ABSTRACT
In this chapter, the author evaluates the role of pH in hypoxic, ischemic, and reperfusion injury to cardiac myocytes and isolated blood-perfused rabbit papillary muscle in recent experiments. This phenomenon is called a “pH paradox” in analogy to the oxygen and calcium paradoxes described previously in heart tissue. Previous work with isolated hepatocytes, perfused liver, and sinusoidal endothelial cells indicates that reperfusion injury involves a “pH paradox”, in which the return from acidotic to physiologic pH, not reoxygenation, initiates lethal reperfusion injury. A similar pH paradox occurs in the isolated perfused rat liver after anoxic stress. This pH paradox may be a universal phenomenon in ischemia/reperfusion injury, since we have also observed a pH paradox in hepatic parenchymal cells and sinusoidal endothelial cells. Our working hypothesis of the pH paradox is that degradative enzymes such as phospholipases and proteases become activated during the adenosine triphosphate depletion of ischemia.
