The evolution of asphyxial defense

From the time animals became dependent upon molecular oxygen as an integral part of their energy-producing processes, they have remained in the shadow of acute asphyxial threat--the blocking of respiratory exchange resulting in the intracellular triad of hypoxia, hypercapnia and acidosis. The most commonly occurring precipitant of acute asphyxia has always been the transfer between air and water environments. Over the last one hundred years studies on a wide range of living organisms, from single cells to complex multicellular organisms like mammals, have demonstrated the presence of well-defined metabolic and cardiovascular-respiratory mechanisms for protecting living things against acute asphyxia. Single-celled animals depend upon anaerobiosis and secondarily hypometabolism. In addition to these processes, animals with gills or lungs utilize "passive" protection such as increased oxygen storage and the "dynamic" cardiovascular adjustments of bradycardia and selective ischemia. These latter changes decrease overall oxygen consumption and hence utilize the oxygen stores in the most economical way to protect the cardiac and cerebral tissue, which are most sensitive to hypoxia and vital to continued survival of the organism. In this article an attempt is made to place these processes into an evolutionary context. As through a glass darkly we glimpse asphyxial defense running like a paleophysiological thread through hundreds of millions of years, being accentuated here and muted there, depending upon the particular needs of individual species.