The primary goals of the cardiovascular physiology lab are: (i) to elucidate the impact of adult stem cell therapy on ventricular function and mechanics; (ii) to understand the biology of myocardial ischemia/reperfusion injury and examine various therapeutic approaches to mitigate this injury; (iii) to explore the effects of genetic manipulations on cardiac function; (iv) to examine the effects of cardiopulmonary arrest on ventricular function and hemodynamics; and (v) to examine the effects of aging on cardiac physiology.
Myocardial ischemia/reperfusion injury: A number of studies currently utilize the in vivo mouse model of myocardial I/R injury that is achieved by temporary occlusion of the left anterior descending coronary artery in anesthetized mice. The procedure requires excellent microsurgical techniques and careful monitoring of numerous physiological parameters throughout the experiment. This model produces myocardial infarction in mice in highly reproducible fashion, and provides an excellent read-out for efficacy of various therapeutic approaches.
Hemodynamic studies: These invasive studies are extremely useful in the assessment of cardiac function and volume in anesthetized mice in vivo. The intraarterial and intracardiac pressures and derived volumes are highly reproducible and provide accurate and physiological measurements.
Myocardial infarct size: This is an essential accompaniment to the myocardial I/R procedure. Myocardial sections are stained with triphenyltetrazolium chloride (TTC) and phthalo blue, and the infarct zone, ischemic zone, and the nonischemic zone are calculated by computerized planimetry.
Induction of cardiopulmonary arrest: This procedure utilizes exsanguination to achieve pulseless electrical activity in mice. Simultaneous discontinuation of mechanical ventilation induces a state that closely mimics cardiopulmonary arrest in humans. This model is very useful for the study of therapeutic approaches for cardiac arrest.
Investigators, trainees, and associates: