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  • Electronic Resource  (2)
  • Adenosine  (1)
  • Cardiac function  (1)
Material
  • Electronic Resource  (2)
Years
  • 1
    ISSN: 1432-1912
    Keywords: Magnesium ; Cardiac function ; Energy metabolism ; Myocardium ; Reperfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of high concentration of magnesium on both mechanical dysfunction and metabolic damage after ischaemia-reperfusion was studied in isolated rat hearts. The heart was perfused by the Langendorff's technique at a constant flow (10 ml/min) with modified Krebs-Henseleit solution and driven at 300 beats/min. The heart was made ischaemic by reducing the flow to 0 ml/min for 25 min, and then reperfused at the constant flow for 15 min. MgSO4 was added to the perfusate for 5 min before the onset of ischaemia, or after the end of ischaemia (after the onset of reperfusion). Ischaemia-reperfusion produced both mechanical dysfunction (as evidenced by an increase in the left ventricular end diastolic pressure and a decrease in the left ventricular developed pressure) and metabolic damage [as evidenced by a decrease in the myocardial adenosine triphosphate (ATP)]. When 15 mmol/l MgSO4 was given before ischaemia, there was no appreciable recovery of mechanical function, whereas when given after ischaemia (during reperfusion), there was a marked recovery of mechanical function. Lower concentrations (10 or 5 mmol/l) of MgSO4 given after ischaemia recovered the mechanical function concentration-dependently. The beneficial effect of 15 mmol/l MgSO4 was minimized by the coexistence of 4.5 mmol/l CaCl2 in the reperfusion solution. The decrease in the myocardial level of ATP induced by ischaemia-reperfusion was attenuated by 15 mmol/l MgSO4 given in the reperfusion solution. These results suggest that high Mg2+ is effective in attenuating both functional and metabolic damage of the post-ischaemic heart, provided it is given after ischaemia.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1615-2573
    Keywords: Heart ; Coronary flow ; Adenosine ; Lactate ; Myoglobin ; Oxygen ; Hypoxia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The contribution of endogenous adenosine to coronary vasodilation induced by global myocardial hypoxia was examined. In isolated rat hearts perfused by means of Langendorff's technique, the relationship between chronological changes in coronary flow and adenosine release during hypoxia was analyzed. The oxygenation level of myoglobin (MbO2), myocardial oxygen uptake, lactate release, and left ventricular pressure (LVP) was also measured. Adenosine was determined by radio-immunoassay, and the MbO2 levels by the optical method. Severe hypoxia (20% O2+75% N2+5% CO2) increased coronary flow, adenosine release, and lactate release and decreased both myocardial oxygen uptake and LVP. Mild hypoxia (50% O2+45%N2+5%CO2) also increased coronary flow, adenosine release, and lactate release, while it affected neither myocardial oxygen uptake nor LVP. These results suggest that the oxygen supply is compensated by an increase in coronary flow in mild hypoxia, whereas this does not occur in severe hypoxia. Changes in MbO2 were the reverse of those in coronary flow during severe hypoxia, confirming that a decrease in intracellular oxygen correlates well with an increase in coronary flow. The pattern of changes in adenosine release, however, was not identical with that in coronary flow in severe and mild hypoxia, indicating that there is no significant relationship between coronary flow and adenosine release in either severe or mild hypoxic hearts. These findings suggest that adenosine is not the only metabolic mediator of regulation of coronary flow in hypoxic hearts.
    Type of Medium: Electronic Resource
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