Abstract
As a sequel to previous evidence that prolonged .beta.-adrenoceptor blockade in young rabbits led to a relative increase in the capillarity of ventricular muscle, an attempt was made to localize and quantify capillary density from epicardium to endocardium in 12 wk old rabbits treated for 6 wk with propranolol (3 mg kg-1) s.c. twice daily and in litter-mates treated with saline (controls). Full-thickness 0.5 .mu.m sections of the left ventricular wall were point-counted in 200 .mu.m steps. In the controls the capillary volume density decreased progressively below the epicardial surface from a value of 9% to reach a minimum of 7.1% at a depth of 2.5 mm. Capillary density when increased again towards the endocardium, reaching a maximum of 11.5% in the trabeculae carnae (depth 3.5 mm). In the treated animals the capillary density was increased in the mid wall at 2.3 and 2.5 mm, but significantly decreased in the trabeculae at 3.7 mm (P < 0.05). A more detailed analysis was undertaken at depths of 0.7 (Epi), 2.3 (Endo) and 3.5 mm (Trab), comprising estimates of capillary number, capillary diameter and intercapillary distance, via the stereological parameters of mean intercept length and mean free distance. In the controls the order was Epi > Trab > Endo for number, Trab > Endo > Epi for diameter and Endo > Epi > Trab for intercapillary distance. In treated rabbits the mean intercapillary distance was significantly reduced in the Epi (by 17.5%, P < 0.05) and End 0 (by 32%, P < 0.005), but was not significantly altered (+ 3.7%, P > 0.05) in the Trab. The non-uniform distribution of capillaries in the controls illustrates that detection of changes in transmural capillary density requires that sample depth be measured from the epicardial surface and not, owing to the presence of trabeculae carnae, from the endocardium. If similar treatment effects were to occur in man, they would suggest that prolonged .beta.-blockade could induce an increase in capillary density which would render the ventricular mid wall less susceptible to ischemia.