A simple fluid-structure coupling algorithm for the study of the anastomotic mechanics of vascular grafts.

Vascular anastomoses constitute a main factor in poor graft performance due to mismatches in distensibility between the host artery and the graft. This work aims at computational fluid-structure investigations of proximal and distal anastomoses of vein grafts and synthetic grafts. Finite element and finite volume models were developed and coupled with a user-defined algorithm.

Participation of macrophages in atherosclerotic lesion morphology in LDLr-/- mice.

Lystbeige (beige) mice crossed with LDL receptor-deficient (LDLr-/-) mice had a distinct atherosclerotic lesion morphology that was not observed in LDLr-/- mice. This morphology is often associated with a stable plaque phenotype. We hypothesized that macrophage expression of the beige mutation accounted for this distinct morphology.

A selective somatostatin type-2 receptor agonist inhibits neointimal thickening and enhances endothelial cell growth and morphology following aortic balloon injury in the rabbit.

Somatostatin analogs have been shown to inhibit vascular smooth muscle cell (VSMC) proliferation and attenuate neointimal thickening following experimental balloon catheter injury. In this study, the effects of a selective agonist for the somatostatin receptor subtype 2, PRL-2486, on neointimal thickening and endothelial cell regrowth 2 weeks following balloon catheterization of male New Zealand White rabbits were determined. Rabbits treated 2 days prior to and 2 weeks after catheter injury with 10 microg/kg/day PRL-2486 (PRL-tx) had decreased I/M ratios (intimal area/medial area x 100; p < 0.

Inflammation in atherosclerosis: lesion formation in LDL receptor-deficient mice with perforin and Lyst(beige) mutations.

Objective: Natural killer (NK) cells have been identified in human vascular pathologies. In this study, we identified NK cells in aortic root atherosclerotic lesions of low density lipoprotein (LDL) receptor-deficient (LDLr-/-) mice. To characterize the role of NK cell-mediated cytolysis in atherosclerosis, we generated C57Bl/6 double-mutant mice by crossing LDLr-/- mice with NK cell-defective Lyst(beige) mice (creating beige,LDLr-/- mice) and with perforin-deficient mice (creating Pfp-/-,LDLr-/- mice).

Effect of gamma-irradiation and bone marrow transplantation on atherosclerosis in LDL receptor-deficient mice.

Bone marrow transplantation (BMT) is commonly used to study the participation of bone marrow-derived cells in atherosclerosis. To determine the effect of this methodology on lesions, 16 male low density lipoprotein (LDL) receptor knockout (LDLr-/-) mice were reconstituted with bone marrow from syngeneic LDLr-/- mice after 10 Gy gamma-irradiation and compared with 12 male LDLr-/- littermates that did not undergo BMT (no-BMT group). Mice were fed a high fat diet (HFD) for 16 weeks to induce atherosclerosis.

Participation of innate and acquired immunity in atherosclerosis.

Coronary artery disease, the major manifestation of atherosclerosis, is the leading cause of death in the Western world. However, the pathogenesis of atherosclerosis is still poorly understood. Controversy exists regarding the participation of innate immunity involving macrophages and natural killer (NK) cells vs antigen-specific acquired immunity involving lymphocytes.

Balloon catheter vascular injury of the alloxan-induced diabetic rabbit: the role of insulin-like growth factor-1.

Neointimal thickening following catheter injury is characterized, in part, by growth factor-induced vascular smooth muscle cell (VSMC) proliferation. It was hypothesized that a reduction in serum insulin-like growth factor-1 (IGF-1), characteristic of chemically-induced diabetes, would result in decreased VSMC proliferation and attenuate neointimal thickening. It was found that alloxan-treated New Zealand White rabbits exhibit varying degrees of glycemia.

Adrenomedullin Does Not Inhibit Human Platelet Aggregation.

BACKGROUND: Adrenomedullin (ADM) is a hypotensive peptide isolated from human pheochromocytoma extracts discovered in 1993 using an assay system designed to monitor its ability to increase rat platelet adenosine 3',5'-cyclic monophosphate (cAMP) levels. Physiological mediators that elevate cAMP levels, such as prostaglandin (PG)E(1) and PGI(2), have also been shown to inhibit platelet aggregation. Therefore, we have chosen to investigate the effect of ADM, a peptide shown to increase platelet cAMP levels, on human platelet aggregation.

Endothelial cell regrowth and morphology after balloon catheter injury of alloxan-induced diabetic rabbits.

Neointimal thickening after catheter injury has been reported to be influenced by the integrity of the vascular endothelium. We have previously shown that neointimal thickening is significantly reduced in alloxan-induced diabetic New Zealand White rabbits after catheter injury compared with euglycemic rabbits. In the present study, it was hypothesized that endothelial cell regrowth, morphology, and endothelium-dependent vasoreactivity after catheter injury are improved in the diabetic rabbit (glucose >/=400 mg/dl) compared with the euglycemic rabbit.