Attenuating Pulmonary Hypertension by Protecting the Integrity of Glycocalyx in Rats Model of Pulmonary Artery Hypertension.

The endothelial glycocalyx has been proved to be a polysaccharide protein complex covering the surface of vascular endothelial cells, playing an important role in vascular permeability, blood flow shear stress induction, and prevention of endothelial cell adhesion. The pathogenesis of PAH includes pulmonary arterial endothelial cell dysfunction and pulmonary arterial smooth muscle cell (PASMCs) proliferation. Based on the physicochemical properties of endothelial glycocalyx involving pathogenesis of pulmonary hypertension. We hypothesized that the endothelial glycocalyx is involved in the development of pulmonary hypertension; pulmonary hypertension can be regulated by protecting the integrity of glycocalyx. Expression of glycocalyx markers including heparin sulfate proteoglycan (HSPG), hyaluronan (HA), and syndecan-1 (SDC-1) was detected in monocrotaline (MCT)-induced PAH in rats and these components were detected when the PAH rats were treated with heparin that protected the role of glycocalyx. Results showed that plasma levels of HSPG, HA, and SDC-1 were increased in MCT group when compared with control group. However, rats in treatment group showed reduced levels of HSPG, HA, and SDC-1. Expression of HSPG, HA, and SDC-1 in pulmonary arteries was also reduced in MCT group when compared with those in the control group. By contrast, expression of HSPG, HA, and SDC-1 in pulmonary arteries increased in treatment group. In conclusion, destruction of glycocalyx was involved in the development of pulmonary hypertension. Pulmonary hypertension can be regulated by protecting the integrity of glycocalyx.