Myointimal thickening in experimental vein grafts is dependent on wall tension

Schwartz, Lewis B.; O’Donohoe, Martin K.; Purut, Cemil M.; Mikat, Eileen M.; Hagen, Per-Otto; McCann, Richard L.

doi:10.1016/0741-5214(92)70026-h

Cited by 80 publications

(54 citation statements)

References 47 publications

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“…It is well established that hypertension induces an increase in the arterial wall thickness as a result of medial hypertrophy and hyperplasia and the deposition of extracellular matrix (20). Similarly, when veins are exposed to arterial pressures, the result is an increase in medial thickness attributed to the pressure-induced elevation of circumferential tension and stress (10,16,17,31). The increase in pressure may also lead to an increase in flow and wall shear stress that results in vasodilatation and remodeling of the vessel wall (28).…”

Section: Discussionmentioning

confidence: 99%

A novel strategy for increasing wall thickness of coronary venules prior to retroperfusion

Choy

Kassab²

2006

American Journal of Physiology-Heart and Circulatory Physiology

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Choy, Jenny Susana, and Ghassan S. Kassab. A novel strategy for increasing wall thickness of coronary venules prior to retroperfusion. Am J Physiol Heart Circ Physiol 291: H972-H978, 2006. First published April 7, 2006 doi:10.1152/ajpheart.00235.2006.-The sudden exposure of veins to arterial pressures during coronary venous retroperfusion may cause rupture of small venules. Our rationale is to first occlude the coronary vein, which will cause an increase in pressure intermediate to arterial and venous values, and hence lead to remodeling and increased wall thickness of the veins prior to retroperfusion. To accomplish this objective, five pigs were subjected to left anterior descending (LAD) vein ligation while six pigs served as sham. Myocardial tissue samples were obtained from the area adjacent to the LAD vein at four transmural locations of the left ventricular free wall: epicardial surface, subepicardium, midmyocardium, and endocardium. Arterioles and venules from the experimental and sham control groups were photographed, and the following measurements were made: inner and outer circumferences, inner and outer areas, major and minor diameters, and intima-media thickness. Each vessel was categorized in four different orders according to lumen diameter. Our results show that intima-media thickness was larger in the experimental group in all four regions of the heart and in all four orders of the vessels, although venules from the epicardial region showed the largest increase in thickness. The intima-media thicknessto-radius ratio was also larger in the experimental group and decreased from epicardial to endocardial region of the heart and from order 1 to order 4 of the vessels. The present study provides a rationale for the development of coronary retroperfusion strategy that avoids vessel rupture and hemorrhage in the postcapillary venules. pressure overload; arterialization; rupture stress; remodeling; ligation BECAUSE THE CORONARY VEINS rarely develop arteriosclerosis (8,23,24), it is desirable to use these vessels as conduits for revascularization. The possibility of coronary retroperfusion was first suggested by Pratt (27) in 1898, when he was able to sustain the mechanical function of a cat's heart by delivering oxygenated blood through the coronary sinus. Almost 50 years after this seminal study, the first attempts at arterialization of the coronary sinus were made by Roberts et al. (30) and Beck et al. (5), independently. In 1943, Roberts et al. (30) suggested the use of coronary veins as conduits to deliver oxygenated blood in a retrograde manner in animal studies. In 1948, Beck and colleagues (5) performed the coronary retroperfusion procedure in humans. The method was abandoned, however, because of the high mortality rate from the edema and hemorrhage in the postcapillary venules that resulted from the elevated pressure (6,8,12,26). To remedy these difficulties, we propose to avoid raising the pressure in the left anterior descending (LAD) vein from venous (10 -20 mmHg) to arterial values (100 ...

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Section: Discussionmentioning

confidence: 99%

A novel strategy for increasing wall thickness of coronary venules prior to retroperfusion

Choy

Kassab²

2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…[3][4][5] In vein grafts, intimal and medial thickening occur in the regions of increased circumferential deformation. 6 Moreover, VSMCs exposed to mechanical strain in vitro exhibit alterations in cell morphology, proliferation, production of vasoactive substances, 2,3 and gene expression. [7][8][9] Many of the effects of thrombin, including inflammation and cell proliferation, are mediated by protease-activated receptor-1 (PAR-1).…”

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Cyclic Strain Increases Protease-Activated Receptor-1 Expression in Vascular Smooth Muscle Cells

et al. 2001

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Abstract-Cyclic strain regulates many vascular smooth muscle cell (VSMC) functions through changing gene expression.This study investigated the effects of cyclic strain on protease-activated receptor-1 (PAR-1) expression in VSMCs and the possible signaling pathways involved, on the basis of the hypothesis that cyclic strain would enhance PAR-1 expression, reflecting increased thrombin activity. Uniaxial cyclic strain (1 Hz, 20%) of cells cultured on elastic membranes induced a 2-fold increase in both PAR-1 mRNA and protein levels. Functional activity of PAR-1, as assessed by cell proliferation in response to thrombin, was also increased by cyclic strain. In addition, treatment of cells with antioxidants or an NADPH oxidase inhibitor blocked strain-induced PAR-1 expression. Preincubation of cells with protein kinase inhibitors (staurosporine or Ro 31-8220) enhanced strain-increased PAR-1 expression, whereas inhibitors of NO synthase, tyrosine kinase, and mitogen-activated protein kinases had no effect. Cyclic strain in the presence of basic fibroblast growth factor induced PAR-1 mRNA levels beyond the effect of cyclic strain alone, whereas no additive effect was observed between cyclic strain and platelet-derived growth factor-AB. Our findings that cyclic strain upregulates PAR-1 mRNA expression but that shear stress downregulates this gene in VSMCs provide an opportunity to elucidate signaling differences by which VSMCs respond to different mechanical forces. (Hypertension. 2001;38: 1038-1043.)

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“…18 Although pulsatility and increased pressure and flow, experienced by veins in the arterial hemodynamic environment, are thought to contribute to triggering the graft remodeling, their specific effects are somewhat conflicting. Arterial conditions are characterized by increased wall tension, associated with the formation of intimal hyperplasia, 19 as well as by increased flow, thought to decrease intimal hyperplasia. 20,21 In the present study, we pursued the early effects (up to 3 days) of ex vivo hemodynamic conditions mimicking either the bypass graft (arterial) or native (venous) environment on gelatinase expression/activation and cell proliferation in matching pairs of human saphenous veins.…”

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confidence: 99%

Early Effects of Arterial Hemodynamic Conditions on Human Saphenous Veins Perfused Ex Vivo

Mavromatis

Fukai

Tate

et al. 2000

ATVB

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Abstract-Exposure to the arterial hemodynamic environment is thought to be a potential trigger for the pathological remodeling of saphenous vein grafts. Using matched pairs of freshly isolated human saphenous vein, we analyzed the early effects of ex vivo hemodynamic conditions mimicking the venous (native) compared with arterial (graft) environment on the key components of vascular remodeling, ie, matrix metalloproteinase (MMP)-9 and MMP-2 and cell proliferation. Interestingly, we found that arterial conditions halved latent MMP-9 (50Ϯ11%, Pϭ0.01) and MMP-2 (44Ϯ6%, Pϭ0.005) levels relative to matched vein pairs maintained ex vivo under venous perfusion for up to 3 days. Immunostaining supported decreased MMP levels in the innermost area of arterially perfused veins. Either decreased synthesis or increased posttranslational processing may decrease MMP zymogen levels. Biosynthetic radiolabeling showed that arterial perfusion actually increased MMP-9 and MMP-2 production. When we then examined potential pathways for MMP zymogen processing, we found that arterial conditions did not affect the expression of MT-MMP-1, a cell-associated MMP activator, but that they significantly increased the levels of superoxide, another MMP activator, suggesting redox-dependent MMP processing. Additional experiments indicated that increased superoxide under arterial conditions was due to diminished scavenging by decreased extracellular superoxide dismutase. Arterial perfusion also stimulated cell proliferation (by 220% to 750%) in the majority of vein segments investigated. Our observations support the hypothesis that arterial hemodynamic conditions stimulate early vein graft remodeling.

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Myointimal thickening in experimental vein grafts is dependent on wall tension

Cited by 80 publications

References 47 publications

A novel strategy for increasing wall thickness of coronary venules prior to retroperfusion

A novel strategy for increasing wall thickness of coronary venules prior to retroperfusion

Cyclic Strain Increases Protease-Activated Receptor-1 Expression in Vascular Smooth Muscle Cells

Early Effects of Arterial Hemodynamic Conditions on Human Saphenous Veins Perfused Ex Vivo

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