ABSTRACT
I. INTRODUCTION In the last decade we have been made increasingly aware of the importance of ischemia and hypoxia on cellular function. At one end of the spectrum, severe hypovolemia and shock can result in rapid death. Even minor degrees of ischemia, however, can cause measurable cellular damage [1]. Moderate degrees of ischemia can predispose to cytokine release and multiorgan failure (MOF) [2]. Severe cellular ischemia can occur in spite of a normal blood pressure [3]. Goris was one of the first to describe the concept of nonbacterial ‘‘sepsis states’’ as a result of mediators such as cytokines, prostinoids, and lysosomes [4]. He proposed that trauma is the ‘‘match’’ that lights the ‘‘fuse’’ (complement) that activates the ‘‘blasting cap’’ (the macrophage) that sets off the ‘‘explosion’’ of mediators that lead to multiple organ injury.
