Regeneration of myocardial phosphocreatine in pigs despite continued moderate ischemia

George Pantely, S. A. Malone, W. S. Rhen, C. G. Anselone, A. Arai, J. Bristow, J. D. Bristow

    Research output: Contribution to journalArticle

    133 Citations (Scopus)

    Abstract

    The effects of 1 hour of mild and moderate reductions in coronary blood flow on myocardial high-energy phosphate levels were evaluated. Thirty anesthetized pigs were instrumented with left anterior descending arterial and venous catheters, crystals for instantaneous wall thickness, and a fluid-filled occluder. Measurement of myocardial blood flow was performed with microspheres, and a series of myocardial biopsies also was performed. In 10 pigs, overall coronary blood flow was lowered by 22%, with a fall in subendocardial-to-subepicardial flow ratio from 1.11 to 0.54 and in wall thickening from 33% to 15%. Subendocardial flow fell 48%. Coronary blood flow and thickening were constant during 1 hour of ischemia. Phosphocreatine (μmol/g wet wt) in the subendocardial third of the ischemic zone fell from 7.6 to 3.8 at 5 minutes of ischemia (p <0.005 versus control) and returned to normal (7.9) at 60 minutes (p = NS), despite ongoing ischemia. Subendocardial ATP (μmol/g wet wt) fell slowly from 4.3 and leveled off at 2.1 at 60 minutes of ischemia (p <0.001 versus control). Similar regeneration of phosphocreatine was found in seven additional pigs, with a 43% transmural reduction in coronary blood flow and a 66% reduction in subendocardial flow. No significant changes in ATP and phosphocreatine were noted in two different control groups (n = 13 pigs). The regeneration of phosphocreatine despite ongoing ischemia and low ATP levels was not related to changes in myocardial oxygen demand or consumption, or in regional function during the period of ischemia. This may reflect 1) a successful downregulation of the energy needs of the ischemic myocardium to maintain cell viability, or 2) a metabolic abnormality in the ability of the cells to produce ATP primarily or by use of phosphocreatine.

    Original languageEnglish (US)
    Pages (from-to)1481-1493
    Number of pages13
    JournalCirculation Research
    Volume67
    Issue number6
    StatePublished - 1990

    Fingerprint

    Phosphocreatine
    Regeneration
    Swine
    Ischemia
    Adenosine Triphosphate
    Microspheres
    Cell Survival
    Myocardium
    Down-Regulation
    Catheters
    Phosphates
    Oxygen
    Biopsy
    Control Groups

    Keywords

    • Adenosine triphosphate
    • Coronary blood flow
    • Myocardial function
    • Myocardial metabolism
    • Myocardial oxygen consumption

    ASJC Scopus subject areas

    • Physiology
    • Cardiology and Cardiovascular Medicine

    Cite this

    Pantely, G., Malone, S. A., Rhen, W. S., Anselone, C. G., Arai, A., Bristow, J., & Bristow, J. D. (1990). Regeneration of myocardial phosphocreatine in pigs despite continued moderate ischemia. Circulation Research, 67(6), 1481-1493.

    Regeneration of myocardial phosphocreatine in pigs despite continued moderate ischemia. / Pantely, George; Malone, S. A.; Rhen, W. S.; Anselone, C. G.; Arai, A.; Bristow, J.; Bristow, J. D.

    In: Circulation Research, Vol. 67, No. 6, 1990, p. 1481-1493.

    Research output: Contribution to journalArticle

    Pantely, G, Malone, SA, Rhen, WS, Anselone, CG, Arai, A, Bristow, J & Bristow, JD 1990, 'Regeneration of myocardial phosphocreatine in pigs despite continued moderate ischemia', Circulation Research, vol. 67, no. 6, pp. 1481-1493.
    Pantely G, Malone SA, Rhen WS, Anselone CG, Arai A, Bristow J et al. Regeneration of myocardial phosphocreatine in pigs despite continued moderate ischemia. Circulation Research. 1990;67(6):1481-1493.
    Pantely, George ; Malone, S. A. ; Rhen, W. S. ; Anselone, C. G. ; Arai, A. ; Bristow, J. ; Bristow, J. D. / Regeneration of myocardial phosphocreatine in pigs despite continued moderate ischemia. In: Circulation Research. 1990 ; Vol. 67, No. 6. pp. 1481-1493.
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    abstract = "The effects of 1 hour of mild and moderate reductions in coronary blood flow on myocardial high-energy phosphate levels were evaluated. Thirty anesthetized pigs were instrumented with left anterior descending arterial and venous catheters, crystals for instantaneous wall thickness, and a fluid-filled occluder. Measurement of myocardial blood flow was performed with microspheres, and a series of myocardial biopsies also was performed. In 10 pigs, overall coronary blood flow was lowered by 22{\%}, with a fall in subendocardial-to-subepicardial flow ratio from 1.11 to 0.54 and in wall thickening from 33{\%} to 15{\%}. Subendocardial flow fell 48{\%}. Coronary blood flow and thickening were constant during 1 hour of ischemia. Phosphocreatine (μmol/g wet wt) in the subendocardial third of the ischemic zone fell from 7.6 to 3.8 at 5 minutes of ischemia (p <0.005 versus control) and returned to normal (7.9) at 60 minutes (p = NS), despite ongoing ischemia. Subendocardial ATP (μmol/g wet wt) fell slowly from 4.3 and leveled off at 2.1 at 60 minutes of ischemia (p <0.001 versus control). Similar regeneration of phosphocreatine was found in seven additional pigs, with a 43{\%} transmural reduction in coronary blood flow and a 66{\%} reduction in subendocardial flow. No significant changes in ATP and phosphocreatine were noted in two different control groups (n = 13 pigs). The regeneration of phosphocreatine despite ongoing ischemia and low ATP levels was not related to changes in myocardial oxygen demand or consumption, or in regional function during the period of ischemia. This may reflect 1) a successful downregulation of the energy needs of the ischemic myocardium to maintain cell viability, or 2) a metabolic abnormality in the ability of the cells to produce ATP primarily or by use of phosphocreatine.",
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    AU - Rhen, W. S.

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    AU - Arai, A.

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    N2 - The effects of 1 hour of mild and moderate reductions in coronary blood flow on myocardial high-energy phosphate levels were evaluated. Thirty anesthetized pigs were instrumented with left anterior descending arterial and venous catheters, crystals for instantaneous wall thickness, and a fluid-filled occluder. Measurement of myocardial blood flow was performed with microspheres, and a series of myocardial biopsies also was performed. In 10 pigs, overall coronary blood flow was lowered by 22%, with a fall in subendocardial-to-subepicardial flow ratio from 1.11 to 0.54 and in wall thickening from 33% to 15%. Subendocardial flow fell 48%. Coronary blood flow and thickening were constant during 1 hour of ischemia. Phosphocreatine (μmol/g wet wt) in the subendocardial third of the ischemic zone fell from 7.6 to 3.8 at 5 minutes of ischemia (p <0.005 versus control) and returned to normal (7.9) at 60 minutes (p = NS), despite ongoing ischemia. Subendocardial ATP (μmol/g wet wt) fell slowly from 4.3 and leveled off at 2.1 at 60 minutes of ischemia (p <0.001 versus control). Similar regeneration of phosphocreatine was found in seven additional pigs, with a 43% transmural reduction in coronary blood flow and a 66% reduction in subendocardial flow. No significant changes in ATP and phosphocreatine were noted in two different control groups (n = 13 pigs). The regeneration of phosphocreatine despite ongoing ischemia and low ATP levels was not related to changes in myocardial oxygen demand or consumption, or in regional function during the period of ischemia. This may reflect 1) a successful downregulation of the energy needs of the ischemic myocardium to maintain cell viability, or 2) a metabolic abnormality in the ability of the cells to produce ATP primarily or by use of phosphocreatine.

    AB - The effects of 1 hour of mild and moderate reductions in coronary blood flow on myocardial high-energy phosphate levels were evaluated. Thirty anesthetized pigs were instrumented with left anterior descending arterial and venous catheters, crystals for instantaneous wall thickness, and a fluid-filled occluder. Measurement of myocardial blood flow was performed with microspheres, and a series of myocardial biopsies also was performed. In 10 pigs, overall coronary blood flow was lowered by 22%, with a fall in subendocardial-to-subepicardial flow ratio from 1.11 to 0.54 and in wall thickening from 33% to 15%. Subendocardial flow fell 48%. Coronary blood flow and thickening were constant during 1 hour of ischemia. Phosphocreatine (μmol/g wet wt) in the subendocardial third of the ischemic zone fell from 7.6 to 3.8 at 5 minutes of ischemia (p <0.005 versus control) and returned to normal (7.9) at 60 minutes (p = NS), despite ongoing ischemia. Subendocardial ATP (μmol/g wet wt) fell slowly from 4.3 and leveled off at 2.1 at 60 minutes of ischemia (p <0.001 versus control). Similar regeneration of phosphocreatine was found in seven additional pigs, with a 43% transmural reduction in coronary blood flow and a 66% reduction in subendocardial flow. No significant changes in ATP and phosphocreatine were noted in two different control groups (n = 13 pigs). The regeneration of phosphocreatine despite ongoing ischemia and low ATP levels was not related to changes in myocardial oxygen demand or consumption, or in regional function during the period of ischemia. This may reflect 1) a successful downregulation of the energy needs of the ischemic myocardium to maintain cell viability, or 2) a metabolic abnormality in the ability of the cells to produce ATP primarily or by use of phosphocreatine.

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