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Preservation of myocyte contractile function after hypothermic, hyperkalemic cardioplegic arrest with 2,3-butanedione monoxime
- Source :
- The Journal of Thoracic and Cardiovascular Surgery. 111(3):621-629
- Publication Year :
- 1996
- Publisher :
- Elsevier BV, 1996.
-
Abstract
- One proposed contributory mechanism for depressed ventricular performance after hypothermic, hyperkalemic cardioplegic arrest is a reduction in myocyte contractile function caused by alterations in intracellular calcium homeostasis. Because 2,3-butanedione monoxime decreases intracellular calcium transients, this study tested the hypothesis that 2,3-butanedione monoxime supplementation of the hyperkalemic cardioplegic solution could preserve isolated myocyte contractile function after hypothermic, hyperkalemic cardioplegic arrest. Myocytes were isolated from the left ventricles of six pigs. Magnitude and velocity of myocyte shortening were measured after 2 hours of incubation under normothermic conditions (37º C, standard medium), hypothermic, hyperkalemic cardioplegic arrest (4º C in Ringer's solution with 20 mEq potassium chloride), and hypothermic, hyperkalemic cardioplegic arrest with 2,3-butanedione monoxime supplementation (4º C in Ringer's solution with 20 mEq potassium chloride and 20 mmol/L 2,3-butanedione monoxime). Because β-adrenergic agonists are commonly employed after cardioplegic arrest, myocyte contractile function was examined in the presence of the β-agonist isoproterenol (25 nmol/L). Hypothermic, hyperkalemic cardioplegic arrest and rewarming reduced the velocity (32%) and percentage of myocyte shortening (27%, p < 0.05). Supplementation with 2,3-butanedione monoxime normalized myocyte contractile function after hypothermic, hyperkalemic cardioplegic arrest. Although β-adrenergic stimulation significantly increased myocyte contractile function under normothermic conditions and after hypothermic, hyperkalemic cardioplegic arrest, contractile function of myocytes exposed to β-agonist after hypothermic, hyperkalemic cardioplegic arrest remained significantly reduced relative to the normothermic control group. Supplementation with 2,3-butanedione monoxime restored β-adrenergic responsiveness of myocytes after hypothermic, hyperkalemic cardioplegic arrest. Thus, supplementation of a hyperkalemic cardioplegic solution with 2,3-butanedione monoxime had direct and beneficial effects on myocyte contractile function and β-adrenergic responsiveness after cardioplegic arrest. A potential mechanism for the effects of 2,3-butanedione monoxime includes modulation of intracellular calcium transients or alterations in sensitivity to calcium. Supplementation with 2,3-butanedione monoxime may have clinical utility in improving myocardial contractile function after hypothermic, hyperkalemic cardioplegic arrest. (J THORAC CARDIOVASC SURG 1996;111:621-9)
- Subjects :
- Pulmonary and Respiratory Medicine
medicine.medical_specialty
Cholinesterase Reactivators
Swine
Potassium
chemistry.chemical_element
Isolated myocytes
Hypokalemia
Left Ventricles
Diacetyl
030204 cardiovascular system & hematology
In Vitro Techniques
Calcium in biology
03 medical and health sciences
0302 clinical medicine
Hypothermia, Induced
Internal medicine
medicine
Myocyte
Animals
Cardioplegic Solutions
030304 developmental biology
0303 health sciences
business.industry
Myocardium
Myocardial Contraction
3. Good health
chemistry
Intracellular calcium homeostasis
Cardiology
Heart Arrest, Induced
Surgery
business
Cardiology and Cardiovascular Medicine
Butanedione monoxime
Subjects
Details
- ISSN :
- 00225223
- Volume :
- 111
- Issue :
- 3
- Database :
- OpenAIRE
- Journal :
- The Journal of Thoracic and Cardiovascular Surgery
- Accession number :
- edsair.doi.dedup.....3fcf3bb8b0f0634d864d07ec054d082f
- Full Text :
- https://doi.org/10.1016/s0022-5223(96)70314-8