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Cardiac endothelin release and infarct size, myocardial blood flow, and ventricular function in canine infarction and
R F Kelly1, T L Hursey, G L Schaer
1Section of Cardiology, Rush Medical College, Rush-Presbyterian-St. Luke's Medical Center, Chicago, IL 60612, USA.
Insights
Increased endothelin-1 (ET-1) release during myocardial infarction correlates with larger infarct size and impaired blood flow. This suggests ET-1 may worsen outcomes in acute myocardial infarction.
Area of Science:
- Cardiology
- Biomedical Science
Background:
- Endothelin-1 (ET-1), a potent vasoconstrictor, is implicated in acute myocardial infarction (AMI) pathophysiology.
- The exact role of ET-1 in AMI, particularly its relationship with infarct size and cardiac function, requires further elucidation.
Purpose of the Study:
- To investigate the interrelationships between cardiac ET-1 release and infarct size.
- To evaluate the association of ET-1 release with myocardial blood flow and ventricular function post-myocardial infarction.
Main Methods:
- Utilized a canine model of coronary artery occlusion and reperfusion (3 hours each).
- Measured coronary sinus and aortic ET-1 levels via radioimmunoassay.
- Assessed left ventricular function (echocardiography) and regional myocardial blood flow (colored microspheres).
- Determined myocardial infarct size using postmortem staining techniques.
Main Results:
- Coronary occlusion and reperfusion significantly elevated coronary sinus ET-1 and cardiac ET-1 release.
- A trend towards increased ET-1 release was observed with larger infarct sizes and in cases of significant no-reflow.
- ET-1 release correlated with increased contractility in nonischemic segments and improved global left ventricular function.
Conclusions:
- Greater cardiac ET-1 release in this canine AMI model was linked to larger infarcts and the no-reflow phenomenon.
- Increased ET-1 release may adversely affect AMI outcomes by reducing reperfused myocardial blood flow and increasing contractility in nonischemic areas.
Background:
The potent vasoconstrictor endothelin-1 (ET) may play an important pathophysiologic role in acute myocardial infarction, but its precise effects are incompletely understood. The purpose of this study was to evaluate the interrelationships between cardiac ET-1 release and infarct size, myocardial blood flow, and ventricular function.
Methods:
Fifteen closed chest dogs underwent 3 hours of coronary artery occlusion followed by 3 hours of reperfusion. Coronary sinus and aortic ET-1 levels during occlusion and after reperfusion were determined by radioimmunoassay. Left ventricular function and regional myocardial blood flow were measured by echocardiography and colored microspheres, respectively. Myocardial infarct size was determined by postmortem staining with blue dye and triphenyl tetrazolium chloride.
Results:
Coronary occlusion and reperfusion produced significant elevations of coronary sinus ET-1 (p < 0.05) and cardiac ET-1 release (p < 0.05), and a trend toward an increase in aortic ET-1 (p = 0.08). A trend toward more ET-1 release was observed in dogs with larger infarcts (p = 0.06), and in dogs with substantial no-reflow in the reperfused territory (p = 0.05). Endothelin-1 release also was associated with increased contractility in nonischemic myocardial segments (p = 0.002), and ET-1 correlated with increased global left ventricular function (p < 0.02).
Conclusions:
In this canine model of coronary occlusion and reperfusion, greater increases in cardiac ET-1 release were observed in dogs with larger infarcts, and increased ET-1 release was associated with the no-reflow phenomenon in the reperfused territory. These data suggest that ET-1 release may have adverse consequences in acute myocardial infarction, including a reduction of myocardial blood flow in the reperfused zone after reperfusion and increased contractility in nonischemic myocardium.