[Effect of pushing manipulation on Qiaogong acupoint on hemodynamics in cynomolgus monkeys with mild carotid atherosclerotic plaques].

OBJECTIVE: To explore the hemodynamic changes in cynomolgus monkeys with mild carotid atherosclerotic (CAS) plaques after therapy with pushing manipulation on Qiaogong acupoint (MPQ). METHODS: Nine cynomolgus monkeys were equally randomized into MPQ group, mild CAS model group and blank control group. Mild CAS models were established in the monkeys in MPQ and model groups, and the monkeys in MPQ group received treatment with MPQ intervention after the modeling. The conditions of the carotid artery and the hemodynamic changes in the 3 groups were evaluated after the treatment. RESULTS: Formation of CAS plaques was detected in monkeys in both MPQ and model groups. The vascular cross?sectional area, plaque cross?sectional area and stenosis rate of the plaques in the two groups all differed significantly from those in the blank control group (P<0.05), but these parameters were similar between MPQ group and the model group (P>0.05). Compared with those in the blank control group, the hemodynamic parameters showed significant changes in MPQ and the model groups (P<0.05) but remained similar between the latter two groups (P>0.05). CONCLUSION: CAS plaques can cause changes in hemodynamic parameters. Short?term therapy with MPQ does not affect the stability of the plaques or cause adverse effects on hemodynamics in cynomolgus monkeys with mild CAS plaques.

P-cresol, but not p-cresylsulphate, disrupts endothelial progenitor cell function in vitro.

BACKGROUND: Patients afflicted with chronic kidney disease (CKD) typically suffer from cardiovascular disease (CVD) which is a leading cause of patient mortality. It has been demonstrated that two distinct physiological events contribute to this disease state. These include the abundance of abnormally high levels of protein-bound uraemic toxins as well as functionally aberrant endothelial progenitor cells (EPCs). Specifically, it has been demonstrated that the uraemic toxin p-cresol (pC; 4-methylphenol) inhibits EPC proliferation and tube formation in previous in vitro studies. More recently, however, it has been demonstrated that circulating pC is actually conjugated and that p-cresylsulphate (pCS) is its main metabolite. Therefore, within the context of this study, we examined the in vitro effects of pC and pCS treatment on cultured human EPCs. METHODS: Late-outgrowth EPCs were treated with physiological concentrations of pC or pCS (10, 40, 80, and 160 or 10, 40, 80, 160 and 320 µg/mL for up to 72 h, respectively) in the presence of 4% human serum albumin (HSA). Cell proliferation was determined using WST-1 assay, while migration and tube formation assays were used to evaluate EPC function in vitro. Cell cycle analyses were also performed to determine the effects of pC and pCS on cell cycle status. RESULTS: With regard to EPC proliferation, data demonstrate that pC in the presence or absence of HSA had an IC50 of 80.1 and 100.8 µg/mL 72 h post-treatment, respectively, while pCS-treated groups did not impair EPC proliferation. Similarly, pC-treated groups showed limited vessel formation and migration compared with controls and no detrimental effects were seen with pCS treatment. Lastly, pC treatment of EPCs caused cells to accumulate in the G2/M phase of the cell cycle with accompanied down-regulation of cyclin B1 and phosphorylated CDK1. pCS had no effect on cell cycle parameters. CONCLUSIONS: Our data demonstrate that pC and pCS have different effects on EPC function. Since there is a dearth of data that have focused on the toxicity of pCS, further research should be performed to determine the exact biological toxicity of pCS on the cardiovascular system.

Hemocompatibility of drug-eluting coronary stents coated with sulfonated poly (styrene-block-isobutylene-block-styrene).

The presence of polymer coating on a coronary stent is a major mediator of coronary inflammation reaction thereby affects re-endothelialization. Poly(styrene-block-isobutylene-block-styrene) (SIBS) is one of the most attractive alternatives to serve as stent coating, but has shown less than optimal biocompatibility. Increasing the sulfonic acid content in the polymer can result in increased strength and hydrophilicity. The present study was undertaken to determine the mechanism of action and in vivo efficacy of sulfonated SIBS (S-SIBS) designed specifically as a stent polymer with reduced inflammatory potential and greater endothelialization preservation potential. The blood compatibility of S-SIBS in vitro and its ability to support the attachment of human umbilical vein endothelial cells (HUVECs) were first assessed to get some insight into its potential use in vivo. Baer metal stent (BMS), S-SIBS-coated stent without drug (BMS Plus S-SIBS), standard drug-eluting stent (DES) and S-SIBS-coated drug-eluting stent (DES Plus S-SIBS) were then implanted in the coronary arteries of a porcine model. Neointimal hyperplasia was evaluated at 28 and 180 days, and re-endothelialization was evaluated at 7 and 28 days post stents implantation. The results showed that DES Plus S-SIBS exhibited similar ability to reduce neointimal hyperplasia but preserved endothelialization compared with standard DES. These results suggest potentially promising performance of S-SIBS-coated stent in human clinical applications of coronary stenting.