Optimal hypothermic preservation of arrested myocardium in isolated perfused rabbit hearts: A 31P NMR study

Glenn Whitman, Robert S. Kieval, James Brown, Ani Banerjee, Michael A. Grosso, Alden H. Harken

Research output: Contribution to journalArticle

Abstract

The purpose of this study was to (1) relate myocardial high-energy phosphate stores to functional recovery after ischemia and reperfusion, (2) assess the bioenergetics and functional influence of clinically relevant myocardial hypothermia, and (3) examine tissue pH as an independent indicator of postischemic recovery of function. Rabbit hearts were perfused via a modified Langendorff technique, monitored for developed pressure (DP) and left ventricular end-diastolic pressure (LVEDP) via an isovolumic left ventricular balloon catheter, and placed in a Brucker NMR magnet (4.7 tesla) to measure phosphocreatine (PCr), adenosine triphosphate (ATP), and pH. Hearts underwent 1 hour of global ischemia at 7 °, 17 °, 27 ° and 37 °C initiated by one dose of K+ cardioplegia followed by 30 minutes of reperfusion. After reperfusion, DP (expressed as a percentage of preischemic control) and LVEDP (mm Hg) in 7 ° and 17 °C hearts were no different (96 + 5% vs 97 ± 3%; 5 ± 2 mm Hg vs 6 ± 2 mm Hg; p = NS), but were better (p <0.01) than 27 ° hearts (72 ± 6%, 17 ± 6 mm Hg) and 37 ° hearts (31 ± 7%, 60 ± 6 mm Hg). PCr was severely depleted in all groups. ATP was 90 ± 7% and 87 ± 5% of preischemic control in the 7 ° and 17 ° hearts, which was significantly better than the 68 ± 3% and 21 ± 3% in the 27 ° and 37 ° groups (p <0.01). The pH at end ischemia was 6.83, 6.89, 6.54, and 5.86 for the 7 °, 17 °, 27 °, and 37 ° hearts, respectively (7 ° vs 27 ° or 37 °, p <0.01; 17 ° vs 27 ° or 37 °, p <0.01). Linear regression of DP on end-ischemic ATP (EIATP) and end-ischemic pH revealed: DP = 0.96 (EIATP) + 20 (r = 0.92) and DP = 60 (pH) -317 (r = 0.86). We conclude that (1) end-ischemic ATP predicts recovery of ventricular function, and, furthermore, there appears a threshold ATP concentration (80% of control) below which full recovery of function will not occur; (2) end-ischemic pH predicts recovery of ventricular function; (3) 7 °C hypothermic ischemia does not cause a clinically significant cold injury; and (4) in a single-dose crystalloid cardioplegia model, end-ischemic pH is linearly related to recovery of function (r = 0.86).

Original languageEnglish (US)
Pages (from-to)100-108
Number of pages9
JournalSurgery
Volume105
Issue number1
StatePublished - 1989
Externally publishedYes

Fingerprint

Myocardium
Recovery of Function
Rabbits
Adenosine Triphosphate
Ischemia
Reperfusion
Pressure
Induced Heart Arrest
Phosphocreatine
Ventricular Function
Blood Pressure
Magnets
Ventricular Pressure
Hypothermia
Energy Metabolism
Linear Models
Catheters
Phosphates

ASJC Scopus subject areas

  • Surgery

Cite this

Whitman, G., Kieval, R. S., Brown, J., Banerjee, A., Grosso, M. A., & Harken, A. H. (1989). Optimal hypothermic preservation of arrested myocardium in isolated perfused rabbit hearts: A 31P NMR study. Surgery, 105(1), 100-108.

Optimal hypothermic preservation of arrested myocardium in isolated perfused rabbit hearts : A 31P NMR study. / Whitman, Glenn; Kieval, Robert S.; Brown, James; Banerjee, Ani; Grosso, Michael A.; Harken, Alden H.

In: Surgery, Vol. 105, No. 1, 1989, p. 100-108.

Research output: Contribution to journalArticle

Whitman, G, Kieval, RS, Brown, J, Banerjee, A, Grosso, MA & Harken, AH 1989, 'Optimal hypothermic preservation of arrested myocardium in isolated perfused rabbit hearts: A 31P NMR study', Surgery, vol. 105, no. 1, pp. 100-108.
Whitman, Glenn ; Kieval, Robert S. ; Brown, James ; Banerjee, Ani ; Grosso, Michael A. ; Harken, Alden H. / Optimal hypothermic preservation of arrested myocardium in isolated perfused rabbit hearts : A 31P NMR study. In: Surgery. 1989 ; Vol. 105, No. 1. pp. 100-108.
@article{d0303da3306e4ce5a77b64363f0277b6,
title = "Optimal hypothermic preservation of arrested myocardium in isolated perfused rabbit hearts: A 31P NMR study",
abstract = "The purpose of this study was to (1) relate myocardial high-energy phosphate stores to functional recovery after ischemia and reperfusion, (2) assess the bioenergetics and functional influence of clinically relevant myocardial hypothermia, and (3) examine tissue pH as an independent indicator of postischemic recovery of function. Rabbit hearts were perfused via a modified Langendorff technique, monitored for developed pressure (DP) and left ventricular end-diastolic pressure (LVEDP) via an isovolumic left ventricular balloon catheter, and placed in a Brucker NMR magnet (4.7 tesla) to measure phosphocreatine (PCr), adenosine triphosphate (ATP), and pH. Hearts underwent 1 hour of global ischemia at 7 °, 17 °, 27 ° and 37 °C initiated by one dose of K+ cardioplegia followed by 30 minutes of reperfusion. After reperfusion, DP (expressed as a percentage of preischemic control) and LVEDP (mm Hg) in 7 ° and 17 °C hearts were no different (96 + 5{\%} vs 97 ± 3{\%}; 5 ± 2 mm Hg vs 6 ± 2 mm Hg; p = NS), but were better (p <0.01) than 27 ° hearts (72 ± 6{\%}, 17 ± 6 mm Hg) and 37 ° hearts (31 ± 7{\%}, 60 ± 6 mm Hg). PCr was severely depleted in all groups. ATP was 90 ± 7{\%} and 87 ± 5{\%} of preischemic control in the 7 ° and 17 ° hearts, which was significantly better than the 68 ± 3{\%} and 21 ± 3{\%} in the 27 ° and 37 ° groups (p <0.01). The pH at end ischemia was 6.83, 6.89, 6.54, and 5.86 for the 7 °, 17 °, 27 °, and 37 ° hearts, respectively (7 ° vs 27 ° or 37 °, p <0.01; 17 ° vs 27 ° or 37 °, p <0.01). Linear regression of DP on end-ischemic ATP (EIATP) and end-ischemic pH revealed: DP = 0.96 (EIATP) + 20 (r = 0.92) and DP = 60 (pH) -317 (r = 0.86). We conclude that (1) end-ischemic ATP predicts recovery of ventricular function, and, furthermore, there appears a threshold ATP concentration (80{\%} of control) below which full recovery of function will not occur; (2) end-ischemic pH predicts recovery of ventricular function; (3) 7 °C hypothermic ischemia does not cause a clinically significant cold injury; and (4) in a single-dose crystalloid cardioplegia model, end-ischemic pH is linearly related to recovery of function (r = 0.86).",
author = "Glenn Whitman and Kieval, {Robert S.} and James Brown and Ani Banerjee and Grosso, {Michael A.} and Harken, {Alden H.}",
year = "1989",
language = "English (US)",
volume = "105",
pages = "100--108",
journal = "Surgery",
issn = "0039-6060",
publisher = "Mosby Inc.",
number = "1",

}

TY - JOUR

T1 - Optimal hypothermic preservation of arrested myocardium in isolated perfused rabbit hearts

T2 - A 31P NMR study

AU - Whitman, Glenn

AU - Kieval, Robert S.

AU - Brown, James

AU - Banerjee, Ani

AU - Grosso, Michael A.

AU - Harken, Alden H.

PY - 1989

Y1 - 1989

N2 - The purpose of this study was to (1) relate myocardial high-energy phosphate stores to functional recovery after ischemia and reperfusion, (2) assess the bioenergetics and functional influence of clinically relevant myocardial hypothermia, and (3) examine tissue pH as an independent indicator of postischemic recovery of function. Rabbit hearts were perfused via a modified Langendorff technique, monitored for developed pressure (DP) and left ventricular end-diastolic pressure (LVEDP) via an isovolumic left ventricular balloon catheter, and placed in a Brucker NMR magnet (4.7 tesla) to measure phosphocreatine (PCr), adenosine triphosphate (ATP), and pH. Hearts underwent 1 hour of global ischemia at 7 °, 17 °, 27 ° and 37 °C initiated by one dose of K+ cardioplegia followed by 30 minutes of reperfusion. After reperfusion, DP (expressed as a percentage of preischemic control) and LVEDP (mm Hg) in 7 ° and 17 °C hearts were no different (96 + 5% vs 97 ± 3%; 5 ± 2 mm Hg vs 6 ± 2 mm Hg; p = NS), but were better (p <0.01) than 27 ° hearts (72 ± 6%, 17 ± 6 mm Hg) and 37 ° hearts (31 ± 7%, 60 ± 6 mm Hg). PCr was severely depleted in all groups. ATP was 90 ± 7% and 87 ± 5% of preischemic control in the 7 ° and 17 ° hearts, which was significantly better than the 68 ± 3% and 21 ± 3% in the 27 ° and 37 ° groups (p <0.01). The pH at end ischemia was 6.83, 6.89, 6.54, and 5.86 for the 7 °, 17 °, 27 °, and 37 ° hearts, respectively (7 ° vs 27 ° or 37 °, p <0.01; 17 ° vs 27 ° or 37 °, p <0.01). Linear regression of DP on end-ischemic ATP (EIATP) and end-ischemic pH revealed: DP = 0.96 (EIATP) + 20 (r = 0.92) and DP = 60 (pH) -317 (r = 0.86). We conclude that (1) end-ischemic ATP predicts recovery of ventricular function, and, furthermore, there appears a threshold ATP concentration (80% of control) below which full recovery of function will not occur; (2) end-ischemic pH predicts recovery of ventricular function; (3) 7 °C hypothermic ischemia does not cause a clinically significant cold injury; and (4) in a single-dose crystalloid cardioplegia model, end-ischemic pH is linearly related to recovery of function (r = 0.86).

AB - The purpose of this study was to (1) relate myocardial high-energy phosphate stores to functional recovery after ischemia and reperfusion, (2) assess the bioenergetics and functional influence of clinically relevant myocardial hypothermia, and (3) examine tissue pH as an independent indicator of postischemic recovery of function. Rabbit hearts were perfused via a modified Langendorff technique, monitored for developed pressure (DP) and left ventricular end-diastolic pressure (LVEDP) via an isovolumic left ventricular balloon catheter, and placed in a Brucker NMR magnet (4.7 tesla) to measure phosphocreatine (PCr), adenosine triphosphate (ATP), and pH. Hearts underwent 1 hour of global ischemia at 7 °, 17 °, 27 ° and 37 °C initiated by one dose of K+ cardioplegia followed by 30 minutes of reperfusion. After reperfusion, DP (expressed as a percentage of preischemic control) and LVEDP (mm Hg) in 7 ° and 17 °C hearts were no different (96 + 5% vs 97 ± 3%; 5 ± 2 mm Hg vs 6 ± 2 mm Hg; p = NS), but were better (p <0.01) than 27 ° hearts (72 ± 6%, 17 ± 6 mm Hg) and 37 ° hearts (31 ± 7%, 60 ± 6 mm Hg). PCr was severely depleted in all groups. ATP was 90 ± 7% and 87 ± 5% of preischemic control in the 7 ° and 17 ° hearts, which was significantly better than the 68 ± 3% and 21 ± 3% in the 27 ° and 37 ° groups (p <0.01). The pH at end ischemia was 6.83, 6.89, 6.54, and 5.86 for the 7 °, 17 °, 27 °, and 37 ° hearts, respectively (7 ° vs 27 ° or 37 °, p <0.01; 17 ° vs 27 ° or 37 °, p <0.01). Linear regression of DP on end-ischemic ATP (EIATP) and end-ischemic pH revealed: DP = 0.96 (EIATP) + 20 (r = 0.92) and DP = 60 (pH) -317 (r = 0.86). We conclude that (1) end-ischemic ATP predicts recovery of ventricular function, and, furthermore, there appears a threshold ATP concentration (80% of control) below which full recovery of function will not occur; (2) end-ischemic pH predicts recovery of ventricular function; (3) 7 °C hypothermic ischemia does not cause a clinically significant cold injury; and (4) in a single-dose crystalloid cardioplegia model, end-ischemic pH is linearly related to recovery of function (r = 0.86).

UR - http://www.scopus.com/inward/record.url?scp=0024575023&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024575023&partnerID=8YFLogxK

M3 - Article

C2 - 2911797

AN - SCOPUS:0024575023

VL - 105

SP - 100

EP - 108

JO - Surgery

JF - Surgery

SN - 0039-6060

IS - 1

ER -