We studied the effects of developing, peak, and stabilized cardiac hypertrophy on the capillary bed of spontaneously hypertensive rats; Wistar-Kyoto rats served as controls. Histological measurements were based on 1.5-/xm cross-sections of left ventricular specimens from perfuse-fixed hearts arrested in diastole. The decline in capillary density, in general, paralleled the decrease in capillary surface area which was lowest at peak hypertrophy (7 months) in spontaneously hypertensive rats. Between 7 and 15 months cardiocyte diameter remained constant and capillary density increased to Wistar-Kyoto rat values. Radioautographic data showed that in 12-month-old spontaneously hypertensive rats, 3H-thymidine labeling of capillary nuclei was more than 2-fold higher than in Wistar-Kyoto rats. Mean capillary diameter increased in both spontaneously hypertensive and Wistar-Kyoto rats between 1 and 2.5 months, but remained constant thereafter. Whereas multiple regression analysis showed that capillary density is the major determinant of capillary surface area, significant changes were detected earlier in capillary surface area than in capillary density. Although peak cardiac hypertrophy affected a 12.5% capillary density decrement in spontaneously hypertensive rats, capillary surface area was 24% lower than in Wistar-Kyoto rats. This substantial decrease in capillary surface area was associated with only a 1.1-jU. m decrease in minimal intercapillary distance. Since mean capillary diameter was similar in the two strains, it is suggested that the drop in capillary surface area during peak hypertrophy was due to a relative decrease in anastomotic and branching capillaries, as well as the decline in capillary density. These data provide morphological evidence that:(1) whereas capillary density is, in general, a good predictor of capillary surface area, the latter is a more sensitive measure of capillarity than the former;(2) the decrement in capillary supply to a cardiocyte during peak, but moderate, hypertrophy is probably substantially greater than that estimated by capillary density; and (3) capillary growth during stabilized hypertrophy is sufficient to reverse the decrements in capillary surface area, capillary density and the increase in minimal intercapillary distance.(Circ Res 51: 295-304, 1982)

IT IS well established that the increase in myocardial mass associated with pressure overload significantly reduces capillary density (Wearn, 1941; Rakusan and Poupa, 1966; Rakusan et al., 1967; Lund and Tomanek, 1978). Such data suggest that capillary growth during this type of cardiac hypertrophy is either inadequate or nonexistent. In contrast, recent work in our laboratory has shown that the decrement in capillary density that occurs during the development of caridac hypertrophy in the spontaneously hypertensive rat is reversed as hypertrophy stabilizes (Tomanek and Hovanec, 1981). Such data suggest that capillary density is normalized by a proliferation of endothelial cells.