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Metabolic deterioration during global ischemia as a function of time in the intact normal dog heart.

Publication ,  Journal Article
Jones, RN; Attarian, DE; Currie, WD; Olsen, CO; Hill, RC; Sink, JD; Wechsler, AS
Published in: J Thorac Cardiovasc Surg
February 1981

High-energy phosphate content and mitochondrial function were analyzed at the initiation and completion of ischemic contracture in dog hearts exposed to normothermic ischemia while on cardiopulmonary bypass. Contracture initiation and completion were detected by a balloon catheter placed within the left ventricle. In seven dogs, inner and outer layers of the myocardium were assayed for adenosine triphosphate (ATP) and creatine phosphate (CP). ATP and CP content in these two layers were compared prior to ischemia and at contracture initiation and completion. Inner layer ATP levels were 23.88 +/- 0.73 (mean +/- SM) mu moles/gm dry weight prior to ischemia, 5.14 +/- 0.49 at initiation, and 0.73 +/- 0.2 at completion. Inner layer CP content was 41.29 +/- 0.87 prior to ischemia, 3.49 +/- 0.34 at initiation, and 4.06 +/- 0.48 at completion. Mitochondrial respiratory control indices (RCI) were assayed in a second group of seven dogs prior to ischemia, at contracture initiation, and at contracture completion and were, respectively, 11.5 +/- 1.18, 3.1 +/- 0.43 and 1.76 +/- 0.29 (alpha ketoglutarate as substrate). Despite the specific degrees of metabolic deterioration associated with the events of contracture, ischemic time required to develop contracture initiation and completion was variable, ranging from 29.5 to 72 minutes for initiation and 60.25 to 101 minutes for completion. A third group of five dogs had biopsy specimens taken for ATP at fixed ischemic time intervals, and at 45 minutes of ischemia they were found to have greater ranges in ATP values than the ranges associated with contracture initiation. In contrast to ischemic time, the physiological events of ischemic contracture are reliable predictors of the degree of metabolic injury in the intact dog heart exposed to normothermic ischemic arrest during cardiopulmonary bypass.

Duke Scholars

Published In

J Thorac Cardiovasc Surg

ISSN

0022-5223

Publication Date

February 1981

Volume

81

Issue

2

Start / End Page

264 / 273

Location

United States

Related Subject Headings

  • Time Factors
  • Respiratory System
  • Phosphocreatine
  • Oxygen Consumption
  • Myocardium
  • Myocardial Contraction
  • Mitochondria, Heart
  • Male
  • Female
  • Dogs
 

Citation

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Jones, R. N., Attarian, D. E., Currie, W. D., Olsen, C. O., Hill, R. C., Sink, J. D., & Wechsler, A. S. (1981). Metabolic deterioration during global ischemia as a function of time in the intact normal dog heart. J Thorac Cardiovasc Surg, 81(2), 264–273.
Jones, R. N., D. E. Attarian, W. D. Currie, C. O. Olsen, R. C. Hill, J. D. Sink, and A. S. Wechsler. “Metabolic deterioration during global ischemia as a function of time in the intact normal dog heart.J Thorac Cardiovasc Surg 81, no. 2 (February 1981): 264–73.
Jones RN, Attarian DE, Currie WD, Olsen CO, Hill RC, Sink JD, et al. Metabolic deterioration during global ischemia as a function of time in the intact normal dog heart. J Thorac Cardiovasc Surg. 1981 Feb;81(2):264–73.
Jones, R. N., et al. “Metabolic deterioration during global ischemia as a function of time in the intact normal dog heart.J Thorac Cardiovasc Surg, vol. 81, no. 2, Feb. 1981, pp. 264–73.
Jones RN, Attarian DE, Currie WD, Olsen CO, Hill RC, Sink JD, Wechsler AS. Metabolic deterioration during global ischemia as a function of time in the intact normal dog heart. J Thorac Cardiovasc Surg. 1981 Feb;81(2):264–273.
Journal cover image

Published In

J Thorac Cardiovasc Surg

ISSN

0022-5223

Publication Date

February 1981

Volume

81

Issue

2

Start / End Page

264 / 273

Location

United States

Related Subject Headings

  • Time Factors
  • Respiratory System
  • Phosphocreatine
  • Oxygen Consumption
  • Myocardium
  • Myocardial Contraction
  • Mitochondria, Heart
  • Male
  • Female
  • Dogs