Crystalloid cardioplegia and hypothermia do not impair endothelium- dependent relaxation or damage vascular smooth muscle of epicardial coronary arteries

P. R B Evora, P. J. Pearson, Hartzell V Schaff, M. R. Oeltjen

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Abstract

Canine hearts were arrested with crystalloid cardioplegic solution (45 minutes at 7° C) to determine whether either cardioplegia or hypothermia impairs the production of endothelium-derived relaxing factor or damages the vascular smooth muscle of epicardial coronary arteries. In addition, isolated coronary artery segments were exposed to either cold (7° C) or warm (37° C) crystalloid cardioplegic solution and physiologic salt solution in vitro for 45 minutes. After cardiac arrest or incubation with the solutions, segments of epicardial coronary artery were prepared and studied in organ chambers. Cardioplegic arrest of the heart or exposure to cardioplegic solution in vitro (7° or 37° C) did not alter endothelium-dependent relaxation of epicardial coronary artery segments in response to adenosine diphosphate or acetylcholine (10-9 to 10-4 mol/L). Cardioplegic arrest did not alter G protein-mediated, endothelium-dependent relaxation in response to sodium fluoride. In addition, smooth muscle contraction in response to potassium ions (voltage-dependent) or prostaglandin F(2α) (receptor-dependent) and relaxation in response to isoproterenol (cyclic adenosine monophosphate- mediated) or sodium nitroprusside (cyclic guanosine monophosphate-mediated) was unaltered after exposure to cardioplegic solution or hypothermia. These experiments demonstrate that hyperkalemic crystalloid cardioplegia does not irreversibly alter function of epicardial coronary arteries. We hypothesize that coronary artery endothelial cell dysfunction identified in previous studies of cardioplegia may have been due to the effects of barotrauma or shear stress on the vasculature and not the effect of cardioplegia per se.

Original languageEnglish (US)
Pages (from-to)1365-1374
Number of pages10
JournalJournal of Thoracic and Cardiovascular Surgery
Volume104
Issue number5
StatePublished - 1992

Fingerprint

Induced Heart Arrest
Hypothermia
Vascular Smooth Muscle
Endothelium
Coronary Vessels
Cardioplegic Solutions
Heart Arrest
Barotrauma
Endothelium-Dependent Relaxing Factors
Sodium Fluoride
Cyclic GMP
Prostaglandins F
Nitroprusside
Muscle Contraction
Isoproterenol
GTP-Binding Proteins
Cyclic AMP
Adenosine Diphosphate
Acetylcholine
Smooth Muscle

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

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abstract = "Canine hearts were arrested with crystalloid cardioplegic solution (45 minutes at 7° C) to determine whether either cardioplegia or hypothermia impairs the production of endothelium-derived relaxing factor or damages the vascular smooth muscle of epicardial coronary arteries. In addition, isolated coronary artery segments were exposed to either cold (7° C) or warm (37° C) crystalloid cardioplegic solution and physiologic salt solution in vitro for 45 minutes. After cardiac arrest or incubation with the solutions, segments of epicardial coronary artery were prepared and studied in organ chambers. Cardioplegic arrest of the heart or exposure to cardioplegic solution in vitro (7° or 37° C) did not alter endothelium-dependent relaxation of epicardial coronary artery segments in response to adenosine diphosphate or acetylcholine (10-9 to 10-4 mol/L). Cardioplegic arrest did not alter G protein-mediated, endothelium-dependent relaxation in response to sodium fluoride. In addition, smooth muscle contraction in response to potassium ions (voltage-dependent) or prostaglandin F(2α) (receptor-dependent) and relaxation in response to isoproterenol (cyclic adenosine monophosphate- mediated) or sodium nitroprusside (cyclic guanosine monophosphate-mediated) was unaltered after exposure to cardioplegic solution or hypothermia. These experiments demonstrate that hyperkalemic crystalloid cardioplegia does not irreversibly alter function of epicardial coronary arteries. We hypothesize that coronary artery endothelial cell dysfunction identified in previous studies of cardioplegia may have been due to the effects of barotrauma or shear stress on the vasculature and not the effect of cardioplegia per se.",
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T1 - Crystalloid cardioplegia and hypothermia do not impair endothelium- dependent relaxation or damage vascular smooth muscle of epicardial coronary arteries

AU - Evora, P. R B

AU - Pearson, P. J.

AU - Schaff, Hartzell V

AU - Oeltjen, M. R.

PY - 1992

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N2 - Canine hearts were arrested with crystalloid cardioplegic solution (45 minutes at 7° C) to determine whether either cardioplegia or hypothermia impairs the production of endothelium-derived relaxing factor or damages the vascular smooth muscle of epicardial coronary arteries. In addition, isolated coronary artery segments were exposed to either cold (7° C) or warm (37° C) crystalloid cardioplegic solution and physiologic salt solution in vitro for 45 minutes. After cardiac arrest or incubation with the solutions, segments of epicardial coronary artery were prepared and studied in organ chambers. Cardioplegic arrest of the heart or exposure to cardioplegic solution in vitro (7° or 37° C) did not alter endothelium-dependent relaxation of epicardial coronary artery segments in response to adenosine diphosphate or acetylcholine (10-9 to 10-4 mol/L). Cardioplegic arrest did not alter G protein-mediated, endothelium-dependent relaxation in response to sodium fluoride. In addition, smooth muscle contraction in response to potassium ions (voltage-dependent) or prostaglandin F(2α) (receptor-dependent) and relaxation in response to isoproterenol (cyclic adenosine monophosphate- mediated) or sodium nitroprusside (cyclic guanosine monophosphate-mediated) was unaltered after exposure to cardioplegic solution or hypothermia. These experiments demonstrate that hyperkalemic crystalloid cardioplegia does not irreversibly alter function of epicardial coronary arteries. We hypothesize that coronary artery endothelial cell dysfunction identified in previous studies of cardioplegia may have been due to the effects of barotrauma or shear stress on the vasculature and not the effect of cardioplegia per se.

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