scholarly journals Modifications to the classical rat aortic ring model to allow vascular degeneration studies

2021 ◽  
Vol 2 (1) ◽  
pp. 100281
Author(s):  
Guillaume Blot ◽  
Thérèse-Marie Sartoris ◽  
Florian Sennlaub ◽  
Xavier Guillonneau
Keyword(s):  
Aortic Ring ◽  
Ring Model ◽  
Rat Aortic Ring Model

Rat Aortic Ring Model to Assay Angiogenesis ex vivo

BIO-PROTOCOL ◽  
2015 ◽  
Vol 5 (20) ◽  
Author(s):  
Isabelle Ernens ◽  
B�n�dicte Lenoir ◽  
Yvan Devaux ◽  
Daniel Wagner
Keyword(s):  
Ex Vivo ◽  
Aortic Ring ◽  
Ring Model ◽  
Rat Aortic Ring Model

scholarly journals Purified Anthocyanin Supplementation Improves Endothelial Function via NO-cGMP Activation in Hypercholesterolemic Individuals

2011 ◽  
Vol 57 (11) ◽  
pp. 1524-1533 ◽  
Author(s):  
Yanna Zhu ◽  
Min Xia ◽  
Yan Yang ◽  
Fengqiong Liu ◽  
Zhongxia Li ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Hdl Cholesterol ◽  
Aortic Ring ◽  
Control Group ◽  
Short Term ◽  
Beneficial Effects ◽  
Ring Model ◽  
Vascular Adhesion ◽  
Rat Aortic Ring Model

BACKGROUND Anthocyanins have been shown to improve endothelial function in animal models. However, whether these compounds have similar beneficial effects in humans is largely unknown. METHODS In a short-term crossover study, 12 hypercholesterolemic individuals were given oral anthocyanins (320 mg) isolated from berries or placebo. Brachial artery flow-mediated dilation (FMD) was assessed before and after the intervention. In a long-term intervention trial (12 weeks), 150 hypercholesterolemic individuals were given anthocyanins (320 mg/day, n = 75) or placebo (n = 75), after which we measured FMD, plasma cGMP, and other serum biomarkers. Another short-term intervention was conducted in the presence of NO-cGMP inhibitors in 6 people and in a rat aortic ring model (n = 8). RESULTS Significant increases of FMD from 8.3% (0.6%) at baseline to 11.0% (0.8%) at 1 h and 10.1% (0.9%) at 2 h were observed after short-term anthocyanin consumption, concomitantly with increases of plasma anthocyanin concentrations (P < 0.05). In the study participants who received long-term anthocyanin intervention, compared with the control group, we observed significant increases in the FMD (28.4% vs 2.2%), cGMP (12.6% vs −1.2%), and HDL-cholesterol concentrations, but decreases in the serum soluble vascular adhesion molecule-1 and LDL cholesterol concentrations (P < 0.05). The changes in the cGMP and HDL cholesterol concentrations positively correlated with FMD in the anthocyanin group (P < 0.05). In the presence of NO-cGMP inhibitors, the effects of anthocyanin on endothelial function were abolished in human participants and in a rat aortic ring model. CONCLUSIONS Anthocyanin supplementation improves endothelium-dependent vasodilation in hypercholesterolemic individuals. This effect involves activation of the NO-cGMP signaling pathway, improvements in the serum lipid profile, and decreased inflammation.

scholarly journals B. anthracisedema toxin increases cAMP levels and inhibits phenylephrine-stimulated contraction in a rat aortic ring model

2013 ◽  
Vol 305 (2) ◽  
pp. H238-H250 ◽  
Author(s):  
Yan Li ◽  
Xizhong Cui ◽  
Steven B. Solomon ◽  
Kenneth Remy ◽  
Yvonne Fitz ◽  
...  
Keyword(s):  
Protective Antigen ◽  
Lethal Factor ◽  
Aortic Ring ◽  
Contractile Force ◽  
Host Cells ◽  
Sprague Dawley ◽  
Adenyl Cyclase Activity ◽  
Ring Model ◽  
Arterial Relaxation ◽  
Rat Aortic Ring Model

B. anthracis edema toxin (ET) and lethal toxin (LT) are each composed of protective antigen (PA), necessary for toxin uptake by host cells, and their respective toxic moieties, edema factor (EF) and lethal factor (LF). Although both toxins likely contribute to shock during infection, their mechanisms are unclear. To test whether ET and LT produce arterial relaxation, their effects on phenylephrine (PE)-stimulated contraction in a Sprague-Dawley rat aortic ring model were measured. Rings were prepared and connected to pressure transducers. Their viability was confirmed, and peak contraction with 60 mM KCl was determined. Compared with PA pretreatment (control, 60 min), ET pretreatment at concentrations similar to those noted in vivo decreased the mean (±SE) maximum contractile force (MCF; percent peak contraction) in rings generated during stimulation with increasing PE concentrations (96.2 ± 7.0 vs. 57.3 ± 9.1) and increased the estimated PE concentration producing half the MCF (EC50; 10−7M, 1.1 ± 0.3 vs. 3.7 ± 0.8, P ≤ 0.002). ET inhibition with PA-directed monoclonal antibodies, selective EF inhibition with adefovir, or removal of the ring endothelium inhibited the effects of ET on MCF and EC50( P ≤ 0.02). Consistent with its adenyl cyclase activity, ET increased tissue cAMP in endothelium-intact but not endothelium-denuded rings ( P < 0.0001 and 0.25, respectively). LT pretreatment, even in high concentrations, did not significantly decrease MCF or increase EC50(all P > 0.05). In rings precontracted with PE compared with posttreatment with PA (90 min), ET posttreatment produced progressive reductions in contractile force and increases in relaxation in endothelium-intact rings ( P < 0.0001) but not endothelium-denuded rings ( P = 0.51). Thus, ET may contribute to shock by producing arterial relaxation.

scholarly journals Green Synthesis of Silver Nanoparticles using Achillea biebersteinii Flower Extract and Its Anti-Angiogenic Properties in the Rat Aortic Ring Model

Molecules ◽  
2014 ◽  
Vol 19 (4) ◽  
pp. 4624-4634 ◽  
Author(s):  
Javad Baharara ◽  
Farideh Namvar ◽  
Tayebe Ramezani ◽  
Nasrin Hosseini ◽  
Rosfarizan Mohamad
Keyword(s):  
Silver Nanoparticles ◽  
Green Synthesis ◽  
Aortic Ring ◽  
Flower Extract ◽  
Ring Model ◽  
Achillea Biebersteinii ◽  
Rat Aortic Ring Model

scholarly journals QUANTIFICATION OF ANGIOGENESIS ON THE RAT AORTIC RING ASSAY

2011 ◽  
Vol 22 (1) ◽  
pp. 43 ◽  
Author(s):  
Silvia Blacher ◽  
Laetitia Devy ◽  
Agnes Noel ◽  
Jean-Michel Foidart
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Image Analysis ◽  
Growth Factor ◽  
Aortic Ring ◽  
Vascular Endothelial ◽  
Microvascular Network ◽  
Ring Model ◽  
Aortic Ring Assay ◽  
Endothelial Growth Factor ◽  
Rat Aortic Ring Model

Image analysis is used to quantify angiogenesis on the rat aortic ring model. This technique allows to determine: (1) the aortic ring area and factor shape; (2) the number of microvessels, the total number of branching, the maximal microvessel length and the number of microvessels in function of the distance to the aortic ring; (3) the total number of isolated fibroblast-like cells and the number of fibroblast-like cells in function of the distance to the aortic ring. We show that this method is suitable to quantify spontaneous angiogenesis as well as to analyse a complex microvascular network induced by vascular endothelial growth factor (VEGF).

scholarly journals Effects of Acrylamide-Induced Vasorelaxation and Neuromuscular Blockage: A Rodent Study

Toxics ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 117
Author(s):  
Wei-De Lin ◽  
Chu-Chyn Ou ◽  
Shih-Hao Hsiao ◽  
Chih-Han Chang ◽  
Fuu-Jen Tsai ◽  
...  
Keyword(s):  
Acetylcholine Receptor ◽  
Phrenic Nerve ◽  
Reproductive Toxicity ◽  
Aortic Ring ◽  
Laboratory Animals ◽  
Ring Model ◽  
Receptor Inhibition ◽  
Nos Inhibitors ◽  
Oxide Synthase ◽  
Rat Aortic Ring Model

Acrylamide (ACR), which is formed during the Maillard reaction, is used in various industrial processes. ACR accumulation in humans and laboratory animals results in genotoxicity, carcinogenicity, neurotoxicity, and reproductive toxicity. In this study, we investigated the mechanisms by which ACR may induce vasorelaxation and neuromuscular toxicity. Vasorelaxation was studied using an isolated rat aortic ring model. The aortic rings were divided into the following groups: with or without endothelium, with nitric oxide synthase (NOS) inhibition, with acetylcholine receptor inhibition, and with extracellular calcium inhibition. Changes in tension were used to indicate vasorelaxation. Neuromuscular toxicity was assessed using a phrenic nerve–diaphragm model. Changes in muscle contraction stimulated by the phrenic nerve were used to indicate neuromuscular toxicity. ACR induced the vasorelaxation of phenylephrine-precontracted aortic rings, which could be significantly attenuated by NOS inhibitors. The results of the phrenic nerve–diaphragm experiments revealed that ACR reduced muscle stimulation and contraction through nicotinic acetylcholine receptor (AChR). ACR-induced vasotoxicity was regulated by NOS through the aortic endothelium. Nicotinic AChR regulated ACR-induced neuromuscular blockage.

scholarly journals 4-Pyridinio-1,4-Dihydropyridines as Calcium Ion Transport Modulators: Antagonist, Agonist, and Dual Action

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Ilona Domracheva ◽  
Iveta Kanepe-Lapsa ◽  
Reinis Vilskersts ◽  
Imanta Bruvere ◽  
Egils Bisenieks ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Neuroblastoma Cell ◽  
Aortic Ring ◽  
Antagonistic Effect ◽  
Human Neuroblastoma Cell ◽  
Human Neuroblastoma ◽  
Ring Model ◽  
A7r5 Cells ◽  
Intracellular Ca ◽  
The Impact

A set of six new 4-pyridinio-1,4-dihydropyridine (1,4-DHP) compounds has been synthesized. The calcium channel modulating activity of these compounds was evaluated in an aorta vascular smooth muscle cell line (A7R5), in an isolated rat aortic ring model, and in human neuroblastoma cell lines (SH-SY5Y). The antagonistic effect of these 1,4-DHP was tested by modulating the impact of carbachol-dependent mobilization of intracellular Ca2+ in SH-SY5Y cells. The intracellular free Ca2+ concentration was measured in confluent monolayers of SH-SY5Y cells and A7R5 cells with the Ca2+-sensitive fluorescent indicator Fluo-4 NW. Only four compounds showed calcium channel blocking activity in SH-SY5Y and A7R5 cells as well as in the aortic ring model. Among them, compound 3 was the most active calcium channel antagonist, which had 3 times higher activity on carbachol-activated SH-SY5Y cells than amlodipine. Two of the compounds were inactive. Compound 4 had 9 times higher calcium agonist activity than the classic DHP calcium agonist Bay K8644. The intracellular mechanism for the action of compound 4 using inhibitor analysis was elucidated. Nicotinic as well as muscarinic receptors were not involved. Sarcoplasmic reticulum (ER) Ca2+ (SERCA) stores were not affected. Ryanodine receptors (RyRs), another class of intracellular Ca2+ releasing channels, participated in the agonist response evoked by compound 4. The electrooxidation data suggest that the studied compounds could serve as antioxidants in OS.

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