Ib. Schipper et al., CARDIAC SYMPATHETIC DENERVATION DOES NOT CHANGE THE LOAD DEPENDENCE OF THE LEFT-VENTRICULAR END-SYSTOLIC PRESSURE-VOLUME RELATIONSHIP IN DOGS, Pflugers Archiv, 425(5-6), 1993, pp. 426-433
It has been shown that in the intact canine heart the left-ventricular
end-systolic pressure/volume relation (ESPVR) depends on loading cond
itions: an increase in arterial vascular resistance causes a leftwards
shift and a steeper slope of the ESPVR, suggesting an increased inotr
opic state. Our purpose was to investigate the possible contribution o
f the sympathetic nervous system to this load sensitivity of the ESPVR
, using intact, but denervated, hearts with normal coronary perfusion
and afterload. We used two types of loading intervention: venous volum
e infusion and gradual occlusion of the descending aorta. ESPVRs were
obtained in six anaesthetized open-chest dogs, both before and after b
ilateral ablation of the stellate ganglia. To exclude the influence of
heart rate changes, bilateral vagotomy was performed and the heart wa
s paced. The absence of (unpaced) heart rate changes in response to pr
essure alterations was used to confirm total denervation. Left ventric
ular pressure was measured with a micromanometer and volume with a con
ductance catheter. ESPVRs were essentially linear and characterized by
their slope (E(es)) and volume intercept at 12 kPa (V-12). We found t
hat E(es) (P ( 0.0001) and V-12 (P < 0.05) were both significantly dif
ferent during pressure and volume interventions (0.67 +/- 0.29 and 0.4
1 +/- 0.18kPa/ml for E(es) and 16.2 +/- 8.2 and 18.2 +/- 8.4 ml for V-
12 respectively). Denervation did not significantly affect the paramet
ers of the ESPVR obtained by either volume infusion or aortic occlusio
n. Two-way analysis of variance revealed no significant interactive ef
fect between denervation and intervention, indicating that the sympath
etic nervous system does not influence the load dependency of the ESPV
R. The dP/dt(max): EDV relationship behaved similarly. These results s
uggest that load dependency is an intrinsic property of the myocardium
.