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Observational study

Pediatrics · Pulmonology · 1 h ago

Hypoxia activates platelets in a mouse model of neonatal pulmonary hypertension

In a neonatal mouse model of hypoxia-induced bronchopulmonary dysplasia-associated pulmonary hypertension, researchers found increased pulmonary platelet accumulation and markers of circulating platelet activation. The findings identify platelet pathways as potential targets for further study, but do not establish a role for platelet-directed treatment in infants.

Bronchopulmonary dysplasia-associated pulmonary hypertension (BPD-PH) can cause substantial morbidity in preterm infants, and current treatments largely target vasoconstriction. In this experimental study, neonatal mice were exposed to hypoxia equivalent to 12% oxygen from 12–24 hours after birth until postnatal day 8 or 15. Investigators assessed lung and heart changes and measured platelet activation using histology, flow cytometry, ELISA and immunohistochemistry. The supplied report does not state the number of animals studied.

Hypoxia produced features of BPD-PH, including simplified alveoli, muscularization of pulmonary vessels, increased right ventricular systolic pressure and right ventricular hypertrophy. At day 15, hypoxic mice had increased pulmonary platelet accumulation and platelet factor 4, disrupting the normal postnatal decline. Circulating platelets showed increased surface P-selectin and activated αIIbβ3 at days 8 and 15. At day 8, they also showed greater agonist-induced P-selectin expression and increased leukocyte-platelet aggregation.

The results support an association between hypoxia, platelet activation and pulmonary vascular disease in this mouse model. They do not show that platelet activation causes the disease or that targeting platelets improves outcomes. The findings are preclinical and require mechanistic investigation before their relevance to treatment or biomarkers in infants can be determined.

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Source

Pediatric Research: Hypoxia-induced platelet activation and pulmonary platelets are increased in a murine model of neonatal chronic lung disease and pulmonary hypertension ↗

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