Changes in the pulmonary vasculature in human hypoxic lung disease and in rats exposed chronically to hypoxia lead to haemodynamic changes. Muscularisation of small vessels occurs internal to the external elastic lamina (EL) and narrows the lumen, increasing resistance. We compare pulmonary haemodynamics with the development of new muscularisation of small intra-acinar (resistance) vessels 22.5-30 mm and < 22.5 mm diameter in rats (n = 3-6/group) kept in normoxia (N), normobaric hypoxia (10 % O2) for 2 or 4 weeks (CH2, CH4), or 2 weeks followed by 2 weeks air recovery period (REC).
After hypoxic exposure the rats were humanely killed by pentobarbitone overdose (100 mg kg-1 I.P.). Series 1: lungs were perfused with plasma substitute (38 °C, basal flow 20 ml min-1) to measure pulmonary artery pressure (Ppa), and pulmonary vascular resistance (PVR) (slope of Ppa/flow line, flow 5-30 ml min-1); lungs were then fixed with formol-saline for histology and heart ventricles weighed to give RV/LV+septum. Series 2: lungs were fixed immediately for histology. Muscularisation of small vessels was assessed by Image-Pro analysis from: (1) area of α-actin in walls after immunostaining; (2) area between external elastic lamina and new internal elastic lamina (ΔEL), after elastin staining (Gomori) (Table 1). CH4 results, not given, were in all respects similar to those of CH2.
The number (n) of small muscular vessels (MV), almost absent in N rats, increased in CH. The number and amount of new muscle was reduced after air recovery REC (22.5-30 mm), being virtually lost in vessels < 22.5 mm. Haemodynamic criteria were also reduced in REC but remained greater than in N. Thus haemodynamic and structural changes were correlated in both chronic hypoxia and after air recovery.
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