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Intact Endothelium (intact + endothelium)
Selected AbstractsComparison of Endovenous Radiofrequency Versus 810 nm Diode Laser Occlusion of Large Veins in an Animal ModelDERMATOLOGIC SURGERY, Issue 1 2002Robert A. Weiss MDArticle first published online: 27 FEB 200 background. Endovenous occlusion using radiofrequency (RF) energy has been shown to be effective for the elimination of sapheno-femoral reflux and subsequent elimination of varicose veins. Recently, endovenous laser occlusion has been introduced with initial clinical reports indicating effective treatment for varicose veins. However, in our practice we note increased peri-operative hematoma and tenderness with the laser. Little is known regarding the mechanism of action of this new laser vein therapy. objective. To better understand the mechanism of action of endovenous laser vs. the endovenous RF procedure in the jugular vein of the goat model. methods. A bilateral comparison was performed using 810 nm diode laser transmitted by a bare-tipped optical fiber vs. the RF delivery by engineered electrodes with a temperature feedback loop using a thermocouple (Closure procedure) in three goat jugular veins. Immediate and one-week results were studied radiographically and histologically. Temperature measurements during laser treatment were performed by using an array of up to five thermocouples, spaced 2 mm apart, placed adjacent to a laser fiber tip during goat jugular vein treatment. results. Immediate findings showed that 100% of the laser-treated veins showed perforations by histologic examination and immediate contrast fluoroscopy. The RF-treated side showed immediate constriction with maintenance of contrast material within the vein lumen and no perforations. The difference in acute vein shrinkage was also dramatic as laser treatments resulted in vein shrinkage of 26%, while RF-treated veins showed a 77% acute reduction in diameter. At one week, extravasated blood that leaked into the surrounding tissue of laser treated veins acutely, continued to occupy space and impinge on surrounding structures including nerves. For the laser treatment, the highest average temperature was 729°C (peak temperature 1334°C) observed flush with the laser fiber tip, while the temperature feedback mechanism of the RF method maintains temperatures at the electrodes of 85°C. conclusion. Vein perforations, extremely high intravascular temperatures, failure to cause significant collagen shrinkage, and intact endothelium in an animal model justify a closer look at the human clinical application of the 810 nm endovenous laser technique. Extravasated blood impinging on adjacent structures may theoretically lead to increased peri-operative hematoma and tenderness. Further study and clinical investigation is warranted. [source] Liver sinusoidal endothelial cells and acute non-oxidative hepatic injury induced by Pseudomonas aeruginosa pyocyaninINTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 6 2008Rajkumar Cheluvappa Summary The liver sinusoidal endothelial cell (LSEC) is damaged by many toxins, including oxidants and bacterial toxins. Any effect on LSECs of the Pseudomonas aeruginosa virulence factor, pyocyanin, may be relevant for systemic pseudomonal infections and liver transplantation. In this study, the effects of pyocyanin on in vivo rat livers and isolated LSECs were assessed using electron microscopy, immunohistochemistry and biochemistry. In particular, the effect on fenestrations, a crucial morphological aspect of LSECs was assessed. Pyocyanin treatment induced a dose-dependent reduction in fenestrations in isolated LSECs. In the intact liver, intraportal injection of pyocyanin (11.9 ,M in blood) was associated with a reduction in endothelial porosity from 3.4 ± 0.2% (n = 5) to 1.3 ± 0.1% (n = 7) within 30 min. There were decreases in both diameter and frequency of fenestrations in the intact endothelium. There was also a decrease in endothelial thickness from 175.8 ± 5.8 to 156.5 ± 4.0 nm, an endothelial pathology finding previously unreported. Hepatocyte ultrastructure, liver function tests and immunohistochemical markers of oxidative stress (3-nitrotyrosine and malondialdehyde) were not affected. Pyocyanin induces significant ultrastructural changes in the LSEC in the absence of immunohistochemical evidence of oxidative stress or hepatocyte injury pointing to a novel mechanism for pyocyanin pathogenesis. [source] A Mechanism of Vasodilatory Action of Polyamines and Acetylpolyamines: Possible Involvement of their Ca2+ Antagonistic PropertiesJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 6 2000CHANG-SEON MYUNG Polyamines, a class of low-molecular weight organic polycations, have been shown to produce relaxing effects in vascular smooth muscles, although the mechanism has not been carefully examined. In this study, the mechanism of vascular action of polyamines and their metabolites, acetylpolyamines, was pharmacologically examined in the rabbit isolated thoracic aorta focusing on an endothelium-dependent component of vasodilatation and Ca2+ influx through plasma membrane channels. Both polyamines and acetylpolyamines (except N1 -acetylputrescine, which produced no response or very slight contraction) caused concentration-dependent relaxation in pre-constricted aortic rings containing an intact endothelium. Aortic rings denuded of endothelium were also responsive to both polyamines and acetylpolyamines. Inhibitors of nitric oxide (reduced haemoglobin and N, -nitro- l -arginine methyl ester), vasodilator prostaglandins (indomethacin) and guanylyl cyclase (methylene blue) did not affect the relaxation induced by both polyamines and acetylpolyamines in either endothelium-intact or -denuded aortic rings. Both polyamines and acetylpolyamines inhibited the concentration-dependent contraction for phenylephrine and K+. The Ca2+ agonist Bay K 8644 induced concentration-dependent contraction in segments of rabbit aorta partially depolarized with 15 mm KCl, and both polyamines and acetylpolyamines relaxed the Bay K 8644-induced contraction in a concentration-dependent manner. Interestingly, both polyamines and acetylpolyamines also decreased contractions evoked by the Ca2+ ionophore A23187. The concentration-response curve to exogenous Ca2+ in K+ -depolarization medium (K+ = 120 mm) was shifted to the right by both polyamines and acetylpolyamines. The response elicited by Ca2+ was increased by Bay K 8644 (10,6m), and this potentiation was also inhibited by both polyamines and acetylpolyamines. The results indicate that both polyamines and acetylpolyamines can induce vasorelaxation of rabbit thoracic aorta by an endothelium-independent mechanism in-vitro and relax vascular smooth muscle by acting at the plasma membrane level, decreasing the influx of Ca2+. Therefore, polyamines and acetylpolyamines may have Ca2+ antagonistic properties which may, in part, be involved in the mechanism of rabbit aortic vascular smooth muscle relaxation. [source] Effect of ropivacaine on endothelium-dependent phenylephrine-induced contraction in guinea pig aortaACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 10 2007P. L. Lin Background:, Previous studies have shown that ropivacaine has biphasic vascular effects, causing vasoconstriction at low concentrations and vasorelaxation at high concentrations. This study was designed to examine the role of the endothelium during accidental intravascular absorption of ropivacaine, and to elucidate the mechanisms responsible. Methods:, Isolated guinea pig aortic rings were suspended for isometric tension recording. The effects of ropivacaine on endothelium-intact and endothelium-denuded aortic rings were assessed. Endothelium-intact aortic rings were pre-contracted with phenylephrine before being exposed to ropivacaine and acetylcholine, in order to generate and compare concentration,response curves. In the absence and presence of yohimbine, propranolol, atropine, indometacin, NG -nitro- l -arginine methyl ester (l -NAME), 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) or methylene blue, the contractile response induced by ropivacaine was assessed on endothelium-intact aortic rings pre-contracted with phenylephrine. Results:, Ropivacaine (3 × 10,4 to 10,2 mol/l) produced vasoconstriction in endothelium-denuded aortic rings, whereas no such response was observed in aortic rings with intact endothelium. In phenylephrine pre-contracted intact aortic rings, ropivacaine induced a greater degree of vasorelaxation than did acetylcholine. Yohimbine, propranolol and atropine all failed to affect the relaxation responses induced by ropivacaine. However, pre-treatment with indometacin (cyclo-oxygenase inhibitor), l -NAME (nitric oxide synthase inhibitor), methylene blue (soluble guanylyl cyclase inhibitor) or ODQ (soluble guanylyl cyclase inhibitor), significantly decreased the ropivacaine-induced relaxation of endothelium-intact aortic rings (3 × 10,4 to 10,2 mol/l). Conclusions:, Ropivacaine elicits an endothelium-dependent vasorelaxation in phenylephrine pre-contracted aortic rings via the nitric oxide,cyclic guanosine 3,,5,-monophosphate pathway and the prostaglandin system. [source] Ischemia,Reperfusion Impairs Ascending Vasodilation in Feed Arteries of Hamster Skeletal MuscleMICROCIRCULATION, Issue 7 2005MIRIAM C. J. DE WITH ABSTRACT Objective: Vasodilation originating within the microcirculation ascends into proximal feed arteries during muscle contraction to attain peak levels of muscle blood flow. Ascending vasodilation (AVD) requires an intact endothelium, as does conducted vasodilation in response to acetylcholine (ACh). Whereas ischemia,reperfusion (I-R) can affect endothelial cell function, the effect of I-R on AVD is unknown. The authors tested the hypothesis that I-R (1h,1h) would impair AVD. Methods: Using the retractor muscle of anesthetized hamsters, contractions were evoked using field stimulation (200 ms at 40 Hz every 2 s for 1 min) and ACh was delivered using microiontophoresis (1 ,m tip, 500,4000 ms pulse at 800 nA). Feed artery responses were monitored 500,1500 ,m upstream. Results: Neither resting (51 ± 4 ,m) nor maximal diameter (81 ± 5 ,m; 10 ,m sodium nitroprusside) following I-R (n = 8) were different from time-matched controls (n = 10). With peak active tension of 23 ± 4 mN · mm,2, control AVD was 26 ± 2 ,m. Following I-R, active tension fell by 48% (p < .05) and AVD by 57% (p < .05). Stimulation at 70 Hz restored active tension but AVD remained depressed by nearly half (p < .05), as did local and conducted responses to ACh. Nevertheless, control responses to 500 ms ACh were restored by increasing stimulus duration to 4000 ms. Conclusions: Ischemia,reperfusion impairs the initiation of feed artery dilation with muscle contraction and with ACh while conduction along the vessel wall is preserved. Respective components of endothelial cell signaling events may differ in their susceptibility to I-R. [source] Interactions of Platelets with Subendothelium and EndotheliumMICROCIRCULATION, Issue 3 2005JUNMEI CHEN PhD ABSTRACT In this review, the authors summarize how platelets interact with subendothelium when the vessel wall is damaged or with intact endothelium in the inflammatory state. When subendothelium is exposed to rapidly flowing blood upon vessel damage, platelets adhere rapidly to the exposed surface, decelerate, and aggregate to arrest bleeding. Under high shear stress, such as is found in the microcirculation, the interaction between subendothelial von Willebrand factor (VWF) and its platelet receptor, glycoprotein (GP) Ib-IX-V, is required to slow down platelets and allow the platelet collagen receptors ,2,1 and GP VI to bind to collagen. GP VI and ,2,1 play important roles to activate platelets in the early stage and work with GP Ib-IX-V to fully activate platelets to form thrombi. GP Ib-IX-V and GP VI employ similar signaling pathways for platelet activation and the signals from both receptors are down-modulated by PECAM-1 (platelet,endothelial,cell adhesion molecule 1) to prevent unnecessary platelet activation under high shear. During inflammatory states, intact endothelial cells release VWF and P-selectin from their Weibel-Palade bodies. Both molecules are ligands for GP Ib-IX-V. The newly released VWF is larger and stickier than the form normally found in plasma and binds platelets spontaneously. Normally, VWF is processed by proteolysis by the plasma metalloprotease ADAMTS-13. Failure of this processing results in the microvascular thrombotic disorder thrombotic thrombocytopenic purpura. In this review, the authors also use available crystal structures of platelet receptors and ligands to explain the details of their interactions. [source] Comparison of the Healing Mechanisms of Myocardial Lesions Induced by Dry Radiofrequency and Microwave Epicardial AblationPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 3 2006ROSA HENRIQUES DE GOUVEIA Background: Histological assessment of the evolution of lesions induced on a pig's left atrium by microwave (MW) epicardial applications and comparison with dry radiofrequency (RF) lesions. Methods: MW (40 W, 40 seconds) and dry RF (80°C, 2 minutes) were epicardially applied on nine pigs' left atrium. Samples were procured following application (n = 2), at day 3 (n = 2), day 7 (n = 2), day 14 (n = 2), and at 1 month (n = 1). They were fixed in formalin, embedded in paraffin, sectioned (2 ,), stained with histochemical dyes, immunomarked, and histologically analyzed. Results: Histological features of acute stage MW lesion are interstitial hemorrhage, adipose, and muscular tissues' coagulation necrosis, thrombosis of myocardial interstitium small vessels at damaged and optically undamaged areas, epicardial coronary branches, and endocardial parietal thrombosis. Day 3,lymphohistiocytic infiltration (lysosyme+) highlights lesion limits. Day 7,lymphohistiocytic infiltration increases, multi-nucleated giant cells appear surrounding/fagocyting necrotic tissue. Neovessels and scarce myofibroblasts appear. Lesion edges are now better defined. Day 14,myofibroblastic proliferation (actin++, vimentin+) creates "young" scar tissue, as in "healing by second intention." Lesions are deeper and wider than appeared at acute stage. One month,dense fibrous tissue scar appears. Endothelial cells covering endocardium are morphologically intact. RF lesions are histologically identical to MW's, although no vessel thrombosis was identified at acute optically undamaged areas and cytomorphologic elements emerge at later stages in the healing process. Conclusions: (1) Microwave scars are deeper and wider than the lesions observed at the acute stage. (2) Evolution of microwave lesions is faster and induces broader scars than dry radiofrequency. (3) Scar formation (both energies) is "healing by second intention." (4) Endocardial thrombosis may occur despite morphologically intact endothelium. [source] Angiotensin-(1-7) is involved in the endothelium-dependent modulation of phenylephrine-induced contraction in the aorta of mRen-2 transgenic ratsBRITISH JOURNAL OF PHARMACOLOGY, Issue 7 2002Virgínia S Lemos The contribution of the local vascular production of angiotensin-(1-7) [Ang-(1-7)] to the control of ,-adrenergic-induced contractions in the aorta of Sprague-Dawley (SD) and TGR(mRen-2)27 [mRen-2] rats was studied. In mRen-2 rats, contractile responses to phenylephrine were diminished as compared to control SD rats in endothelium containing but not in endothelium-denuded vessels. L -NAME increased contractile responses to phenylephrine in mRen-2 rats and, after nitric oxide synthase blockade, responses to phenylephrine became comparable in both strains. Inhibition of angiotensin-converting enzyme (ACE) by captopril potentiated contractile responses in mRen-2 rats and diminished contractile responses in SD rats, both effects being dependent on the presence of a functional endothelium. The effect of captopril in mRen-2 rats was abolished in vessels pre-incubated with Ang-(1-7). Blockade of Ang-(1-7) and bradykinin (BK) receptors by A-779 and HOE 140 respectively, increased phenylephrine-induced contraction in mRen-2, but not in SD rats. This effect was seen only in endothelium-containing vessels. Angiotensin II AT1 and AT2 receptor blockade by CV 11974 and PD 123319 did not affect the contractile responses to phenylephrine in aortas of transgenic animals but diminished the response in SD rats. This effect was only seen in the presence of a functional endothelium. It is concluded that the decreased contractile responses to phenylephrine in aortas of mRen-2 rats was dependent on an intact endothelium, the local release and action of Ang-(1-7) and bradykinin. British Journal of Pharmacology (2002) 135, 1743,1748; doi:10.1038/sj.bjp.0704630 [source] | ||||||||||