@article{a9162789e6c94369b4c21ce8ace4b7c5,
title = "High energy phosphate in lethal myocardial ischemic injury",
author = "Jennings, \{R. B.\} and Hawkins, \{H. K.\} and Reimer, \{K. A.\} and Lowe, \{J. E.\}",
note = "Funding Information: THE RELATIONSHIP BETWEEN ISCHEMIC CONTRACTURE AND TXE ONSET OF nNO-REFLOW' IN 'THE ISOLATED RAT HFX!RT. Humphrey, S.M., Seelye, R.N. and J.B. Gavin. Department of Pathology, University of Auckland School of Medicine, Auckland, New Zealand. Glob'al ischemia of the isolated rat heart produces an ischemic contracture of the ventricles which has reproduceable onset and duratior.. Fluorescein was used to trace the distribution of flow upon reperfusion after various intervals of ischemia. Whereas maximum contracture was achieved by 25 minutes, subendocardial areas of {"}no reflow{"} were observr.': only after 45 minutes of ischemia. Perfusion of the hearts with hyaluronidase (4U/ml) prior to ischemia caused maximum contracture by 20 minutes, but even transmural flow was sl.ill observed after 60 minute:: of{\textquoteleft} ischemia. Thus the development of {"}no reflow{"} In i.he subendocardiun? is nut directly related to ischemic contrac{\textquoteleft}ture the ventriclilar \textasciitilde{}311::. Perl'usion of the myocardium with hyalurorlicXLse ta ischemia accelerates ischemic contrscture but slgrli:'icani,ly delays the develnpmtzn? of llno reflow{"}. (Supported by a grant from the Medical Resilnrch Council \#of New \%aland). Funding Information: HIGH ENERGY PHOSPHATE IN LETHAL MYOCARDIAL ISCHEMIC INJURY: Robert B. Jennings, Hal K. Hawkins, Keith A. Reimer and James E. Lowe. Department of Pathology, I)uke University Medical Center, Durham, N.C. The effect of progressive periods of severe myocardial ischemia --in vivo on tissue high energy phosphate was assessed in open chest dogs in relation to the ultrastructural and functional changes characteristic of irreversible cell injury. Ischemia was induced by proximal ligation of the circumflex coronary artery in 29 dogs for periods of 15,30, 45,60, 120 or 240 minutes. Ischemic tissue was identified by injecting thioflavine S, 5-10 seconds prior to excision of the heart. Severely ischemic non-fluorescent tissue from the posterior papillary muscle (PP) was compared with nonischemic muscle from the anterior papillary muscle W). The loss of 65\% of the ATP and 55\% of the total adenine nucleotides (CAd) after 15 minutes of ischemia (reversible injury) was associated with minimal ultrastructural changes and no significant alterations in ionic gradients or the diffusible space (IDS) of incubated slices. By 40 minutes (irreversible injury), only 6\% of the ATP and 31\% the CAd remained. Incubated slices of this tissue failed to maintain ionic gradients and showed an increase in the IDS. Moreover, myocytes of those slices showed myofibrillar contraction bands and breaks in the plasmalemma. These results indicate that there is a close association between irreversible cellular injury, marked depletion of sP04 and CAd and the development of structural defects in the cell membrane. Marked depletion of SPO and CM and defective membrane function appear to be early and charac\$eristic features of irreversible injury.(NIH Grant No.,HL23138)",
year = "1979",
doi = "10.1016/0022-2828(79)90159-7",
language = "English (US)",
volume = "11",
pages = "29",
journal = "Journal of Molecular and Cellular Cardiology",
issn = "0022-2828",
publisher = "Academic Press",
number = "1 SUPPL.",
}