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.

Improvement by isosorbide dinitrate of exercise-induced regional myocardial dysfunction

1980 ◽  
Vol 239 (3) ◽  
pp. H399-H405
Author(s):  
T. Kumada ◽  
K. P. Gallagher ◽  
M. Miller ◽  
M. McKown ◽  
F. White ◽  
...  
Keyword(s):  
Isosorbide Dinitrate ◽  
Myocardial Function ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Segment Length ◽  
Wall Thickening ◽  
Regional Myocardial Function ◽  
Exercise Induced ◽  
Coronary Obstruction ◽  
Control Exercise

Sonomicrometry was used in 10 conscious dogs to measure regional segment length and dynamic wall thickness by telemetry in a zone supplied by the left circumflex coronary artery after implantation of an ameroid constrictor. When coronary obstruction was nearly complete and collaterals had developed (24-42 days), control exercise and exercise runs after oral isosorbide dinitrate were carried out. During control runs, significant increases occurred in hemodynamic parameters, and percent shortening in normal segments increased (P < 0.01). During the repeat runs after isosorbide dinitrate, there were smaller increases in left ventricular systolic and end-diastolic pressures and significantly reduced end-diastolic dimensions. In addition, percent wall thickening and percent segment shortening in the ischemic zone did not deteriorate significantly during exercise. In this animal model, which appears to mimic chronic single-vessel coronary heart disease, isosorbide dinitrate can prevent exercise-induced deterioration of regional myocardial function.

Pre-Clinical Evaluation of a Novel, Pneumatic, Ventricular Assist Device (Medos® HIA-VAD®) under Pathophysiological Conditions

1997 ◽  
Vol 20 (7) ◽  
pp. 389-396 ◽  
Author(s):  
F.R. Waldenberger ◽  
B. Meyns ◽  
H. Reul ◽  
R. Eilers ◽  
W. Flameng
Keyword(s):  
Coronary Artery ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Assisted Circulation ◽  
Wall Thickening ◽  
Base Line ◽  
Assist Device ◽  
Circumflex Artery ◽  
Group I ◽  
Group Ii

To evaluate a new cardiac assist system, the Medos® HIA-VAD®, we studied the effects of mechanical unloading on regional and global myocardial dysfunction. As a model for the regional temporary contractile dysfunction we chose an anesthetized, open chest preparation in sheep. We occluded the diagonal coronary artery for 15 minutes and reperfused for 90 minutes. Hemodynamic parameters and wall thickening were monitored. Unloading with the 60-ml Medos® HIA-VAD® was performed either during ischemia (group II) or during reperfusion (group III). The recovery of non-uniformity indicated by post-ejection wall thickening was significantly faster (p<0.05) in both groups if compared to the non-assisted group (group I) (all groups n=4). Recovery of systolic wall thickening in the postischemic region in group I was only 76±12%, while it was 103±11% and 92±11% in groups II and III, respectively (p<0.05). In a canine model of global left ventricular failure, we occluded the left anterior descending coronary artery for 20 min, and after 5 minutes of reperfusion, the circumflex artery for 45 min (group I, n=5). After 5 min of CX occlusion in group II we performed assisted circulation for 90 min with the 10-ml (n=5) and the 25-ml (n=5) Medos® HIA-VAD®. In group I, no dog survided, in group II, all survided 4 hours of reperfusion (n=10). Lactate at the end of the experiment was 1.1±0.9 mmol/L (10-ml) and 1.1±0.2 mmol/L (25-ml) (p>0.05 vs. base line). We conclude that the Medos® HIA-VAD® is a reliable assist device that enhances myocardial recovery and allows sufficient peripheral circulation in the case of cardiogenic shock.

Effects of yohimbine and desipramine on cardiac noradrenaline release and ventricular arrhythmias during acute coronary artery occlusion and reperfusion in anesthetized dogs

1987 ◽  
Vol 65 (11) ◽  
pp. 2244-2253 ◽  
Author(s):  
Nobuharu Yamaguchi ◽  
Daniel Lamontagne ◽  
Ghislain Boudreau ◽  
Reginald Nadeau ◽  
Jacques de Champlain
Keyword(s):  
Coronary Artery ◽  
Nerve Stimulation ◽  
Left Ventricular Pressure ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Neuronal Uptake ◽  
Ischemic Region ◽  
Anesthetized Dogs ◽  
Na Release

Effects of yohimbine (YHMB, an α2-antagonist) and desipramine (DMI, a neuronal uptake inhibitor) were compared on cardiac noradrenaline (NA) release either upon left ansa subclavia nerve stimulation during acute occlusion of the left anterior descending coronary artery (LAD) or upon subsequent LAD reperfusion without stimulation in anesthetized dogs. In control dogs, before LAD occlusion, coronary sinus (CS) NA output increased from 5.4 ± 1.0 to 26.8 ± 4.0 ng/min (p < 0.05) upon stimulation (2 Hz, 30 s). The response to stimulation remained unchanged 25 min after LAD occlusion. During reperfusion 60 min after occlusion, the output of CS-NA and lactate increased from 6.1 ± 0.8 to 51.3 ± 19.4 ng/min (p < 0.05) and from 2.7 ± 0.5 to 6.7 ± 1.3 mg/min (p < 0.05), respectively. In dogs treated with YHMB, the stimulation-induced increase in NA output was potentiated at least fourfold (p < 0.05) either before or during LAD occlusion, but not during reperfusion. In dogs receiving DMI, stimulation-induced CS-NA output was enhanced to a similar extent (approximately twofold, p < 0.05) either before or during occlusion, while reperfusion-induced NA output was markedly potentiated by approximately ninefold (p < 0.05). Maximum dP/dt of left ventricular pressure remained unchanged upon reperfusion in all groups. The total arrhythmic ratio in the drug-treated groups did not significantly differ from the ratio in control dogs upon either stimulation or reperfusion. The data suggest that an abrupt increase in NA output upon reperfusion may result from a washout of NA locally accumulated in the ischemic and (or) peri-ischemic region during the preceding occlusion period, and that N A thus released does not have substantial hemodynamic effects. The results indicate that in the presence of YHMB or DMI, the potentiated increase in NA release in response to either nerve stimulation during LAD occlusion or to reperfusion without stimulation did not aggravate ventricular arrhythmia, most probably owing to the antiarrhythmic properties of these substances.

Cardiopulmonary resuscitation in a rat model of chronic myocardial ischemia

2006 ◽  
Vol 101 (4) ◽  
pp. 1091-1096 ◽  
Author(s):  
Xiangshao Fang ◽  
Wanchun Tang ◽  
Shijie Sun ◽  
Lei Huang ◽  
Yun-Te Chang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Coronary Artery ◽  
Cardiopulmonary Resuscitation ◽  
Myocardial Ischemia ◽  
Rat Model ◽  
Myocardial Dysfunction ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Control Group ◽  
Chronic Myocardial Ischemia

Our group has developed a rat model of cardiac arrest and cardiopulmonary resuscitation (CPR). However, the current rat model uses healthy adult animals. In an effort to more closely reproduce the event of cardiac arrest and CPR in humans with chronic coronary disease, a rat model of coronary artery constriction was investigated during cardiac arrest and CPR. Left coronary artery constriction was induced surgically in anesthetized, mechanically ventilated Sprague-Dawley rats. Echocardiography was used to measure global cardiac performance before surgery and 4 wk postsurgery. Coronary constriction provoked significant decreases in ejection fraction, increases in left ventricular end-diastolic volume, and increases left ventricular end-systolic volume at 4 wk postintervention, just before induction of ventricular fibrillation (VF). After 6 min of untreated VF, CPR was initiated on three groups: 1) coronary artery constriction group, 2) sham-operated group, and 3) control group (without preceding surgery). Defibrillation was attempted after 6 min of CPR. All the animals were resuscitated. Postresuscitation myocardial function as measured by rate of left ventricular pressure increase at 40 mmHg and the rate of left ventricular pressure decline was more significantly impaired and left ventricular end-diastolic pressure was greater in the coronary artery constriction group compared with the sham-operated group and the control group. There were no differences in the total shock energy required for successful resuscitation and duration of survival among the groups. In summary, this rat model of chronic myocardial ischemia was associated with ventricular remodeling and left ventricular myocardial dysfunction 4 wk postintervention and subsequently with severe postresuscitation myocardial dysfunction. This model would suggest further clinically relevant investigation on cardiac arrest and CPR.

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.

Cumulative deterioration of myocardial function after repeated episodes of exercise-induced ischemia

1989 ◽  
Vol 256 (5) ◽  
pp. H1462-H1471 ◽  
Author(s):  
D. C. Homans ◽  
D. D. Laxson ◽  
E. Sublett ◽  
P. Lindstrom ◽  
R. J. Bache
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Coronary Stenosis ◽  
Myocardial Dysfunction ◽  
Wall Thickening ◽  
The Third ◽  
Single Period ◽  
Exercise Period ◽  
Exercise Induced ◽  
Systolic Wall Thickening

To determine whether progressive regional myocardial dysfunction occurs after repetitive episodes of exercise-induced ischemia, 10 dogs were instrumented with ultrasonic microcrystals for determination of regional myocardial wall thickening, circumflex artery electromagnetic flow probes, and hydraulic coronary artery occluders. Dogs performed treadmill exercise in the presence of a coronary artery stenosis, which limited coronary blood flow to control levels. Dogs performed a single 10-min exercise period one day and three identical runs separated by 1-h rest periods on the alternate day. At rest before the first exercise period, circumflex wall thickening was 18.8 +/- 6.7% and increased to 25.5 +/- 10.6% during exercise before the application of coronary stenosis. On the day that three exercise trials were performed, circumflex systolic wall thickening at rest before the third exercise period (9.7 +/- 4.0%) and during exercise without coronary stenosis (17.3 +/- 7.3%) were both significantly lower than during the first exercise period (P less than 0.0125). During exercise with stenosis, circumflex systolic wall thickening fell to 4.6 +/- 4.7% during a single run, and 5.0 +/- 2.0% during the third of three consecutive runs. Wall thickening was significantly lower 2 h after the third consecutive run (9.1 +/- 2.4%) than 2 h after a single period of exercise-induced ischemia (14.8 +/- 7.6%; P 0.0125). Transmural myocardial blood flow to circumflex myocardium during the third period of exercise-induced ischemia (0.93 +/- 0.47 ml.min-1.g-1) was not different than during the single period of exercise (0.84 +/- 0.47 ml.min-1.g-1). It is concluded that repetitive episodes of exercise-induced ischemia result in cumulative postexercise regional myocardial dysfunction.

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.

Effects of ischemia on cardiac afferent sympathetic and vagal reflexes in dog

1988 ◽  
Vol 255 (1) ◽  
pp. H26-H35 ◽  
Author(s):  
H. Inoue ◽  
B. T. Skale ◽  
D. P. Zipes
Keyword(s):  
Coronary Artery ◽  
Time Course ◽  
Coronary Occlusion ◽  
Test Site ◽  
Left Ventricular ◽  
Balloon Occlusion ◽  
Diagonal Branch ◽  
Control Value ◽  
Ischemic Area ◽  
Ischemic Region

To determine the time course of afferent sympathetic and vagal denervation after coronary occlusion and that of neural recovery after reperfusion, we measured the vasopressor responses to bradykinin and the vasodepressor responses to nicotine applied in a felt pad to the left ventricular epicardium of open-chest dogs. Shortly after latex injection of a diagonal branch of the left anterior descending coronary artery (LAD), the vasopressor response to bradykinin applied to the transmural ischemic area (n = 7) or apically to it (n = 6) was interrupted or attenuated. In contrast, nontransmural ischemia produced by ligation of the diagonal branch did not attenuate the response to bradykinin applied to the ischemic region (n = 6) or apically to it (n = 7). Transmural ischemia produced by occlusion of a diagonal branch of the LAD and a lateral marginal branch of the left circumflex coronary artery (n = 8) or by intraluminal balloon occlusion of the LAD (n = 7) decreased the vasopressor response to bradykinin applied within or apically to the ischemic area in less than 13 min. The vasopressor response to bradykinin became attenuated when the myocardial blood flow in the epicardial test site decreased to approximately 40% or less of the control value. Nontransmural ischemia produced by occlusion of a diagonal branch (n = 7) attenuated the vasodepressor response to nicotine applied to the nonischemic area apically to the occlusion in less than 13 min. A 15-min coronary occlusion followed by reperfusion produced reversible attenuation of afferent neural responses. We conclude that ischemia interrupts afferent sympathetic and vagal cardiac reflex responses to bradykinin and nicotine and that these alterations are reversible after reperfusion.

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.

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