Abstract
Cannabidiol (CBD) is known for its vasorelaxant (including in the human pulmonary artery), anti-proliferative and anti-inflammatory properties. The aim of our study was to examine the potential preventive effect of chronic CBD administration (10 mg/kg/day for three weeks) on monocrotaline (MCT)-induced pulmonary hypertension (PH) rats. PH was connected with elevation of right ventricular systolic pressure; right ventricle hypertrophy; lung edema; pulmonary artery remodeling; enhancement of the vasoconstrictor and decreasing vasodilatory responses; increases in plasma concentrations of tissue plasminogen activator, plasminogen activator inhibitor type 1 and leukocyte count; and a decrease in blood oxygen saturation. CBD improved all abovementioned changes induced by PH except right ventricle hypertrophy and lung edema. In addition, CBD increased lung levels of some endocannabinoids (anandamide, N-arachidonoyl glycine, linolenoyl ethanolamide, palmitoleoyl ethanolamide and eicosapentaenoyl ethanolamide but not 2-arachidonoylglycerol). CBD did not affect the cardiopulmonary system of control rats or other parameters of blood morphology in PH. Our data suggest that CBD ameliorates MCT-induced PH in rats by improving endothelial efficiency and function, normalization of hemostatic alterations and reduction of enhanced leukocyte count determined in PH. In conclusion, CBD may be a safe, promising therapeutic or adjuvant therapy agent for the treatment of human pulmonary artery hypertension.
Highlights
Pulmonary artery hypertension (PAH) is a complex, chronic and multi-factorial disease which can lead, among other complications, to an increase in right ventricle pressure (RVP), resulting in progressive right heart failure and premature death
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Three weeks after MCT injection we observed increases in the following, parameters of the pulmonary (but not systemic heart rate (HR) and systolic blood pressure (SBP)) circulation, which are characteristic for pulmonary hypertension (PH)—(1) right ventricular systolic pressure (RVSP) by about 115%, (2) RV hypertrophy expressed as Fulton index (RV/LV and septum ratio) by about 55% and (3) the adjusted weight of the lungs suggesting lung edema [28]
Summary
Pulmonary artery hypertension (PAH) is a complex, chronic and multi-factorial disease which can lead, among other complications, to an increase in right ventricle pressure (RVP), resulting in progressive right heart failure and premature death. PAH is associated with endothelial dysfunction, excessive constriction of pulmonary arteries (PAs), vascular remodeling (smooth muscle cell proliferation and hypertrophy), infiltration of inflammatory cells into the lung and thrombosis. It has a broad therapeutic potential resulting from its anti-inflammatory, antioxidant, anticonvulsant, antipsychotic, anxiolytic and antiproliferative properties. It is approved by the US Food and Drug Administration for the treatment of resistant epilepsy, and it is indicated in the therapy of neuropathic pain in multiple sclerosis and other diseases [2,3]
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