Abrupt reoxygenation of the anoxic potassium-arrested perfused rat heart: a study of myocardial enzyme release
D. J. Hearse, S. M. Humphrey, E. B. Chain

Some evolutionary biologists argue that we evolved despite oxygen rather than because of it. In fact, the demise of the dinosaurs has been attributed, by some, to their inability to deal with rising atmospheric PO2...

Effect of alpha-tocopherol on hypoxic-perfused and reoxygenated rabbit heart muscle
C. Guarnieri, R. Ferrari, O. Visioli, C. M. Caldarera, W. G. Nayler

As reviewed in the preceding review, in 1973 Hearse and colleagues had shown that reoxygenation of the heart after a period of hypoxia results in oxidative injury and enzyme leakage...

The “wavefront phenomenon” of myocardial ischemic cell death. II. Transmural progression of necrosis within the framework of ischemic bed size (myocardium at risk) and collateral flow
K. A. Reimer, R. B. Jennings

By 1979, the idea that it may be possible to salvage the acutely ischemic myocardium by pharmacological intervention had received much attention...

ATP-regulated K+ channels in cardiac muscle
A. Noma

Having previously observed an outward current induced by metabolic inhibition in cardiac cells, in this paper Akinori Noma describes for the first time the identity of the underlying channel—the ATP-sensitive potassium channel (KATP)...

Direct measurement of free radical generation following reperfusion of ischemic myocardium
J. L. Zweier, J. T. Flaherty, M. L. Weisfeldt

By 1987, many pharmacological studies had implicated oxygen-derived free radicals in the genesis of reperfusion injury...

Role of intracellular Na+ in Ca2+ overload and depressed recovery of ventricular function of reperfused ischemic rat hearts. Possible involvement of H+-Na+ and Na+-Ca2+ exchange
M. Tani, J. R. Neely

Michel Lazdunski came up in 1985 with what became known as the Lazdunski Hypothesis. In the course of describing the properties of the Na/H exchanger, Lazdunski proposed a mechanism by which Na and Ca load during reperfusion may exacerbate injury...

The hibernating myocardium
S. H. Rahimtoola

It’s a lesson to us all—if you want your discovery to make an impact, it needs a snappy name! In 1980, Rahimtoola tried to raise awareness of what he refered to as “chronic painless persistent severe reversible myocardial ischemia at rest”—no wonder no one took any notice!...

Cardiac stress protein elevation 24 hours after brief ischemia or heat stress is associated with resistance to myocardial infarction
M. S. Marber, D. S. Latchman, J. M. Walker, D. M. Yellon

Synthesis of heat-shock or stress proteins (HSPs) in response to environmental stress is evolutionarily ancient and was well known and described in the late 1970s...

Reperfusion injury induces apoptosis in rabbit cardiomyocytes
R. A. Gottlieb, K. O. Burleson, R. A. Kloner, B. M. Babior, R. L. Engler

The seminal papers selected for this volume tell a story. Reimer and Jennings clearly demonstrated that early reperfusion is the only way for severely ischemic myocytes to survive, and the exact timing of the transition from reversibly injured to irreversibly injured cells is largely determined by the extent of residual collateral flow...

Mitochondrial non-specific pores remain closed during cardiac ischaemia, but open upon reperfusion
E. J. Griffiths, A. P. Halestrap

In the mid 1990s, the search for the Holy Grail of a single “end-effector,” either responsible for injury or capable of protecting against injury, following myocardial ischemia/reperfusion was still booming...