Objective:To observe the effects of inhibition of glycolysis with iodoacetate (IAA) on calcium homeostasis and functional recovery of stunned myocardium in anesthetized dogs. Methods: Atomic absorption spectrophotomet...Objective:To observe the effects of inhibition of glycolysis with iodoacetate (IAA) on calcium homeostasis and functional recovery of stunned myocardium in anesthetized dogs. Methods: Atomic absorption spectrophotometry was employed to measure myocyte calcium and magnesium contents. Hemodynamics were monitored with a multichannel electrophysiologic recorder. Results: In nonischemic canine hearts (control), IAA's inhibition of glycolysis failed to change the [Ca2+] and [Mg2+] levels and cardiac functional conditions, whereas in hearts subjected to 15-minute ischemia , [Ca2+] increased from nonischemic 1.40±0. 20μmol/g to ischemic 1.80±0.17 μmol/g (P<0. 05), while [Mg2+] decreased. After 30 min of reperfusion,[Ca2+] continued to increase from 1.57±0.21 μmol/g (nonischemic area)to 2. 26±0. 09 μmol/g (abnormal area) and 60 min of reperfusion saw a slight restoration (1.54±0. 16 μmol/g in nonischemic area and 2. 21±0.20 μmol/g in abnormal area). In the glycolysis-inhibiting group, the calcium level registered a significant rise after 30 min of reperfusion: 1.57±0.07 μmol/g in nonischemic area and 2. 90? 0.25 μmol/g in abnormal area (P<0. 01).There was a significant difference between the glycolysis-inhibiting group and the group to which IAA was not applied. [Mg2+] maintained at a relatively low level and registered a more remarkable drop during inhibition of glycolysis, P<0.01 in comparison with the non IAA-administered group,suggesting that inhibition of glycolysis could cause severe calcium overload to sustain, in addition to an obvious harm to cardiac function. Left ventricular end-diastolic pressure and diastolic factor T were augmented andp/dt(max)declined. Conclusion: Since in vivo inhibition of glycolysis seemed to lead to severe calcium overload and hemodynamics changes,it might indicate that glycolysis played an importent role in the restoration of calcium homeostasis in postischemic myocardium,and that ATP derived from glycolysis took a significant part in myocardial ion transport both at the展开更多
A comparative study was performed of the permeability of cell membranous structures in canine stunned myocardium and that of infarct myocardium by using colloidal lanthanum nitrate as an ultrastructure probe. Stunned ...A comparative study was performed of the permeability of cell membranous structures in canine stunned myocardium and that of infarct myocardium by using colloidal lanthanum nitrate as an ultrastructure probe. Stunned myocardium was characterized by mitochondrial swelling, vacuolar formation, a few lanthanum granules deposrting inside cells and intact structure of such membranes as cell membrane, mitochondrial membrane and lysosome membrane.Infarct myocardium was characterized by a large number of lanthanum granules passing through ruptured cell membrane and depositing in the cytoplasm and mitochondria. These results suggest that membranous structure remained intact during the occurrence of stunned myocardium.展开更多
文摘Objective:To observe the effects of inhibition of glycolysis with iodoacetate (IAA) on calcium homeostasis and functional recovery of stunned myocardium in anesthetized dogs. Methods: Atomic absorption spectrophotometry was employed to measure myocyte calcium and magnesium contents. Hemodynamics were monitored with a multichannel electrophysiologic recorder. Results: In nonischemic canine hearts (control), IAA's inhibition of glycolysis failed to change the [Ca2+] and [Mg2+] levels and cardiac functional conditions, whereas in hearts subjected to 15-minute ischemia , [Ca2+] increased from nonischemic 1.40±0. 20μmol/g to ischemic 1.80±0.17 μmol/g (P<0. 05), while [Mg2+] decreased. After 30 min of reperfusion,[Ca2+] continued to increase from 1.57±0.21 μmol/g (nonischemic area)to 2. 26±0. 09 μmol/g (abnormal area) and 60 min of reperfusion saw a slight restoration (1.54±0. 16 μmol/g in nonischemic area and 2. 21±0.20 μmol/g in abnormal area). In the glycolysis-inhibiting group, the calcium level registered a significant rise after 30 min of reperfusion: 1.57±0.07 μmol/g in nonischemic area and 2. 90? 0.25 μmol/g in abnormal area (P<0. 01).There was a significant difference between the glycolysis-inhibiting group and the group to which IAA was not applied. [Mg2+] maintained at a relatively low level and registered a more remarkable drop during inhibition of glycolysis, P<0.01 in comparison with the non IAA-administered group,suggesting that inhibition of glycolysis could cause severe calcium overload to sustain, in addition to an obvious harm to cardiac function. Left ventricular end-diastolic pressure and diastolic factor T were augmented andp/dt(max)declined. Conclusion: Since in vivo inhibition of glycolysis seemed to lead to severe calcium overload and hemodynamics changes,it might indicate that glycolysis played an importent role in the restoration of calcium homeostasis in postischemic myocardium,and that ATP derived from glycolysis took a significant part in myocardial ion transport both at the
文摘A comparative study was performed of the permeability of cell membranous structures in canine stunned myocardium and that of infarct myocardium by using colloidal lanthanum nitrate as an ultrastructure probe. Stunned myocardium was characterized by mitochondrial swelling, vacuolar formation, a few lanthanum granules deposrting inside cells and intact structure of such membranes as cell membrane, mitochondrial membrane and lysosome membrane.Infarct myocardium was characterized by a large number of lanthanum granules passing through ruptured cell membrane and depositing in the cytoplasm and mitochondria. These results suggest that membranous structure remained intact during the occurrence of stunned myocardium.
