Intralipid, a clinically safe compound, protects the heart against ischemia-reperfusion injury more efficiently than cyclosporine-A

Anesthesiology. 2012 Oct;117(4):836-46. doi: 10.1097/ALN.0b013e3182655e73.

Abstract

Background: We have recently shown that postischemic administration of intralipid protects the heart against ischemia-reperfusion injury. Here we compared the cardioprotective effects of intralipid with cyclosporine-A, a potent inhibitor of the mitochondrial permeability transition pore opening.

Methods: In vivo rat hearts or isolated Langendorff-perfused mouse hearts were subjected to ischemia followed by reperfusion with intralipid (0.5%, 1% and 2% ex-vivo, and 20% in vivo), cyclosporine-A (0.2 μM, 0.8 μM, and 1.5 μM ex- vivo and 10 mg/kg in vivo), or vehicle. The hemodynamic function, infarct size, calcium retention capacity, mitochondrial superoxide production, and phosphorylation levels of protein kinase B (Akt)/glycogen synthase kinase-3β (GSK-3β) were measured. The values are mean ± SEM.

Results: Administration of intralipid at reperfusion significantly reduced myocardial infarct size compared with cyclosporine-A in vivo (infarct size/area at risk)%: 22.9 ± 2.5% vs. 35.2 ± 3.5%; P = 0.030, n = 7/group). Postischemic administration of intralipid at its optimal dose (1%) was more effective than cyclosporine-A (0.8 μM) in protecting the ex vivo heart against ischemia-reperfusion injury, as the rate pressure product at the end of reperfusion was significantly higher (mmHg · beats/min: 12,740 ± 675 [n = 7] vs. 9,203 ± 10,781 [n = 5], P = 0.024), and the infarct size was markedly smaller (17.3 ± 2.9 [n = 7] vs. 29.2 ± 2.7 [n = 5], P = 0.014). Intralipid was as efficient as cyclosporine-A in inhibiting the mitochondrial permeability transition pore opening (calcium retention capacity = 280 ± 8.2 vs. 260.3 ± 2.9 nmol/mg mitochondria protein in cyclosporine-A, P = 0.454, n = 6) and in reducing cardiac mitochondrial superoxide production. Unlike intralipid, which increased phosphorylation of Akt (6-fold) and GSK-3β (5-fold), cyclosporine-A had no effect on the activation of these prosurvival kinases.

Conclusions: Although intralipid inhibits the opening of the mitochondrial permeability transition pore as efficiently as cyclosporine-A, intralipid is more effective in reducing the infarct size and improving the cardiac functional recovery.

Publication types

  • Comparative Study
  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Anterior Wall Myocardial Infarction / pathology
  • Blotting, Western
  • Calcium / metabolism
  • Calcium / pharmacology
  • Cardiotonic Agents*
  • Coronary Vessels / physiology
  • Cyclosporine / pharmacology*
  • Dose-Response Relationship, Drug
  • Electron Spin Resonance Spectroscopy
  • Emulsions / pharmacology
  • Fat Emulsions, Intravenous / pharmacology*
  • Glycogen Synthase Kinase 3 / metabolism
  • Glycogen Synthase Kinase 3 beta
  • Heart Function Tests
  • Immunosuppressive Agents / pharmacology*
  • In Vitro Techniques
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mitochondria, Heart / drug effects
  • Myocardial Reperfusion Injury / pathology
  • Myocardial Reperfusion Injury / prevention & control*
  • Necrosis
  • Oncogene Protein v-akt / metabolism
  • Permeability
  • Phospholipids / pharmacology*
  • Rats
  • Rats, Sprague-Dawley
  • Reactive Oxygen Species / analysis
  • Reactive Oxygen Species / metabolism
  • Soybean Oil / pharmacology*

Substances

  • Cardiotonic Agents
  • Emulsions
  • Fat Emulsions, Intravenous
  • Immunosuppressive Agents
  • Phospholipids
  • Reactive Oxygen Species
  • soybean oil, phospholipid emulsion
  • Soybean Oil
  • Cyclosporine
  • Glycogen Synthase Kinase 3 beta
  • Gsk3b protein, mouse
  • Gsk3b protein, rat
  • Oncogene Protein v-akt
  • Glycogen Synthase Kinase 3
  • Calcium