There is an extensive literature to show that volatile anesthetics limit myocardial ischemia-reperfusion injury and reduce the size of the consequent myocardial infarction. These beneficial effects are found both immediately (first window) and 24-48 hrs (second window) after ischemia. Many intracellular signaling pathways interact to confer myocardial protection and a key final stage is a change in mitochondrial permeability. Increased mitochondrial permeability results in swelling, loss of function, and cell death.
Dr. Christopher Lotz and colleagues from the Department of Physiology, Division of Cardiology, University of California at Los Angeles, Los Angeles, California, investigated the role of the mitochondrial respiratory chain in limiting ischemia-reperfusion injury in the murine myocardium exposed to isoflurane. Their results are published in this month’s issue of Anesthesia and Analgesia and discussed in the article titled “Isoflurane Protects the Myocardium Against Ischemic Injury via the Preservation of Mitochondrial Respiration and Its Supramolecular Organization.”
The researchers undertook a comprehensive examination of cardiac mitochondrial functionality during the second window of protection (24-48 hrs after ischemia). Mice receiving 1.0 MAC isoflurane had a decreased infarct size, preserved respiratory complex III, stabilized supercomplexes of oligomers from complex I/III/IV, decreased oxidative damage, and reduced mitochondrial swelling.
These results complement findings obtained investigating the first window of protection (immediate) that also showed the importance of the preservation of mitochondrial function. The methodologies used to study isolated mitochondria cannot replicate conditions in vivo, but there is now considerable evidence to show that the “powerhouse of the aerobic cell” plays a vital role in ischemia-reperfusion injury with the volatile anesthetics maintaining mitochondrial function to mitigate injury.