Circulation, Vol 68, 170-182, Copyright © 1983 by American Heart Association
M Matsuzaki, KP Gallagher, WS Kemper, F White and J Ross Jr
Prolonged nontransmural ischemia was produced and the early and late
effects of reperfusion were studied in 10 conscious dogs instrumented over
the long term. Five hours of partial circumflex coronary artery stenosis
was produced with a hydraulic occluder, followed by gradual release over 20
min, with measurements of left ventricular pressure, regional myocardial
function (systolic wall thickening by sonomicrometry), coronary blood flow
velocity (pulsed Doppler), and myocardial blood flow (microspheres). During
coronary stenosis the occluder was adjusted frequently to maintain a
reduction of systolic wall thickening to 50% to 75% of control (average
62.6% of control). Myocardial blood flow in the ischemic area at 4 hr of
partial coronary stenosis was reduced in the inner layers of the myocardium
(subendocardium, from 0.81 +/- 0.18 at control to 0.36 +/- 0.08 SD, p less
than .01; midwall, from 0.77 +/- 0.20 to 0.46 +/- 0.07 ml/min/g, p less
than .01), accompanied by significant ST segment elevation on the
subendocardial electrogram (0.83 +/- 0.96 to 4.58 +/- 4.10 mV; p less than
.05) and decreased left ventricular dP/dt (3503 +/- 462 to 2991 +/- 339 mm
Hg/sec; p less than .01). Within a few minutes after complete release of
partial coronary stenosis, ST segments returned to control and myocardial
blood flow of the inner layers was increased (subendocardium, 1.37 +/-
0.39, p less than .01; midwall, 0.97 +/- 0.28, p less than .05), but
systolic wall thickening and left ventricular dP/dt were significantly
depressed and remained reduced at 24, 48, and 72 hr when myocardial blood
flow was normal. By seven days, systolic wall thickening and left
ventricular dP/dt had returned to control (94.1 +/- 7.0% of control, 3353
+/- 605 mm Hg/sec, respectively; NS). Histologic changes caused by ischemia
constituted only 2.7% (average) of the tissue between the crystals in the
ischemic wall, but ischemic damage in the posterior papillary muscle, which
did not contain crystals, was 31.9%. Thus, regional myocardial dysfunction
reduced by nontransmural ischemia for 5 hr persisted for at least 3 days,
with only slight damage to the left ventricular free wall but considerable
infarction of the posterior papillary muscle. Full recovery of regional and
global contractile function of the free wall then occurred within a period
of 1 week.
ARTICLES
Sustained regional dysfunction produced by prolonged coronary stenosis: gradual recovery after reperfusion
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