Response of the intact canine left ventricle to increased afterload and increased coronary perfusion pressure in the presence of coronary flow autoregulation
Mk. Karunanithi et al., Response of the intact canine left ventricle to increased afterload and increased coronary perfusion pressure in the presence of coronary flow autoregulation, CIRCULATION, 100(14), 1999, pp. 1562-1568
Citations number
37
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Background-Increased left ventricular (LV) contractile force or oxygen cons
umption has been documented with increased coronary arterial pressure (CAP)
and flow (Gregg phenomenon). We investigated whether the increase in contr
actile force with increased LV afterload might be mediated by the concomita
nt increase in CAP when coronary autoregulation is intact.
Methods and Results-The LV of 6 autonomically blocked open-chest dogs was p
erfused through the left main coronary artery by a cannula with a side gate
to the aortic root. With the gate open, CAP increased from 77+/-20 to 93+/
-20 mm I-Ig (P<0.05) with aortic constriction (AC). With the gate closed, C
AP was maintained at a constant level of 100 mmHg. A small reduction in the
slope of the preload recruitable stroke work (PRSW) relationship was obser
ved with AC, but this response was not altered by the coronary perfusion ga
te position. The end-systolic pressure-volume (ESPV) relationship shifted u
pward significantly with AC (P<0.001), but this shift was not greater with
open-gate perfusion than with closed-gate perfusion. Furthermore, with coro
nary autoregulation intact, wide changes in CAP (between 60 and 180 mm Hg,
n=5) did not alter either the PRSW or ESPV relationship. In contrast, when
autoregulation was abolished with intracoronary adenosine (n=6), both index
es of contractility increased progressively with increased CAP.
Conclusions The concomitant increase in CAP with increased afterload in the
intact canine LV does not contribute to the afterload-induced increase in
contractile force. Coronary perfusion pressure per se does not influence LV
contractile function. Coronary perfusion pressure influences contractility
only when coronary flow changes.