Cardiac work and capillary density in normal and vascularly compromised hearts.

Capillary density and cardiac work were measured in several groups of rabbits, with normal hearts (controls) and hearts vascularly compromised by left ventricular volume-overload hypertrophy or subendocardial necrosis elicited by a high dose of noradrenaline. Measurements were also made in these same three groups after four weeks of atrial bradycardial pacing, and also in two groups treated for four weeks with coronary vasodilators (adenosine or a xanthine derivative HWA 285). Chronic bradycardial pacing, with decreased heart rate by about 50%, resulted in increased capillary density in both control and hypertrophied hearts. Increased capillary density was also induced by long-term i.v. infusion of adenosine or HWA 285. Since pacing or vasodilator infusion did not alter the heart weights or fibre diameters, the increase in capillary density can be interpreted as due to capillary growth. Increased capillary density was also found in noradrenaline-treated hearts--both unpaced and paced--and was due to a drastic reduction in fibre cross sectional area (and consequently reduced diffusion distances). Heart performance, estimated by maximal cardiac work, was increased in all paced hearts (control, hypertrophied, noradrenaline-damaged) and in hearts infused with HWA 285, but not with adenosine. Thus increased capillary density and shortening of diffusion distances do not guarantee improved heart performance. Since pacing of hypertrophied and noradrenaline-damaged hearts and infusion of HWA 285 increased subendo/subepicardial capillary density ratio, the importance of homogeneous transmural or preferential higher subendocardial capillary supply for cardiac work is discussed.