The Impact of Balloon Embolectomy on the Function and Morphology of the Endothelium

Jerius, Hilde; Bagwell, Drew; Beall, Arthur C.; Brophy, Colleen M.

doi:10.1006/jsre.1996.4908

Cited by 7 publications

(7 citation statements)

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“…Most studies describing vascular reactivity after arterial injury in vivo have used Fogarty balloons to induce injury. [27][28][29] These studies are therefore hard to compare with our results. The only in vivo study reporting semiacute effects of BA using a percutaneous transluminal angioplasty (PTA) balloon catheter on vascular reactivity demonstrated a lack of tone and reactivity to vasoconstrictors (ergonovine) that remained for 4 weeks.…”

Section: Behavior Of Ba Arteriesmentioning

confidence: 63%

Function and Structure of Pressurized and Perfused Porcine Carotid Arteries

Perree

Leeuwen

Kerindongo

et al. 2003

The American Journal of Pathology

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In this report we describe the application of an in vitro pressure-perfusion system for study of functional/structural changes after in vitro balloon dilation injury. Pig carotid arteries were perfused at P = 100 mm Hg and Q = 100 ml/min, balloon angioplastied (BA), and cultured under these hemodynamic conditions for 4 or 8 days (n = 5 BA and 6 controls for each time point). To assess endothelial function, outer diameter changes in response to bradykinin (BK) were measured daily. Remodeling was determined from the shift in pressure-passive diameter relation, as obtained after papaverine addition. Arterial samples were processed for histology. Control arteries showed spontaneous tone, BK-induced relaxation, and inward remodeling that was more pronounced at day 8 (ratio end-to-start passive diameter at P = 100 mm Hg, 0.69 +/- 0.04; P < 0.001) than at day 4 (0.85 +/- 0.03, P = 0.03). Intimal hyperplasia was detectable in these control vessels at day 8 with accumulation of alpha-smooth muscle actin-positive cells around the lumen. Angioplasty caused ruptures and dissections and abolished tone that returned after 5 days of perfusion along with BK-dependent relaxation. No significant inward remodeling or intimal hyperplasia was observed at day 8 after angioplasty. Thus, BA inhibits remodeling, which occurs after in vitro perfusion of conductance arteries.

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Section: Behavior Of Ba Arteriesmentioning

confidence: 63%

Function and Structure of Pressurized and Perfused Porcine Carotid Arteries

Perree

Leeuwen

Kerindongo

et al. 2003

The American Journal of Pathology

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“…Our previous reports (26,43) have indicated that there is pharmacological and physiological evidence for NOS activation in VSM. Bovine carotid smooth muscle contractions induced by 5-HT or norepinephrine were shown to be attenuated by preincubation with L-NMMA.…”

Section: Discussionmentioning

confidence: 97%

Functional expression of NOS 1 in vascular smooth muscle

Brophy

Knoepp²,

Xin

et al. 2000

American Journal of Physiology-Heart and Circulatory Physiology

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Substances that increase intracellular calcium concentration ([Ca(2+)](i)), such as serotonin, are known to induce vascular smooth muscle (VSM) contraction. However, increases in [Ca(2+)](i) also activate Ca(2+)/calmodulin-dependent nitric oxide synthases (NOS), which leads to increases in cGMP and activation of cGMP-dependent protein kinase (PKG). One recently identified substrate protein of PKG is the small heat shock protein, HSP20. The purpose of this study was to determine if serotonin activates a Ca(2+)-dependent NOS in VSM. Strips of bovine carotid arterial smooth muscle denuded of endothelium were stimulated with serotonin in the presence and absence of the nonspecific NOS inhibitor N-monomethyl-L-arginine (L-NMMA). Activation of NOS was determined by increases in cGMP and in the phosphorylation of HSP20. Immunohistochemical and Western blotting techniques were performed to identify specific NOS isoforms in bovine carotid arterial smooth muscle preparations. Serotonin stimulation led to significant increases in cGMP and in the phosphorylation of HSP20, which were inhibited by pretreatment with L-NMMA. Antibodies against NOS 1 stained the media of bovine carotid and human renal arteries, whereas antibodies against NOS 3 stained only the endothelium. Additionally, the conversion of radiolabeled L-arginine to L-citrulline NOS activity demonstrated a consistent amount of activity present in the endothelium-denuded smooth muscle preparations that was reduced by 99% with an NOS 1 specific inhibitor. Finally, an NOS 1 specific inhibitor, 7-nitroindazole, augmented contractions induced by high extracellular KCl. This study demonstrates that NOS 1 is present in VSM and may effect physiological contractile responses.

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“…If either of these is the case, then despite the failure of initial endothelial balloon denudation to augment the injury to the tunica media, it could have a positive impact on the success of sclerotherapy in vivo. Further, previous studies have shown that balloon injury impairs endothelial-dependent vessel relaxation19,20 and promotes vessel spasm which is likely to facilitate early vessel closure following administration of foam sclerotherapy. Thus further evaluation of this technique is required.…”

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confidence: 99%