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Laboratory for Physiology, Institute for Cardiovascular Research, Vrije Universiteit Amsterdam, 1081 BT Amsterdam, The Netherlands
The
perfusion-induced increase in cardiac contractility (Gregg phenomenon)
is especially found in heart preparations that lack adequate coronary
autoregulation and thus protection of changes in capillary pressure. We
determined in the isolated perfused papillary muscle of the rat whether
cardiac muscle contractility is related to capillary perfusion. Oxygen
availability of this muscle is independent of internal perfusion, and
perfusion may be varied or even stopped without loss of function.
Muscles contracted isometrically at 27°C
(n = 7). During the control state
stepwise increases in perfusion pressure resulted in all muscles in a
significant increase in active tension. Muscle diameter always
increased with increased perfusion pressure, but muscle segment length
was unaffected. Capillary perfusion was then obstructed by plastic
microspheres (15 µm). Flow, at a perfusion pressure of 66.6 ± 26.2 cmH2O, reduced from 17.6 ± 5.4 µl/min in the control state to 3.2 ± 1.3 µl/min after
microspheres. Active tension developed by the muscle in the unperfused
condition before microspheres and after microspheres did not differ
significantly (
12.8 ± 29.4% change). After microspheres similar perfusion pressure steps as in control never resulted in an
increase in active tension. Even at the two highest perfusion pressures
(89.1 ± 28.4 and 106.5 ± 31.7 cmH2O) that were applied a
significant decrease in active tension was found. We conclude that the
Gregg phenomenon is related to capillary perfusion.
Gregg phenomenon; microspheres; rat; perfused papillary muscle; wall shear
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