TY - JOUR
T1 - Preconditioning and postconditioning: Innate cardioprotection from ischemia-reperfusion injury
AU - Vinten-Johansen, Jakob
AU - Zhao, Zhi-Qing
AU - Jiang, Rong
AU - Zatta, Amanda
AU - Dobson, Geoffrey
PY - 2007
Y1 - 2007
N2 - Preconditioning
and postconditioning: innate cardioprotection from ischemia-reperfusion injury.
J Appl Physiol 103: 1441a??1448, 2007; doi:10.1152/japplphysiol.00642.2007.a??
Reperfusion is the definitive treatment to salvage ischemic myocardium from
infarction. A primary determinant of infarct size is the duration of ischemia. In
myocardium that has not been irreversibly injured by ischemia, reperfusion induces
additional injury in the area at risk. The heart has potent innate cardioprotective
mechanisms against ischemia-reperfusion that reduce infarct size and other
presentations of postischemic injury. Ischemic preconditioning (IPC) applied
before the prolonged ischemia exerts the most potent protection observed
among known strategies. It has been assumed that IPC exerts protection during
ischemia. However, recent data suggest that cardioprotection is also exerted
during reperfusion. Postconditioning (PoC), defined as brief intermittent cycles
of ischemia alternating with reperfusion applied after the ischemic event, has
been shown to reduce infarct size, in some cases equivalent to that observed
with IPC. Although there are similarities in mechanisms of cardioprotection by
these two interventions, there are key differences that go beyond simply
exerting these mechanisms before or after ischemia. A significant limitation of
IPC has been the inability to apply this maneuver clinically except in situations
where the ischemic event can be predicted. On the other hand, PoC is applied
at the point of service in the hospital (cath-lab for percutaneous coronary
intervention, coronary artery bypass grafting, and other cardiac surgery) where
and when reperfusion is initiated. Initial clinical studies are in agreement with
the success and extent to which PoC reduces infarct size and myocardial injury,
even in the presence of multiple comorbidities.
AB - Preconditioning
and postconditioning: innate cardioprotection from ischemia-reperfusion injury.
J Appl Physiol 103: 1441a??1448, 2007; doi:10.1152/japplphysiol.00642.2007.a??
Reperfusion is the definitive treatment to salvage ischemic myocardium from
infarction. A primary determinant of infarct size is the duration of ischemia. In
myocardium that has not been irreversibly injured by ischemia, reperfusion induces
additional injury in the area at risk. The heart has potent innate cardioprotective
mechanisms against ischemia-reperfusion that reduce infarct size and other
presentations of postischemic injury. Ischemic preconditioning (IPC) applied
before the prolonged ischemia exerts the most potent protection observed
among known strategies. It has been assumed that IPC exerts protection during
ischemia. However, recent data suggest that cardioprotection is also exerted
during reperfusion. Postconditioning (PoC), defined as brief intermittent cycles
of ischemia alternating with reperfusion applied after the ischemic event, has
been shown to reduce infarct size, in some cases equivalent to that observed
with IPC. Although there are similarities in mechanisms of cardioprotection by
these two interventions, there are key differences that go beyond simply
exerting these mechanisms before or after ischemia. A significant limitation of
IPC has been the inability to apply this maneuver clinically except in situations
where the ischemic event can be predicted. On the other hand, PoC is applied
at the point of service in the hospital (cath-lab for percutaneous coronary
intervention, coronary artery bypass grafting, and other cardiac surgery) where
and when reperfusion is initiated. Initial clinical studies are in agreement with
the success and extent to which PoC reduces infarct size and myocardial injury,
even in the presence of multiple comorbidities.
UR - http://jap.physiology.org/content/103/4/1441.full.pdf
M3 - Article
SN - 8750-7587
VL - 103
SP - 1441
EP - 1448
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
IS - 4
ER -