Heat dissipation and its effects on tissue and blood interfaces are co
mmon problems associated with the development and increased use of art
ificial hearts, because all of the implantable actuators for artificia
l hearts generate waste heat due to inefficiencies of energy conversio
n. To determine the mechanisms of heat dissipation from artificial hea
rts, heated disks producing constant heat fluxes of 0.08 watts/cm(2) w
ere implanted adjacent to the left lung and the latissimus dorsi muscl
e in calves for 2 weeks, 4 weeks, and 7 weeks. At the end of each expe
riment, a series of acute studies was performed in which blood perfusi
on to the heated tissue was decreased or stopped to observe the contri
bution of blood perfusion to heat dissipation. The cooling effect of v
entilation was also examined to determine its relative contribution to
heat dissipation in lung tissue by decreasing the minute ventilation
volume. The importance of blood perfusion for heat dissipation was dem
onstrated by the temperature rise after cessation of blood perfusion t
o the heated tissue. The contribution of ventilation to heat dissipati
on in the heated lung tissue was minimal. Contribution of total blood
perfusion to heat dissipation was increased with time in the muscle ti
ssue, which has relatively low resting blood perfusion, but not in the
lung tissue, which has relatively high blood perfusion. In the heated
muscle tissue, the in vivo adaptive response to chronic heat was func
tionally shown by the increased perfusion. In conclusion, blood perfus
ion was the main mechanism of heat dissipation from tissues that were
adjacent to an implanted power source.