Background
If the blood supply to an organ or a tissue is impaired for a short time (usually less than five minutes) then restored so that blood flow is resumed, and the process repeated two or more times, the cells downstream of the tissue or organ are robustly protected from a final ischemic insult when the blood supply is cut off entirely and permanently.
The protective effect which is imparted by IPC has two windows of protection. The first, lasts between 4–6 hours and has been named classical or early preconditioning. The second window begins at 24 hours lasting up to 72 hours post the ischaemia and reperfusion stimulus.
In an experimental setting if the left anterior descending coronary artery of the animal is ligated the downstream cardiac cellular mass is infarcted and will be injured and then die. If, on the other hand the tissue is subjected to IPC the downstream cellular mass will sustain only minimal to modest damage. IPC protects the tissue by initiating a cascade of biochemical events that allows for an up-regulation of the energetics of the tissue. The locus of this phenomenon is the intracellular organelle, the mitochondrion.
Investigations of various exogenous circulating ligands such as the delta active opiates and opioids simulate the phenomenon of IPC thus protecting the downstream tissues without the IPC intermittent ligating procedure.
Methods to either mimic or elicit IPC have been attempted in clinical practice, in the area of coronary heart disease in an attempt to limit the injury caused to the heart via ischemia and reperfusion injury. Such injury would occur when a patient has an acute myocardial infarct followed by reperfusion by either percutaneous coronary intervention or thrombolysis.
Read more about this topic: Ischemic Preconditioning
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