Effect of Propofol on Regional Myocardial Function and Metabolism in the Canine Stunned Myocardium.
10.4097/kjae.1998.34.6.1073
- Author:
Sang Hyun KWAK
1
;
Kyung Yeon YOO
;
Dae Hyun KIM
;
Woong Mo IM
Author Information
1. Department of Anesthesiology, Chonnam National University, Medical School, Kwangju, Korea.
- Publication Type:Original Article
- Keywords:
Anesthetics, intravenous: propofol;
Animal: dog;
Heart, myocardial function: systolic;
diastolic;
Heart: ischemia-reperfusion
- MeSH:
Anesthesia;
Animals;
Coronary Vessels;
Depression;
Dogs;
Halothane;
Lactic Acid;
Metabolism*;
Myocardial Stunning*;
Myocardium;
Necrosis;
Oxygen;
Oxygen Consumption;
Propofol*;
Reperfusion;
Stroke;
Ventricular Dysfunction;
Ventricular Pressure
- From:Korean Journal of Anesthesiology
1998;34(6):1073-1085
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: A brief period of coronary artery occlusion followed by reperfusion is known to produce prolonged period of ventricular dysfunction without necrosis (myocardial stunning). The present study was aimed to investigate the effects of propofol on regional myocardial functions and metabolism in postischemic stunned myocardium in an open-chest canine model. METHODS: Twenty-two dogs were acutely instrumented under halothane anesthesia to measure aortic and left ventricular pressure, pulmonary, left anterior descending (LAD) and circumflex (LCX) coronary artery flow, and subendocardial segment length in both the regions supplied by LAD and LCX. All animals were then subjected to a 15 min of LAD occlusion and subsequent reperfusion. In the expermental group (n=12), after 30 min of reperfusion halothane was replaced by a bolus of 5 mg.kg 1 of propofol followed by a continuous infusion for 30 min at 0.2 (baseline), 0.3, 0.4, and 0.5 mg.kg 1.min 1, whereas halothane was maintained without propofol infusion throughout the reperfusion period in the control group (n=10). Percent segment shortening (%SS) and the preload recruitable stroke work slope (Mw), as an index of regional myocardial contractility, and peak lengthening rate (dL/dtmax) and percent post-systolic shortening (%PSS), as an index of regional diastolic function, were evaluated. Metabolic data were determined from simultaneous arterial and coronary venous measurements of oxygen and lactate. RESULTS: Significant and dose-dependent decreases in both %SS (8.8 +/- 1.7 at 0.2 to 6.5 +/-1.6% at the 0.5 mg.kg 1.min 1 infusion) and Mw (1.45 +/- 0.15 at 0.2 to 0.87 +/- 0.07 erg.cm 3.104 at the 0.5 mg.kg 1.min 1) in the LAD region were observed. Concomitant decrease in dL/dtmax (52.4 +/- 3.9 at 0.2 to 40.2 +/- 3.6 mm.sec 1 at the 0.5 mg.kg 1.min 1 infusion) in the LAD region was also observed. In contrast, %SS, Mw, and dL/dtmax in the LCX region as well as %PSS in both regions remained unchanged throughout the infusion period. Propofol infusion was accompanied by progressive Although propofol produced progressive decreases in coronary blood flow and myocardial oxygen consumption in both regions, its administration was not associated with any changes in oxygen and lactate extraction ratios. CONCLUSION: The results indicate that propofol produces a greater depression on both regional systolic and diastolic functions in stunned myocardium than those in normal myocardium. However, propofol does not impair myocardial aerobic metabolism in both stunned and normal myocardium.
