Effects of Volatile Anesthetics on Sarcolemmal Calcium Transport and Sarcoplasmic Reticulum Calcium Content in Isolated Myocytes

Abstract

These results suggest that isoflurane and sevoflurane inhibit Ca(2+) transport from the cell via the sarcolemmal Ca(2+)-adenosine triphosphatase. This effect seems to counteract the decrease in Ca(2+) influx through sarcolemmal L-type Ca(2+) channels and maintains sarcoplasmic reticulum Ca(2+) stores.

Cardioprotection Via Activation of Protein Kinase C-δ Depends on Modulation of the Reverse Mode of the Na + /Ca 2+ Exchanger

“…11,12 However, sevoflurane can increase intracellular (SR) Ca 2ϩ load, 2,13 and in this study we specif- ically demonstrate that sevoflurane augments force development after low Na ϩ superfusion, confirming that sevoflurane can facilitate NCX-mediated Ca 2ϩ influx. Several explanations may account for these contradictory results.…”

“…1 Sevoflurane reduces myocardial Ca 2ϩ availability, but paradoxically increases sarcoplasmic reticulum (SR) Ca 2ϩ content. 2 Changes in cellular SR Ca 2ϩ load are associated with activation of survival and/or death signaling pathways, 3 and therefore provide a potential mechanism for cardioprotective signaling. Sevoflurane reduces Ca 2ϩ influx via the L-type Ca 2ϩ channels, 4 and therefore another Ca 2ϩ -loading mechanism may be involved.…”

Hyperglycemia Attenuates Myocardial Preconditioning of Remifentanil

“…Thus, approaches to lessen ischemia-reperfusion injury have been extensively studied, and administration of pharmacologic agents such as anesthetics was demonstrated to produce pharmacologic preconditioning against ischemia-reperfusion injury [11,12]. Anesthetic agents have been shown to prevent the accumulation of intracellular Ca 2þ that occurs during myocardial hypoxia or ischemia, which can induce cell apoptosis leading to cardiomyopathy and heart failure [13][14][15]. However, it is controversial whether anesthetic preconditioning is preserved under diseased status such as diabetes or hyperglycemia.…”

Increased tolerance to hypoxic metabolic inhibition and reoxygenation of cardiomyocytes from apolipoprotein E-deficient mice

“…Mice were anesthetized with pentobarbital (60 mg/kg ip, Nembutal, Abbott Laboratories; North Chicago, IL), and the hearts were rapidly excised. Cardiomyocytes were dissociated as previously described (15). In brief, hearts were perfused via aortic cannulation with a cold, calcium-free oxygenated buffer solution containing (in mM) 75 NaCl, 2.4 KCl, 1 MgCl2, 10 HEPES, 58 sucrose, 10 dextrose, 5 NaHCO 3, and 2.5 glutamic acid (pH 7.2 with KOH) until clear of blood.…”