Anesthetic Preconditioning Enhances Ca2+Handling and Mechanical and Metabolic Function Elicited by Na+–Ca2+Exchange Inhibition in Isolated Hearts
| Autor: | Jianzhong An, Ming Tao Jiang, David F. Stowe, Zeljko J. Bosnjak, Ming Tian, Samhita S. Rhodes |
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| Rok vydání: | 2006 |
| Předmět: |
medicine.medical_specialty
Guinea Pigs chemistry.chemical_element Calcium-Transporting ATPases Calcium Ryanodine receptor 2 Sodium-Calcium Exchanger Sarcoplasmic Reticulum Calcium-Transporting ATPases Internal medicine medicine Animals Anesthetics Calcium metabolism Aniline Compounds Sodium-calcium exchanger business.industry Ryanodine receptor Myocardium Phenyl Ethers Thiourea Phospholamban Anesthesiology and Pain Medicine Endocrinology chemistry Anesthesia Ischemic Preconditioning Myocardial Reticular connective tissue Ischemic preconditioning business |
| Zdroj: | Anesthesiology. 105:541-549 |
| ISSN: | 0003-3022 |
| Popis: | Background Anesthetic preconditioning (APC) is well known to protect against myocardial ischemia-reperfusion injury. Studies also show the benefit of Na+-Ca2+ exchange inhibition on ischemia-reperfusion injury. The authors tested whether APC plus Na+-Ca2+ exchange inhibitors given just on reperfusion affords additive protection in intact hearts. Methods Cytosolic [Ca2+] was measured by fluorescence at the left ventricular wall of guinea pig isolated hearts using indo-1 dye. Sarcoplasmic reticular Ca2+-cycling proteins, i.e., Ca2+ release channel (ryanodine receptor [RyR2]), sarcoplasmic reticular Ca2+-pump adenosine triphosphatase (SERCA2a), and phospholamban were measured by Western blots. Hearts were assigned to seven groups (n = 8 each): (1) time control; (2) ischemia; (3, 4) 10 microM Na+-Ca2+ exchange inhibitor KB-R7943 (KBR) or 1 microM SEA0400 (SEA), given during the first 10 min of reperfusion; (5) APC initiated by sevoflurane (2.2%, 0.41 +/- 0.03 mm) given for 15 min and washed out for 15 min before ischemia-reperfusion; (6, 7) APC plus KBR or SEA. Results The authors found that APC reduced the increase in systolic [Ca2+], whereas KBR and SEA both reduced the increase in diastolic [Ca2+] on reperfusion. Each intervention improved recovery of left ventricular function. Moreover, APC plus KBR or SEA afforded better functional recovery than APC, KBR, or SEA alone (P < 0.05). Ischemia-reperfusion-induced degradation of major sarcoplasmic reticular Ca2+-cycling proteins was attenuated by APC, but not by KBR or SEA. Conclusions APC plus Na+-Ca2+ exchange inhibition exerts additive protection in part by reducing systolic and diastolic Ca2+ overload, respectively, during ischemia-reperfusion. Less degradation of sarcoplasmic reticular Ca2+-cycling proteins may also contribute to cardiac protection. |
| Databáze: | OpenAIRE |
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