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  • 1
    ISSN: 1435-1803
    Keywords: Anoxia ; glycolysis ; heart ; ischemia ; myocardialmetabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Coronary artery disease causes an increase in glutamate uptake and alanine output by the heart. We assessed the effects of acute myocardial ischemia on alanine and glutamate exchange and ammonia production in 10 anesthetized open-chest domestic swine (46.9±0.7 kg). Coronary blood flow was controlled through an extracorporal perfusion circuit. After a nonischemic control period (aerobic) the blood flow in the left anterior descending coronary artery was reduced by 60%. Arterial and anterior interventricular venous samples where drawn before and during 35 min of ischemia. Subendocardial blood flow, measured using radiolabeled microspheres, decreased from 1.27±0.16 to 0.25±0.09 (ml/g)/min, and left-ventricular wall-thickening fell to 47% of aerobic values. Ischemia resulted in a significant increase in the rate of glucose uptake (p〈0.05) and a switch to net lactate production (p〈0.01). Ischemia did not affect the rates of alanine output (−0.9±1.0 vs. −0.3±0.3 μmol/min) or glutamate uptake (−0.4±1.1 vs. 0.3±0.6 μmol/min), but did increase the venous-arterial difference for ammonia (−4.1±4.1 to 52.7±5.5 μM, p〈0.0001) and the ammonia output (−0.33±0.24 to 1.34±0.14 μmol/min, p〈0.0001). In conclusion, acute ischemia did not stimulate greater alanine output or glutamate uptake. However, acute ischemia did cause an increase in anaerobic glycolysis rate and ammonia output, which reflects a profound disruption in myocardial energy metabolism.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1435-1803
    Keywords: Cardiac ; glycolysis ; heart ; myocardial ; metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The purpose of this investigation was to assess the effects of ischemia and reperfusion on the transmural levels of glucose and lactate in the interstitium in 11 open-chest swine. Microdialysis probes were used to estimate changes in interstitial metabolities across the ventricular wall. Probes were placed in the subepicardium and the subendocardium of the left anterior descending (LAD) coronary artery perfusion bed and in the midmyocardium of the circumflex (CFX) perfusion bed. The LAD coronary artery was cannulated and perfused with blood from the femoral artery through an extracorporal perfusion circuit. Ischemia was induced in the LAD perfusion bed by reducing the flow of the LAD perfusion pump by 60% for 50 min, and was followed by 30 min of reperfusion. Regional myocardial blood flow was assessed with fluorescent microspheres. Ischemia resulted in a transmural gradient in blood flow, with the most severe reduction in flow occurring in the subendocardium (p〈0.05). We found a significant reduction in interstitial glucose in both the LAD subepicardium (1.26±0.24 mM) (p=0.0009) and subendocardium (0.89±0.21 mM) (p=0.0001) during ischemia compared to the aerobic (non-ischemic) period (1.97±0.25 mM, 2.03±0.29 mM for the subepicardium and subendocardium, respectively). This coincided with a significant reduction in glucose delivery (LAD pump flow* arterial glucose) to the LAD perfusion bed during ischemia (54.5±8.5 μmol/min) compared to aerobic values (182.1±25.3 μmol/min) (p〈0.05). Interstitial lactate levels were significantly increased during ischemia in the LAD subendocardium (3.39±0.46 mM) compared to the aerobic values (1.73±0.46 mM) (p〈0.0029). A transmural gradient in interstitial lactate levels was observed during ischemia: this gradient was not seen during the aerobic period and was negated upon reperfusion. In conclusion, ischemia resulted in a decrease in interstitial glucose in both the LAD subepicardium and subendocardium, and an increase in interstitial lactate in the LAD subendocardium. Further, a transmural gradient in interstitial lactate levels was observed during ischemia, with the highest lactate values appearing in the subendocardium.
    Type of Medium: Electronic Resource
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