Mice chronically exposed to hypoxia and given fucoidans exhibited improved vascular remodeling, right ventricular (RV) function, and an attenuated inflammatory response, according to study results published in the American Journal of Respiratory and Critical Care Medicine.

Mice induced with pulmonary hypertension (PH) by chronic hypoxia for 35 days were given either fucoidan (from Fucus vesiculosus), anti-P-selectin antibody (Rb40.34), or saline by intraperitoneal injection from days 21 through 35. Parameters associated with PH such as RV function, vascular morphometry, and inflammatory responses were compared between groups.

Hypoxia exposure for 35 days resulted in significant RV hypertrophy confirming the occurrence of PH. Control mice also exhibited RV dilatation, increased RV systolic pressure, decreased stroke volume and cardiac output, and overall impaired RV function.

Fucoidan treatment led to a marked decrease in RV internal diameter as well as an increase in stroke volume, cardiac output, and tricuspid annular plane systolic excursion. Fucoidan treatment had no effect on RV systolic pressure. Overall, fucoidan significantly improves RV function in chronic hypoxia-induced PH. Furthermore, lung morphometry demonstrated that fucoidan significantly decreased the number of fully muscularized pulmonary arteries and significantly decreased the level of CD3-positive lymphocytes.

The researchers wrote, “Although fucoidan did not affect RV hypertrophy and RV [systolic pressure], our data clearly indicate that it significantly improved pulmonary remodeling and RV function and in parallel decreased [pulmonary vascular resistance index].”

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Reference

Novoyatleva T, Kojonazarov B, Owczarek A, et al. Evidence for fucoidan-p-selectin axis as a therapeutic target on hypoxia-induced pulmonary hypertension [published December 17, 2018]. Am J Respir Crit Care Med. doi:10.1164/rccm.201806-1170OC

This article originally appeared on Pulmonology Advisor