MECHANISM OF ENLARGEMENT OF MAJOR CEREBRAL COLLATERAL ARTERIES IN RABBITS

Major cerebral collateral arteries enlarge following bilateral ligation of the common and internal carotid arteries. The purpose of this investigation was to determine the relative contribution of cellular hypertrophy versus cellular hyperplasia to this vessel change in a morphometric analysis as well as the functional properties of remodeled vessels in an in vitro study. We assessed cell number and vessel dimensions by morphometric analysis of 16 perfusion-fixed rabbit basilar arteries. Results demonstrated significant increases in luminal diameter from 761 to 946-mu-m (p < 0.01), medial cross-sectional area from 5.1 x 10(4) to 7.6 x 10(4)mu-m2 (p < 0.005), smooth muscle cell volume from 9.19 x 10(5) to 1.44 x 10(6)mu-m3 (p < 0.0005), and overall arterial length from 17.41 to 20.36 mm (p < 0.005) in basilar arteries from the eight ligated rabbits compared with the eight sham-operated controls. Smooth muscle cell volume fraction and cell numerical density were unchanged whereas the number of cells per unit length of artery was increased significantly from 21.5 to 31.0 cells/mu-m (p < 0.05). These data indicate that smooth muscle cell hyperplasia rather than hypertrophy contributes to increases in vessel mass. Functional properties of the basilar arteries from 10 ligated and 10 normal control rabbits were analyzed in vitro. Results showed increased contraction to potassium chloride (approximately 74%) (p < 0.01) and increased sensitivity of smooth muscle to acetylcholine (p < 0.05) while maximal relaxation was the same as control in the ligated animals. In our study, basilar arteries subjected to increased load became remodeled into longer, thicker, wider arteries by the process of hyperplasia and exhibited greater contractility and capacity for vasodilation.