Effects of Intracoronary Epinephrine on Coronary Blood Flow, Oxidative Metabolism and Mechanical Function in Normal and Stunned Myocardium in Dogs.
10.4097/kjae.2000.39.4.568
- Author:
Kyung Yeon YOO
1
;
Myoung Gi NO
;
Mi Kyoung KIM
;
Myung Ha YOON
;
Sung Su CHUNG
Author Information
1. Department of Anesthesiology, Chonnam National University, College of Dentistry Medical School & Hospital, Kwangju, Korea.
- Publication Type:Original Article
- Keywords:
Heart: coronary circulation;
myocardial ischemia;
reperfusion;
Sympathetic nervous system, pharmacology: epinephrine
- MeSH:
Anesthesia;
Animals;
Dogs*;
Enflurane;
Epinephrine*;
Flowmeters;
Heart Rate;
Ischemia;
Lactic Acid;
Metabolism*;
Myocardial Ischemia;
Myocardial Stunning*;
Myocardium;
Oxygen;
Oxygen Consumption;
Reperfusion;
Thoracic Surgery;
Vasodilation;
Ventricular Pressure
- From:Korean Journal of Anesthesiology
2000;39(4):568-577
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Epinephrine is frequently administered during cardiac surgery. The vascular response to epinephrine might be altered by ischemia and reperfusion, since altered vascular control has been demonstrated even after a short period of ischemia. To test the hypothesis, the effects of epinephrine on regional myocardial contractility, coronary blood flow (CBF) and myocardial oxygen consumption (MVO2) were investigated before and after ischemia in an open-chest canine myocardium. METHODS: Fifteen dogs were acutely instrumented under enflurane anesthesia to measure aortic and left ventricular pressures, pulmonary and left anterior descending (LAD) blood flows via Doppler flowmeter, and subendocardial segment length in the region supplied by LAD. Incremental doses of epinephrine (4, 10, 20, 30 ng/mL of LAD flow) were infused directly into LAD before (normal) and after a 15 min of LAD occlusion and subsequent 30 min-reperfusion (stunned). Segment shortening (%SS), as an index of regional myocardial contractility was evaluated. Simultaneous arterial and coronary venous contents of oxygen and lactate were measured during epinephrine (0.0, 4, 10, and 30 ng/mL) infusion. Effectiveness of metabolic vasodilation was determined from oxygen extraction ratio (EO2). RESULTS: Epinephrine infusions before ischemia resulted in dose-dependent increases in %SS and MVO2. These changes were accompanied by excessive increases in CBF, resulting in decreased EO2. After the ischemia and reperfusion, %SS was depressed and lactate extraction (Elac) was reduced, but similar mechanical responses to epinephrine were observed. However, in the stunned myocardium, CBF increased in parallel with increases in MVO2, resulting in unaltered EO2. Epinephrine infusion further decreased Elac dose-dependently in stunned myocardium. Heart rate and left ventricular systolic and diastolic pressures were little but similarly affected during epinephrine infusions before and after myocardial ischemia. CONCLUSIONS: The results suggest that epinephrine exerts positive inotropic effects in both normal and stunned myocardium, and that epinephrine causes direct coronary vasodilation in normal myocardium, but this effect is abolished in stunned myocardium in dogs. It is also suggested that epinephrine infusion depresses Elac dose-dependently in stunned myocardium.
