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Does monocrotaline-induced pulmonary hypertension impair right ventricular coronary capillary hemodynamics and glycocalyx thickness in rats?
Does monocrotaline-induced pulmonary hypertension impair right ventricular coronary capillary hemodynamics and glycocalyx thickness in rats?
Pulmonary hypertension induces right ventricular coronary capillary remodeling, reduces glycocalyx thickness, and impairs capillary hemodynamics, which may contribute to right heart failure.
Glycocalyx loss may impair RV perfusion in PH; leaves open translational role in human right heart failure.
We hypothesized that coronary capillary function is impaired with a decreased glycocalyx layer and uneven inner wall remodeling in right ventricles that are hypertrophied due to pulmonary hypertension (PH). Five-week-old male Sprague-Dawley rats were divided into 2 groups (PH: n=25, control: n=27). In the PH group, Monocrotaline (60 mg/kg SC) was administrated at 5 weeks. Coronary capillary hemodynamics was visualized in vivo at 8 weeks of age using our high-resolution intravital videomicrosopy, and RBC velocities in RV capillaries were evaluated, along with capillary diameters. Configuration of the capillary cast was assessed by a confocal laser scanning microscope. The thickness of the glycocalyx on the capillary endothelial surface was evaluated with Alcian blue 8GX by electron microscopy. RV systolic pressure increased in PH (by 142%, p<0.01). The diameters of capillaries were uneven in PH (coefficient of variation of diameters along capillary trees; 24±8% vs. 11±3%, p<0.05). The thickness of the glycocalyx in PH was less than half that of control (0.20±0.05 vs. 0.45±0.14 μm, p<0.05). RBC velocity was decreased in PH (820±110 vs. 1,100±230 μm/sec, p<0.05). The capillary flow reduction in PH may be closely related to the changes in the glycocalyx and vessel irregularity, resulting in insufficient oxygen supply to the heart.
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Masahito Kajiya (2008) studied this question.
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