Myocardial stunning in exercise-induced ischemia in dogs: lack of late preconditioning

2001 ◽  
Vol 280 (1) ◽  
pp. H302-H310 ◽  
Author(s):  
Olivier Parent De Curzon ◽  
Bijan Ghaleh ◽  
Renaud Tissier ◽  
Jean-François Giudicelli ◽  
Luc Hittinger ◽  
...  
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Myocardial Stunning ◽  
Time Course ◽  
Reactive Hyperemia ◽  
Coronary Artery Occlusion ◽  
Left Ventricular ◽  
Wall Thickening ◽  
Late Preconditioning ◽  
Exercise Induced

Late preconditioning (PC) against myocardial stunning develops after coronary artery occlusion (CAO) at rest and subsequent reperfusion. We investigated whether late PC occurs after exercise-induced ischemia (high-flow ischemia) in dogs. A circumflex coronary artery stenosis (by using occluders) was set up before the onset of treadmill exercise in nine chronically instrumented dogs to suppress exercise-induced increase in mean coronary blood flow velocity (CBFV, Doppler) without simultaneously affecting left ventricular (LV) wall thickening (Wth) at rest. Two similar exercises were performed 24 h apart. On day 1, LV Wth was reduced by 84 ± 5% ( P < 0.01), and exercise-induced increases in transmural myocardial blood flow (MBF, fluorescent microspheres) in the ischemic zone were blunted. LV Wth was depressed throughout the first 10 h and returned to its baseline value after 24 h. On day 2, changes in LV Wth and MBF were similar as was the time course for LV Wth recovery, indicating lack of late PC. Also, CBFV responses to acetylcholine, nitroglycerin, and reactive hyperemia (20-s CAO) were not significantly different on days 1 and 2. Similar results were obtained in a subgroup of four additional dogs with more severe stenosis during exercise. Late PC against myocardial stunning was confirmed to occur in a model of 10-min CAO followed by coronary artery reperfusion (CAR) in another four dogs. Thus in contrast with CAO at rest followed by CAR, severe myocardial ischemia in coronary flow-limited exercising dogs does not induce late PC against myocardial stunning.

Differences in myocardial stunning following coronary artery occlusion in conscious dogs, pigs, and baboons

1996 ◽  
Vol 270 (4) ◽  
pp. H1312-H1322 ◽  
Author(s):  
Y. T. Shen ◽  
S. F. Vatner
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Myocardial Stunning ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Conscious Dogs ◽  
Wall Thickening ◽  
Systolic Wall Thickening

To determine whether myocardial stunning differs among dogs, pigs, and baboons and is reproducible within species, we examined the effects of 10-min coronary artery (CA) occlusion (CAO) on 9 conscious dogs, 12 minipigs, and 6 baboons. During 10-min CAO, systolic wall thickening in the ischemic zone fell similarly in dogs (-108 +/- 5.6%), pigs (-102 +/- 1.8%), and baboons (-107 +/- 5.7%), but blood flow fell more (P < 0.05) in the subepicardium in pigs (0.07 +/- 0.01 ml.min-1.g-1) and baboons (0.07 +/- 0.02 ml.min-1.g-1) than in dogs (0.18 +/- 0.03 ml.min-1.g-1). At 1 h after CA reperfusion (CAR), wall thickening was reduced more (P < 0.05) in dogs (-40 +/- 4.2%) than in pigs (-22 +/- 2.1%) and baboons (-4 +/- 2.4%). In five dogs and five pigs, three separate 10-min CAO, each 2 days apart, were also examined. In dogs, reductions in wall thickening after CAR were significantly less following the second (-26 +/- 4.2%) or third (-30 +/- 3.2%) CAO, compared with the first CAO (-47 +/- 4.9%). In contrast, repetitive CAO did not induce differences in recovery of wall thickening in pigs. These results indicate that myocardial stunning is less severe in conscious pigs and baboons, compared with conscious dogs, despite more intense transmural ischemia. The dogs demonstrated a "preconditioning-like effect" with serial brief CAO, which was not exhibited in pigs.

Differential effects of postconditioning on myocardial stunning and infarction: a study in conscious dogs and anesthetized rabbits

2006 ◽  
Vol 291 (3) ◽  
pp. H1345-H1350 ◽  
Author(s):  
Nicolas Couvreur ◽  
Laurence Lucats ◽  
Renaud Tissier ◽  
Alain Bize ◽  
Alain Berdeaux ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Infarct Size ◽  
Myocardial Stunning ◽  
Ischemia Reperfusion ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Segment Length ◽  
Wall Thickening ◽  
Area At Risk

Postconditioning, i.e., brief intermittent episodes of myocardial ischemia-reperfusion performed at the onset of reperfusion, reduces infarct size after prolonged ischemia. Our goal was to determine whether postconditioning is protective against myocardial stunning. Accordingly, conscious chronically instrumented dogs (sonomicrometry, coronary balloon occluder) were subjected to a control sequence (10 min coronary artery occlusion, CAO, followed by coronary artery reperfusion, CAR) and a week apart to postconditioning with four cycles of brief CAR and CAO performed at completion of the 10 min CAO. Three postconditioning protocols were investigated, i.e., 15 s CAR/15 s CAO ( n = 5), 30 s CAR/30 s CAO ( n = 7), and 1 min CAR/1 min CAO ( n = 6). Left ventricular wall thickening was abolished during CAO and similarly reduced during subsequent stunning in control and postconditioning sequences (e.g., at 1 h CAR, 33 ± 4 vs. 34 ± 4%, 30 ± 4 vs. 30 ± 4%, and 33 ± 4 vs. 32 ± 4% for 15 s postconditioning, 30 s postconditioning, and 1 min postconditioning vs. corresponding control, respectively). We confirmed this result in anesthetized rabbits by demonstrating that shortening of left ventricular segment length was similarly depressed after 10 min CAO in control and postconditioning sequences (4 cycles of 30 s CAR/30 s CAO). In additional rabbits, the same postconditioning protocol significantly reduced infarct size after 30 min CAO and 3 h CAR (39 ± 7%, n = 6 vs. 56 ± 4%, n = 7 of the area at risk in postconditioning vs. control, respectively). Thus, contrasting to its beneficial effects on myocardial infarction, postconditioning does not protect against myocardial stunning in dogs and rabbits. Conversely, additional episodes of ischemia-reperfusion with postconditioning do not worsen myocardial stunning.

Effect of superoxide dismutase and catalase on regional dysfunction after exercise-induced ischemia

1992 ◽  
Vol 263 (2) ◽  
pp. H392-H398 ◽  
Author(s):  
D. C. Homans ◽  
R. Asinger ◽  
T. Pavek ◽  
M. Crampton ◽  
P. Lindstrom ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Coronary Artery ◽  
Myocardial Stunning ◽  
Coronary Artery Stenosis ◽  
Left Ventricular ◽  
Artery Stenosis ◽  
Regional Myocardial Blood Flow ◽  
Wall Thickening ◽  
Regional Wall ◽  
Exercise Induced

This study was designed to test the hypothesis that the oxygen free radical scavengers superoxide dismutase (SOD) and catalase may reduce myocardial “stunning” after exercise-induced ischemia. To test this hypothesis, 8 mongrel dogs performed treadmill exercise for 10 min in the presence of a flow-limiting coronary artery stenosis. Regional left ventricular function was measured with ultrasonic microcrystals implanted to measure regional wall thickening. Regional myocardial perfusion was measured with radioactive microspheres. The combination of SOD (5 mg/kg iv) and catalase (5 mg/kg iv) did not affect heart rate, blood pressure, coronary artery flow, or regional myocardial blood flow at rest, during exercise, or in the postexercise period. SOD and catalase had no effect on regional wall thickening at rest before exercise. During exercise in the absence of a coronary artery stenosis, thickening was slightly lower during SOD and catalase infusion (27 +/- 11.0 vs. 30.8 +/- 11.5%, SOD vs. control P = 0.05). During exercise in the presence of a coronary artery stenosis, there was no difference in thickening. Infusion of SOD and catalase affected neither the transient rebound function occurring early after exercise nor the prolonged period of stunning. These results indicate that the myocardial stunning that follows exercise-induced ischemia is unlikely to be mediated by oxygen free radicals.

Reduction in postsystolic wall thickening during late preconditioning

2007 ◽  
Vol 292 (1) ◽  
pp. H158-H164 ◽  
Author(s):  
Xavier Monnet ◽  
Laurence Lucats ◽  
Patrice Colin ◽  
Geneviève Derumeaux ◽  
Jean-Luc Dubois-Rande ◽  
...  
Keyword(s):  
Myocardial Stunning ◽  
Time Course ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Wall Thickening ◽  
Circumflex Artery ◽  
Late Preconditioning ◽  
Rapid Ventricular Pacing ◽  
Systolic Wall Thickening ◽  
Similar Decrease

Brief coronary artery occlusion (CAO) and reperfusion induce myocardial stunning and late preconditioning. Postsystolic wall thickening (PSWT) also develops with CAO and reperfusion. However, the time course of PSWT during stunning and the regional function pattern of the preconditioned myocardium remain unknown. The goal of this study was to investigate the evolution of PSWT during myocardial stunning and its modifications during late preconditioning. Dogs were chronically instrumented to measure (sonomicrometry) systolic wall thickening (SWT), PSWT, total wall thickening (TWT = SWT + PSWT), and maximal rate of thickening (dWT/d tmax). Two 10-min CAO (circumflex artery) were performed 24 h apart ( day 0 and day 1, n = 7). At day 0, CAO decreased SWT and increased PSWT. During the first hours of the subsequent stunning, evolution of PSWT was symmetrical to that of SWT. At day 1, baseline SWT was similar to day 0, but PSWT was reduced (−66%), while dWT/d tmax and SWT/TWT ratio increased (+48 and +14%, respectively). After CAO at day 1, stunning was reduced, indicating late preconditioning. Simultaneously vs. day 0, PSWT was significantly reduced, and dWT/d tmax as well as SWT/TWT ratio were increased, i.e., a greater part of TWT was devoted to ejection. Similar decrease in PSWT was observed with a nonischemic preconditioning stimulus (rapid ventricular pacing, n = 4). In conclusion, a major contractile adaptation occurs during late preconditioning, i.e., the rate of wall thickening is enhanced and PWST is almost abolished. These phenotype adaptations represent potential approaches for characterizing stunning and late preconditioning with repetitive ischemia in humans.

Mechanical Unloading Properties of Axial Flow Pumps and their Effect on Myocardial Stunning

1995 ◽  
Vol 18 (12) ◽  
pp. 766-771 ◽  
Author(s):  
F. R. Waldenberger ◽  
B. Meyns ◽  
P. Wouters ◽  
E. De Ruyter ◽  
E. Pongo ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Myocardial Stunning ◽  
Myocardial Dysfunction ◽  
Axial Flow ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Wall Thickening ◽  
Myocardial Wall Motion ◽  
Mechanical Unloading ◽  
Artery Disease

Postischemic myocardial dysfunction affects morbidity and mortality in patients with coronary artery disease. It is known that mechanical unloading of the left heart ventricle can positively influence postischemic myocardial dysfunction. In this respect we tested two miniaturised axial flow pumps, i.e. the 14-F and the 21-F Hemopump®. An experimental study was carried out on 30 open chest sheep where regional myocardial wall motion was followed using sonomicrometry in a preparation of transient coronary artery occlusion. Only the larger 21-F Hemopump® showed hemodynamically significant unloading of the left ventricle. Furthermore, as far as stunning is concerned, systolic wall thickening recovered better when this type of pump was used during reperfusion. Also postejection thickening, which is an indication of diastolic postischemic dysfunction, is reduced significantly in the postischemic area (ANOVA, p<0.05). Thus, the 21F Hemopump®, but not the 14F Hemopump®, provides adequate mechanical unloading in order to beneficially influence myocardial stunning.

Effects of beta-blockade on regional myocardial flow and function during exercise

1984 ◽  
Vol 247 (1) ◽  
pp. H52-H60 ◽  
Author(s):  
M. Matsuzaki ◽  
J. Patritti ◽  
T. Tajimi ◽  
M. Miller ◽  
W. S. Kemper ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Myocardial Dysfunction ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Beta Blockade ◽  
Wall Thickening ◽  
Ischemic Area ◽  
Ischemic Region ◽  
Exercise Induced ◽  
Control Exercise

We examined the effects of a cardioselective beta-blocking drug on exercise-induced regional myocardial ischemia in 10 conscious dogs with chronic coronary artery stenosis. An ameroid constrictor, Doppler flowprobe, and hydraulic cuff were placed around the left circumflex coronary artery, and left ventricular pressure (LVP), systolic wall thickening (% delta WT; by sonomicrometry), and myocardial blood flow (MBF; microspheres) were measured during control standing, control treadmill exercise, and identical exercise after atenolol (1 mg/kg po). Prior to study, in every dog % delta WT and MBF in the ischemic area were normal at rest, indicating collateral development. During control exercise, % delta WT in the ischemic region markedly decreased from 27 to 4%, and transmural ischemia was evident in that region. Heart rate, systolic LVP, and LV (+)dP/dt were significantly lower during exercise after atenolol than during control exercise. % delta WT in the normal area was only 81% of that during control exercise, but dysfunction in the ischemic area was improved (77% increase compared with control exercise). Accompanying the improved function was a significant increase of MBF/beat and relative MBF in the ischemic zone; the endocardial-to-epicardial ratio increased from 0.27 to 0.47. Thus atenolol improved regional MBF distribution, thereby diminishing exercise-induced regional myocardial dysfunction and accelerating its recovery.

A new thermal sensor for surface-based measurement of local myocardial perfusion

1983 ◽  
Vol 244 (3) ◽  
pp. H449-H453
Author(s):  
F. S. Castellana ◽  
R. B. Case ◽  
R. Skalak ◽  
J. M. Cho
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Reactive Hyperemia ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Tissue Blood Flow ◽  
Thermal Sensor ◽  
Epicardial Surface ◽  
Continuous Surface ◽  
Flow Changes

The transient response of a new thermal sensor for continuous surface-based measurement of local tissue blood flow was evaluated in the beating dog heart. The sensor is 2.5 mm square, tests on the heart, and responds to flow changes only within a region of tissue 3-4 mm below its location on the epicardial surface. Initial studies demonstrate excellent sensitivity, good frequency response with a time constant of the order of 10-11 s, and an ability to continuously monitor changes in local myocardial blood flow during a variety of well-understood interventions, including coronary artery occlusion, reactive hyperemia, and intravenous administration of nitroglycerin and dipyridamole.

Responses to coronary artery occlusion in conscious dogs with selective cardiac denervation

1988 ◽  
Vol 255 (3) ◽  
pp. H525-H533 ◽  
Author(s):  
Y. T. Shen ◽  
D. R. Knight ◽  
S. F. Vatner ◽  
W. C. Randall ◽  
J. X. Thomas
Keyword(s):  
At Risk ◽  
Blood Flow ◽  
Coronary Artery ◽  
Infarct Size ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Conscious Dogs ◽  
Wall Thickening ◽  
Area At Risk ◽  
Cardiac Denervation

The extent to which cardiac denervation alters responses to myocardial ischemia remains controversial. This study compared responses to 24-h coronary artery occlusion (CAO) on measurements of wall thickness (ultrasonic crystals), regional myocardial blood flow (microspheres), and infarct size (triphenyltetrazolium chloride technique) in three groups of conscious dogs with 1) selective posterior left ventricular (LV) wall denervation, 2) selective ventricular denervation, or in 3) intact dogs. After CAO, hemodynamic changes were not different among the three groups. Wall thickening in the ischemic zone became akinetic or paradoxical early after CAO and did not recover in any group over the 24-h monitoring period. Blood flow in the area at risk fell similarly in all groups. Infarct size, as a percentage of the area at risk, was 45 +/- 7% in intact, 48 +/- 6% in posterior LV wall-denervated, and 48 +/- 8% in ventricular-denervated group. There was, however, a lower (P less than 0.05) frequency of arrhythmic beats per minute after 3 h of CAO in the ventricular-denervated group (3.2 +/- 1.4) compared with the intact (11.3 +/- 4.1) or posterior wall-denervated (12.6 +/- 3.2) group. An additional group of ventricular-denervated dogs was studied to determine the effects of sequential, brief 2-min CAO at 2, 4, and 8 wk after denervation. Responses of regional wall thickening to CAO were not affected significantly even after 8 wk following ventricular denervation. Thus, in conscious dogs, neither selective ventricular denervation nor selective denervation of the posterior LV wall improved collateral blood flow, affected regional function favorably, or reduced infarct size after CAO.

Depression of regional blood flow and wall thickening after brief coronary occlusions

1978 ◽  
Vol 234 (6) ◽  
pp. H653-H659 ◽  
Author(s):  
G. R. Heyndrickx ◽  
H. Baig ◽  
P. Nellens ◽  
I. Leusen ◽  
M. C. Fishbein ◽  
...  
Keyword(s):  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Coronary Occlusion ◽  
Reactive Hyperemia ◽  
Left Ventricular ◽  
Regional Myocardial Blood Flow ◽  
Wall Thickening ◽  
Flow Ratio ◽  
Systolic Wall Thickening ◽  
Regional Myocardial Blood

The effects of a 15-min coronary occlusion and subsequent reperfusion were investigated in conscious dogs previously instrumented for measurement of left ventricular pressure, dP/dt, regional wall thickening, electrograms, and myocardial blood flow. Coronary occlussion reduced overall left ventricular function only slightly but eliminated systolic wall thickening in the ischemic zone and reduced regional myocardial blood flow in the ischemic zone from 1.04 +/- 0.04 to 0.27 +/- 0.02 ml/min per g and the endo/epi flow ratio from 1.23 +/- 0.04 to 0.44 +/- 0.04, while S-T segment elevation increased from 1.1 +/- 0.3 to 8.2 +/- 0.9 mV. After release of the occlusion, S-T segment elevation disappeared within 1 min while reactive hyperemia in the previously occluded artery and a transient increase in cardiac diastolic wall thickness occurred and then subsided by 15 min. In contrast, systolic wall thickening and the endo/epi flow ratio remained significantly depressed for more than 3 h. Thus reperfusion after a 15 minute coronary occlusion results in a prolonged period of reduced regional myocardial blood flow, particularly in the endocardial layers, which correlates with the prolonged depression of regional myocardial shortening and wall thickening.

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