Coronary arterial inflow is impeded and venous outflow is increased as a re
sult of the decrease in coronary vascular volume due to cardiac contraction
. We evaluated whether cardiac contraction is influenced by interfering wit
h the changes of the coronary vascular volume over the heart cycle. Length-
tension relationships were determined in Tyrode-perfused rat papillary musc
le and when coronary vascular volume changes were partly inhibited by filli
ng it with congealed gelatin or perfusing it with a high viscosity dextran
buffer. Also, myocyte thickening during contraction was reduced by placing
a silicon tube around the muscle. Increasing perfusion pressure from 8 to 8
0 cmH(2)O, increased developed tension by similar to 40%. When compared wit
h the low perfusion state, developed tension of the gelatin-filled vasculat
ure was reduced to 43 +/- 6% at the muscle length where the muscle generate
s the largest developed tension (n = 5, means +/- SE). Dextran reduced deve
loped tension to 73 +/- 6% (n = 6). The silicon tube, in low perfusion stat
e, reduced the developed tension to 83 +/- 7% (n = 4) of control. Time-cont
rol and oxygen-lowering experiments show that the findings are based on mec
hanical effects. Thus interventions to prevent myocyte thickening reduce de
veloped tension. We hypothesize that when myocyte thickening is prevented,
intracellular pressure increases and counteracts the force produced by the
contractile apparatus. We conclude that emptying of the coronary vasculatur
e serves a physiological purpose by facilitating cardiomyocyte thickening t
hereby augmenting force development.