Pulmonary artery pressure in rats with hereditary platelet function defect.

Pulmonary vasoactivity of several biochemical components produced or stored in platelet was the justification for the study of pulmonary artery pressure in fawn-hooded rats (FHR) with hereditary platelet storage pool deficiency. Anesthetized (pentobarbital 35 mg kg-1 i.p.) FHR had higher right ventricular systolic pressure compared with normal Wistar rats (NWR) matched in sex and age (57.7 +/- 6.8 vs. 34.8 +/- 1.2 mm Hg; p less than 0.01). The incidence of higher pulmonary artery pressure (greater than means + 2 SD of NWR) was 68% among FHR. A significant difference was recorded between FHR and NWR in the relative weight of the right ventricle (0.092 +/- 0.021 vs. 0.048 +/- 0.001 g/100 g; p less than 0.05). Rise in pulmonary artery pressure in FHR after 4 weeks of normobaric hypoxia was found to be comparable to that seen posthypoxically in NWR. Morphological consequences of pulmonary hypertension, ranging from moderate medial hypertrophy of small arteries to muscularization of pulmonary arterioles, were recorded in about 50% of FHR with increased pulmonary artery pressure.