current online versions of the manuscripts have been corrected. Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesInfusion of Light Chains From Patients With Cardiac Amyloidosis Causes Diastolic Dysfunction in Isolated Mouse HeartsRonglih Liao, et al. Circulation. 2001;104:1594-1597Adventitial Cells Do Not Contribute to Neointimal Mass After Balloon Angioplasty of the Rat Common Carotid ArteryHector De Leon, et al. Circulation. 2001;104:1591-1593 September 10, 2013Vol 128, Issue 11 Advertisement Article InformationMetrics © 2013 American Heart Association, Inc.https://doi.org/10.1161/CIR.0b013e3182a8c0d6 Originally publishedSeptember 10, 2013 PDF download Advertisement

High Spatial and Temporal Resolution Observations of Pulsatile Changes in Blood Echogenicity in the Common Carotid Artery of Rats

Previous studies have found that ultrasound backscatter from blood in vascular flow systems varies under pulsatile flow, with the maximum values occurring during the systolic period. This phenomenon is of particular interest in hemorheology because it is contrary to the well-known fact that red blood cell (RBC) aggregation, which determines the intensity of ultrasound backscatter from blood, decreases at a high systolic shear rate. In the present study, a rat model was used to provide basic information on the characteristics of blood echogenicity in arterial blood flow to investigate the phenomenon of RBC aggregation under pulsatile flow. Blood echogenicity in the common carotid arteries of rats was measured using a high-frequency ultrasound imaging system with a 40-MHz probe. The electrocardiography-based kilohertz visualization reconstruction technique was employed to obtain high-temporal-resolution and high-spatial-resolution time-course B-mode cross-sectional and longitudinal images of the vessel. The experimental results indicate that blood echogenicity in rat carotid arteries varies during a cardiac cycle. Blood echogenicity tends to decrease during early systole and reaches its peak during late systole, followed by a slow decline thereafter. The time delay of the echogenicity peak from peak systole in the present results is the main difference from previous in vitro and in vivo observations of backscattering peaks during early systole, which may be caused by the very rapid heart rates and low RBC aggregation tendency of rats compared with humans and other mammalian species. The present study may provide useful information elucidating the characteristics of RBC aggregation in arterial blood flow.

A ginkgo biloba extract promotes proliferation of endogenous neural stem cells in vascular dementia rats.

The ginkgo biloba extract EGb761 improves memory loss and cognitive impairments in patients with senile dementia. It also promotes proliferation of neural stem cells in the subventricular zone in Parkinson's disease model mice and in the hippocampal zone of young epileptic rats. However, it remains unclear whether EGb761 enhances proliferation of endogenous neural stem cells in the brain of rats with vascular dementia. In this study, a vascular dementia model was established by repeatedly clipping and reperfusing the bilateral common carotid arteries of rats in combination with an intraperitoneal injection of a sodium nitroprusside solution. Seven days after establishing the model, rats were intragastrically given EGb761 at 50 mg/kg per day. Learning and memory abilities were assessed using the Morris water maze and proliferation of endogenous neural stem cells in the subventricular zone and dentate gyrus were labeled by 5-bromo-2-deoxyuridine immunofluorescence in all rats at 15 days, and 1, 2, and 4 months after model establishment. The escape latencies in Morris water maze tests of rats with vascular dementia after EGb761 treatment were significantly shorter than the model group. Immunofluorescence staining showed that the number and proliferation of 5-bromo-2-deoxyuridine-positive cells in the subventricular zone and dentate gyrus of the EGb761-treated group were significantly higher than in the model group. These experimental findings suggest that EGb761 enhances proliferation of neural stem cells in the subventricular zone and dentate gyrus, and significantly improves learning and memory in rats with vascular dementia.

Influence of Hypoxia on Endothelium-Derived NO-Mediated Relaxation in Rat Carotid, Mesenteric and Iliac Arteries

Individual vascular beds exhibit differences in vascular reactivity. The present study examined the influence of hypoxia on endothelium-dependent, especially nitric oxide (NO)-mediated, relaxation in the isolated rat common carotid, superior mesenteric and external iliac arteries. Hypoxia for 1 and 3 h had no effects on the relaxations caused by acetylcholine (ACh) and sodium nitroprusside (SNP) in common carotid and external iliac arteries. In addition, NO synthase inhibitor N^G-nitro-<smlcap>L</smlcap>-arginine (<smlcap>L</smlcap>-NA, 10 μmol/l)-resistant, endothelium-dependent relaxations by ACh were also unaffected by hypoxia in these arteries. On the other hand, ACh-induced relaxation in superior mesenteric arteries was significantly impaired by exposure to hypoxia, while this condition did not affect the relaxation induced by SNP or ACh in the presence of <smlcap>L</smlcap>-NA. This impairment was partially prevented by treatment with tempol (3 mmol/l), a superoxide scavenger. These findings demonstrate a marked heterogeneity in response to hypoxia in rat arteries. Briefly, acute hypoxia induces impairment of endothelium-derived NO-mediated relaxation through the decrease in its bioavailability in the superior mesenteric, but not in common carotid or external iliac, arteries. Furthermore, superoxide seems to be one causal factor responsible for the undesirable effect of hypoxia.

Effects of diabetes and vascular occlusion on adenosine-induced relaxant response of rat common carotid artery

The aim of this study was to investigate effect of adenosine on isolated rat common carotid artery (CA) submitted to occlusion in non-diabetic or diabetic animals, and to determine whether endothelium denudation or potassium conductance block affects adenosine action. Experiments were conducted on Wistar rat CA with or without endothelium. Diabetes was induced by alloxan. Occlusion of CA was performed in randomly selected non-diabetic or diabetic animals anesthetized with urethane. Thus, experiments were performed in four groups of rats: non-operated (control) animals without or with diabetes and operated animals submitted to the occlusion of CA without or with diabetes. Concentration-response curves for adenosine were obtained in a cumulative fashion on precontracted arteries. Adenosine produced concentration-dependent and endothelium-independent relaxation of CA with comparable maximal effects in all groups. Analysis of pEC50 values showed that responsiveness of CA decreased in following order: [diabetes (-) / occlusion (-)] = [diabetes (-) / occlusion (+)] > [diabetes (+) / occlusion (-)] > [diabetes (+) / occlusion (+)]. In the presence of high K(+) maximal relaxant response of CA from non-operated rats without diabetes was reduced. The recorded inhibition was even stronger in animals subjected to CA occlusion. Conversely, in non-operated diabetic animals obtained reduction of adenosine effect was less pronounced in regard to non-diabetic rats. Adenosine produced equi-effective endothelium-independent relaxation of CA in all groups. Pharmacological potency of adenosine was reduced in diabetic animals solely, but even more in diabetic rats submitted to CA occlusion. The enhanced potassium transmembrane flow has certain protective role on adenosine-induced action in occluded CA from non-diabetic rats. Conversely, diabetes solely inhibited adenosine-evoked cascade connected to increased potassium conductance.

Suppression of JAK2/STAT3 Signaling Reduces End-to-End Arterial Anastomosis Induced Cell Proliferation in Common Carotid Arteries of Rats

BackgroundJAK2/STAT3 pathway was reported to play an essential role in the neointima formation after vascular intima injury. However, little is known regarding this pathway to the whole layer injury after end-to-end arterial anastomosis (AA). Here, we investigated the role of JAK2/STAT3 pathway in common carotid arterial (CCA) anastomosis-induced cell proliferation, phenotypic change of vascular smooth muscle cells (VSMCs) and re-endothelialization.MethodsCCAs of adult male Wistar rats were resected at 3, 7, 14, and 30 days after end-to-end CCA anastomosis. Activation of JAK2/STAT3 pathway was detected by Western blotting and Immunofluorescence, and expression of proliferating cell nuclear antigen (PCNA) was detected by Q-PCR and Western blotting. Under the treatment with AG490 (a JAK2 inhibitor), protein levels of JAK2, STAT3 and PCNA, morphological changes of artery, phenotypic change of VSMCs, and re-endothelialization were measured by Western blotting, H&E, Q-PCR, and Evans blue staining respectively.ResultsThe protein levels of p-JAK2, p-STAT3, and PCNA were up-regulated, peaked on the 7th day in the vessel wall after AA. AG490 down-regulated the levels of p-JAK2, p-STAT3, and PCNA on the 7th-day-group, resulting in reduced vessel wall proliferation on the 7th and 14th day after AA. Besides, AG490 switched the phenotypic change of VSMCs after AA representing inhibited mRNA levels of synthetic phase markers (osteopoitin and SMemb) and up-regulated contractile phase markers (ASMA, SM2 and SM22α). Furthermore, AG490 did not affect the re-endothelialization process on all indicated time points after AA (the 3rd, 7th, 14th, and 30th day).ConclusionOur study indicated that JAK2/STAT3 signaling pathway played an important role on cell proliferation of the injured vessel wall, and probably a promising target for the exploration of drugs increasing the patency or reducing the vascular narrowness after AA.

The Effect of Short-term Intra-arterial Delivery of Paclitaxel on Neointimal Hyperplasia and the Local Thrombotic Environment after Angioplasty

To evaluate the effects of short-term intra-arterial delivery of paclitaxel on neointimal hyperplasia and the local thrombotic environment after angioplasty. An experimental common carotid artery injury model was established in 60 rats, which were divided into experimental groups (40 rats) and controls (20 rats). Local intra-arterial administration of paclitaxel was applied at 2 doses (90 and 180μg/30μl), and the effects of short-term delivery of paclitaxel on neointimal hyperplasia and the expression of tissue factor (TF), plasminogen activator inhibitor-1 (PAI-1) and tissue-type plasminogen activator (t-PA) were evaluated at days 15 and 30 by hematoxylin and eosin staining and immunohistochemistry. At 15 and 30days after injury, neointimal thickness and area, the ratio of intimal area to medial area and the stenotic rate were all significantly decreased in the group provided the high concentrations (180μg/30μl) of paclitaxel for 2min or 10min and in the group provided the low concentration (90μg/30μl) of paclitaxel for 10min (p<0.05). At 30days after injury, there were no significant changes in TF expression among all experimental groups. PAI-1 expression increased in the neointima of the high concentration 10min group (p<0.05), while t-PA expression decreased in the neointima of the high concentration 2min group (p<0.05). In the rat common carotid artery injury model, the short-term delivery of paclitaxel could effectively inhibit neointimal hyperplasia in the long term, with very little influence on the local expression of TF and PAI-1.

The effect of Gαi2 on neuronal apoptosis in cerebral ischemia-reperfusion injury model of rats

Objective To discuss the levels of inhibitory protein Gαi2 （Gcxi2） in hippocampus of brain and the effects of Gαi2 on neuronal intracellular Ca^2＋ level in cerebral ischemia reperfusion injury model of rats. Methods Ninety SD rats were randomly （ random number） assigned to sham group （ n = 30 ）, ischemic - reperfusion （IR） group （ n = 30）, Pertussis toxin （PT） group （ n = 30）. The blood flow of right common carotid artery of rat was blocked for 90 mix to make ischemia reperfusion model. The levels of Gαi2 in hippocampus was assayed by immunohistochemistry and Western blotting after ischemia reperfu - sion for 6, 12, 24 h in each group. The average fluorescence values of intracellular Ca^2＋ levels in hippocampus of rats in three groups were detected by using Flow CytoMeter （FCM）. Neuronal cell apoptosis was measured by TUNEL. Results After restoration of middle cerebral artery blood flow for different lengths of time, the levels of hippocampus God2 and Ca2 ＋ levels in IR group were significantly higher than those in Sham group （P 〈0. 01 ）. The hippocampus Ca^2＋ levels in PT group were higher than those in IR group （P 〈0. 01 ） . The apoptotic rates of neurons in PT group were lower than those in IR group （P 〈 0. 05 ）. Conclusions The level of Gαi2 in cerebral ischemia reperfusion injury model was increased. Gαi2 might reduce the calcium ion concentration of neurons after cerebral ischemia and reduce the neuronal cell apoptosis in this model. Gαi2 might play a role in protecting neuron from cerebral ischemia reperfusion Key words: Gαi2; Cerebral isehemia reperfusion injury; Hippocampus; Pertussis toxin; Apoptosis ; Neuron ; Ca^2＋ ; Death

The effect of 2,3,4′,5-tetrahydroxystilbene-2-0-β-d glucoside on neointima formation in a rat artery balloon injury model and its possible mechanisms

2,3,4′,5-tetrahydroxystilbene-2-0-β-d glucoside (TSG) has been recognized to suppress the proliferation of vascular smooth muscle cells (VSMCs). The aim of the present study was to determine whether TSG inhibits neointimal hyperplasia in a rat carotid arterial balloon injury model. Balloon injury was induced in the left common carotid artery of rats. TSG (30, 60, 120mg/kg/day) was treated from 3 days prior to, until 14 days after the induction of balloon injury. The ratio of intima-to-media was significantly reduced in the TSG-treated rats at 14 days after the induction of injury, which was associated with reduced expressions of proliferating cell nuclear antigen (PCNA), α-smooth muscle actin (α-SMA) and platelet-derived growth factor-BB (PDGF-BB), as markers of VSMCs proliferation and migration. Additionally, TSG significantly inhibited PDGF-BB induced cell migration in cultured VSMCs. Furthermore, we explored the underlying mechanisms for such effects of TSG. The result showed that TSG markedly reduced balloon injury-induced AKT, extracellular signal-regulated kinase (ERK1/2) and nuclear factor kappaB (NF-κB) activation as well as mRNA expressions of c-myc, c-fos and c-jun, which is important signal pathway for VSMCs proliferation. And in both vivo and vitro model, TSG markedly regulated matrix metalloproteinase-2, 9 expressions and collagen I, III expressions, which are key factors in extracellular matrix for VSMCs migration. These results suggest that the anti-proliferative and anti-migrative effects of TSG on VSMCs could help to explain the beneficial effects of TSG on neointima hyperplasia induced by balloon injury.

Training a Sophisticated Microsurgical Technique: Interposition of External Jugular Vein Graft in the Common Carotid Artery in Rats

Neointimal hyperplasia is one the primary causes of stenosis in arterialized veins that are of great importance in arterial coronary bypass surgery, in peripheral arterial bypass surgery as well as in arteriovenous fistulas.(1-5) The experimental procedure of vein graft interposition in the common carotid artery by using the cuff-technique has been applied in several research projects to examine the aetiology of neointimal hyperplasia and therapeutic options to address it. (6-8) The cuff prevents vessel anastomotic remodeling and induces turbulence within the graft and thereby the development of neointimal hyperplasia. Using the superior caval vein graft is an established small-animal model for venous arterialization experiment.(9-11) This current protocol refers to an established jugular vein graft interposition technique first described by Zou et al., (9) as well as others.(12-14) Nevertheless, these cited small animal protocols are complicated. To simplify the procedure and to minimize the number of experimental animals needed, a detailed operation protocol by video training is presented. This video should help the novice surgeon to learn both the cuff-technique and the vein graft interposition. Hereby, the right external jugular vein was grafted in cuff-technique in the common carotid artery of 21 female Sprague Dawley rats categorized in three equal groups that were sacrificed on day 21, 42 and 84, respectively. Notably, no donor animals were needed, because auto-transplantations were performed. The survival rate was 100 % at the time point of sacrifice. In addition, the graft patency rate was 60 % for the first 10 operated animals and 82 % for the remaining 11 animals. The blood flow at the time of sacrifice was 8±3 ml/min. In conclusion, this surgical protocol considerably simplifies, optimizes and standardizes this complicated procedure. It gives novice surgeons easy, step-by-step instruction, explaining possible pitfalls, thereby helping them to gain expertise fast and avoid useless sacrifice of experimental animals.

Training a Sophisticated Microsurgical Technique: Interposition of External Jugular Vein Graft in the Common Carotid Artery in Rats

Training a Sophisticated Microsurgical Technique: Interposition of External Jugular Vein Graft in the Common Carotid Artery in Rats

Alloxan-induced diabetes alters rat common carotid artery response to adenosine

Background It is well established that diabetes mellitus represents an important risk factor for endothelial dysfunction and associated cardiovascular events. Accordingly, vascular responsiveness of different isolated blood vessels was shown to be altered in experimental diabetes. The aim of this study was to investigate the effect of adenosine on intact or denuded isolated rat common carotid arteries obtained from healthy or diabetic rats.

Mechanism Underlying the Protective Effect of Glycine in Energetic Disturbances in Brain Tissues under Hypoxic Conditions

Glycine stabilizes energetics of brain mitochondria under conditions of brain hypoxia in vivo modeled by ligation of the common carotid artery in rats. Hypoxia reduced respiratory control in brain cortex mitochondria from 7.7 ± 0.5 to 4.5 ± 0.3. Preliminary oral administration of glycine almost completely prevented this decrease. In both in vitro models of hypoxia, similar phosphorylation disturbances were detected in both cortical slices and isolated brain mitochondria; they were effectively prevented by glycine. Hypoxia activates H(2)O(2) generation in mitochondrial suspension. The process is significantly reduced in the presence of 5 mM glycine. It is concluded that both in the model of hypoxia in vivo and during in vitro modeling of hypoxia in cortical slices and mitochondria, glycine acts as a protector inhibiting generation of reactive oxygen species in mitochondria and preventing energetics disturbances in brain mitochondria.

Effect of erythropoietin (EPO) on plasticity of nervous synapse in CA1 region of hippocampal of vascular dementia (VaD) rats

The effects of erythropoietin (EPO) on plasticity of nervous synapse in CA1 region of hippocampal of vascular dementia (VaD) rats were studied. The Wistar rats reaching standard were randomly divided into three groups: Sham control group, VaD group, VaD + EPO injection treatment (E) group. The bilateral common carotid arteries of rats were permanently ligated to establish VaD model. Special study and memory were observed by Y-maze test. The expressions relative rate of MAP-2 and SYN in CA1 region of hippocampus at different time were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Immunohistochemistry (ICH). 4, 8 and 12 weeks after operation, there were obvious decrease in MAP-2 and SYN expression in both VaD and E groups, while it was much more for VaD group. EPO could comparatively increase the MAP-2 and SYN protein and mRNA expression in the hippocampal CA1 region of VaD rats. These results suggested that EPO might develop its improvement by regulating the plasticity of nervous synapse, which were in terms of increasing MAP-2 and SYN protein and mRNA expression in the CA1 region of hippocampal of VaD rats. Key words: Erythropoietin, vascular dementia, nervous synapse, MAP-2, SYN.

Heparin-Modified Small-Diameter Nanofibrous Vascular Grafts

Due to high incidence of vascular bypass procedures, an unmet need for suitable vessel replacements exists, especially for small-diameter vascular grafts. Here we produced 1-mm diameter vascular grafts with nanofibrous structure via electrospinning, and successfully modified the nanofibers by the conjugation of heparin using di-amino-poly(ethylene glycol) (PEG) as a linker. Antithrombogenic activity of these heparin-modified scaffolds was confirmed in vitro. After 1 month implantation using a rat common carotid artery bypass model, heparin-modified grafts exhibited 85.7% patency, versus 57.1% patency of PEGylated grafts and 42.9% patency of untreated grafts. Post-explant analysis of patent grafts showed complete endothelialization of the lumen and neovascularization around the graft. Smooth muscle cells were found in the surrounding neo-tissue. In addition, greater cell infiltration was observed in heparin-modified grafts. These findings suggest heparin modification may play multiple roles in the function and remodeling of nanofibrous vascular grafts, by preventing thrombosis and maintaining patency, and by promoting cell infiltration into the three-dimensional nanofibrous structure for remodeling.

Novel nanocomposite stent coating releasing resveratrol and quercetin reduces neointimal hyperplasia and promotes re-endothelialization

Late-term thrombosis associated with drug-eluting stents may be due to the non-selective actions of antimitogenic drugs on endothelial cells, leading to delayed vascular healing after stenting angioplasty. Currently, there is a need for stent-based therapies that can both attenuate neointimal hyperplasia and promote re-endothelialization. The aim of this study was to compare the effects of a resveratrol (R)- and quercetin (Q)-eluting stent with that of a bare metal stent (BMS) on neointimal hyperplasia and re-endothelialization in a rat model of arterial angioplasty and stenting. Miniature stents (2.5×1.25mm) were sprayed with nanocomposite coatings containing two concentrations of R:Q (50:25μg/cm2 (RQ1) or 150:75μg/cm2 (RQ2)). The stents were deployed into the common carotid artery of rats and their impact on vascular remodeling was compared to that of BMS. Luminal stenosis in arteries stented with RQ2-eluting stents was reduced by 64.6% (p<0.05) compared to arteries stented with BMS. Accompanying this effect was a 59.8% reduction in macrophage infiltration (p<0.05). There were no differences found between RQ1 and BMS. Finally, the RQ2-coated stent accelerated re-endothelialization by 50% compared with BMS (p<0.05). Thus, compared with BMS, local delivery of R and Q from a stent platform significantly reduced in-stent stenosis, while promoting re-endothelialization. These data suggest that R and Q may be favorable candidates for novel stent coatings, potentially reducing the risk of late thrombosis associated with drug-eluting stents.

Early monitoring of cerebral hypoperfusion in rats by laser speckle imaging and functional photoacoustic microscopy

Because cerebral hypoperfusion brings damage to the brain, prevention of cerebrovascular diseases correlative to hypoperfusion by studying animal models makes great sense. Since complicated cerebrovascular adaptive changes in hypoperfusion could not be revealed only by cerebral blood flow (CBF) velocity imaging, we performed multi-parameter imaging by combining laser speckle imaging and functional photoacoustic microscopy. The changes in CBF, hemoglobin oxygen saturation (SO(2)), and total hemoglobin concentration (HbT) in single blood vessels of ipsilateral cortex were observed during transient cerebral hypoperfusion by ligating the unilateral common carotid artery in rats. CBF, SO(2), and HbT, respectively, decreased to 37 ± 3%, 71 ± 7.5%, and 92 ± 1.3% of baseline in 6 s immediately after occlusion, and then recovered to 77 ± 4.8%, 84 ± 8%, and 96 ± 2% of baseline in 60 s. These parameters presented the decrease with different degree and the following recovery over time after ligation, the recovery of SO(2) lagged behind those of CBF and HbT, which had the similar response. The results demonstrated that complete monitoring of both cerebral hemodynamic response and oxygen metabolic changes occurred at the earliest period of cerebral hypoperfusion was possible by using the two image modalities with high temporal and spatial resolution.