Circulation, Vol 87, 1275-1285, Copyright © 1993 by American Heart Association
SG De Hert, TC Gillebert and DL Brutsaert
BACKGROUND. High-power intracavitary ultrasound abbreviates left
ventricular (LV) ejection duration, thereby decreasing mechanical LV
performance, presumably by selective impairment of endocardial endothelial
function. METHODS AND RESULTS. Effects of ultrasound were evaluated in the
ejecting LV of anesthetized, open-chest dogs under different conditions of
LV volume and contractile state and after mild selective alpha 1-adrenergic
stimulation. LV pressures, left atrial pressures, and regional segment
lengths were measured in anterior and posterior midwall. A cylindrical
ultrasound probe (0.9 MHz, 25 W) mounted on a catheter was inserted into
the LV cavity through the apex and was activated for 4 minutes in each
condition. In protocol A (n = 7), LV volume was altered with caval vein
occlusion and intravenous dextran infusion. The ultrasound probe was
activated at low (4.1 +/- 0.9 mm Hg), mid (10.6 +/- 1.5 mm Hg), and high
(17.9 +/- 1.8 mm Hg) LV end-diastolic pressure (EDP). Effects of ultrasound
were less pronounced at higher EDP. For example, the time interval from
end- diastole to peak (-)dP/dt decreased by 7.5 +/- 2.3% at low, 4.4 +/-
2.2% at mid, and 1.9 +/- 1.6% at high LVEDP (p < 0.001). In protocol B
(n = 7), LV inotropic state was altered by slow intravenous infusion of
low-dose calcium. The ultrasound probe was activated before and after
calcium. Effects of ultrasound were less pronounced after calcium. Time
from end-diastole to peak (-)dP/dt decreased by 8.4 +/- 3.1% at baseline
and by 3.5 +/- 2.1% after calcium (p < 0.001). In protocol C (n = 7),
activation of the ultrasound probe was performed at baseline and after mild
selective alpha 1-adrenergic stimulation (propranolol plus phenylephrine).
Effects of ultrasound were similar at baseline and after propranolol but
increased after phenylephrine. Time from end- diastole to peak (-)dP/dt
decreased by 5.2 +/- 2.4% at baseline, by 5.3 +/- 1.9% after propranolol,
and by 8.9 +/- 3.2% after phenylephrine (p < 0.05). CONCLUSIONS. Effects
of intracavitary ultrasound, which are presumably mediated through
modulation of endocardial endothelial function, were more important at low
volume, lower calcium, and under mild selective alpha 1-adrenergic
stimulation.
ARTICLES
Alteration of left ventricular endocardial function by intracavitary high-power ultrasound interacts with volume, inotropic state, and alpha 1-adrenergic stimulation
Department of Physiology and Medicine, University of Antwerp, Belgium.
This article has been cited by other articles:
 |
|
 |
|
  D. L. Brutsaert Cardiac Endothelial-Myocardial Signaling: Its Role in Cardiac Growth, Contractile Performance, and Rhythmicity Physiol Rev, January 1, 2003; 83(1): 59 - 115. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Ay, X. Havaux, G. Van Camp, B. Campanelli, G. Gisellu, A. Pasquet, J.-F. Denef, J. A. Melin, and J.-L. J. Vanoverschelde Destruction of Contrast Microbubbles by Ultrasound: Effects on Myocardial Function, Coronary Perfusion Pressure, and Microvascular Integrity Circulation, July 24, 2001; 104(4): 461 - 466. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. U Sys, G. W De Keulenaer, and D. L Brutsaert Physiopharmacological evaluation of myocardial performance: how to study modulation by cardiac endothelium and related humoral factors? Cardiovasc Res, July 1, 1998; 39(1): 136 - 147. [Full Text] [PDF]
|
|
|
|
|
|
D. L. Brutsaert, P. Fransen, L. J. Andries, G. W. De Keulenaer, and S. U. Sys Cardiac endothelium and myocardial function Cardiovasc Res, May 1, 1998; 38(2): 281 - 290. [Abstract] [Full Text] [PDF]
|
|