The Direct Effects of Propofol on Myocyte Contractile Function After Hypothermic Cardioplegic Arrest
| Autor: | Raymond C. Roy, Francis G. Spinale, Latha Hebbar, B. H. Dorman |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
medicine.medical_specialty
Swine Adrenergic beta-Antagonists Plasma Substitutes Isolated myocytes Ventricular Function Left Contractility Hypothermia Induced Internal medicine Image Processing Computer-Assisted medicine Animals Myocyte Rewarming Cardioplegic Solutions Propofol Cells Cultured Microscopy Video Dose-Response Relationship Drug business.industry Myocardium Direct effects Isoproterenol Heart Crystalloid Solutions Adrenergic beta-Agonists Myocardial Contraction Anesthesiology and Pain Medicine medicine.anatomical_structure Ventricle Anesthesia Heart Arrest Induced Potassium Cardiology Isotonic Solutions business Anesthetics Intravenous medicine.drug |
| Zdroj: | Anesthesia & Analgesia. 83:949-957 |
| ISSN: | 0003-2999 |
| DOI: | 10.1097/00000539-199611000-00010 |
| Popis: | Propofol is being used more often in cardiac surgery, particularly after hypothermic, hyperkalemic cardioplegic arrest (HHCA). The purpose of this study was to examine the effects of propofol on isolated myocyte contractile function under both normothermic conditions and after simulated HHCA and rewarming. Myocytes were isolated from the left ventricle of eight pigs. Myocyte contractile function was measured under both normothermic conditions and after simulated HHCA (incubation at 4 degrees C for 2 h in crystalloid cardioplegia; K+ = 24 mEq/L) using computer-assisted videomicroscopy in the presence of 2, 4, and 6 micrograms/mL propofol (11.2, 22.4, and 33.6 microM/L, respectively). Isoproterenol (25 nM) was then added and contractile function measurements repeated. Propofol caused significant dose-dependent reductions in myocyte velocity of shortening (baseline = 67 +/- 2 microns/s; propofol = 2 micrograms/mL, 45 +/- 4 microns/s; and propofol = 6 micrograms/mL, 27 +/- 3 microns/s; P < 0.05). HHCA and rewarming caused a significant reduction in myocyte velocity of shortening (29 +/- 0.9 microns/s, P < 0.05), with further significant dose-dependent reductions in contractile function after the addition of propofol. Propofol caused a decrease in beta-adrenergic responsiveness under normothermic conditions, but not after simulated HHCA. Results from the present study demonstrated for the first time that the reduction in isolated myocyte contractile function after simulated HHCA is further decreased by propofol administration. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
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