Is post-hypoxic-ischemic cell damage associated with excessive ATP consumption rather than a failure of ATP production?
Secondary cell damage after ATP depletion due to hypoxia or ischemia is clinically important because it correlates with residual effects; post-hypoxic-ischemic fits can be associated with later cerebral palsy. The mechanisms involved in delayed secondary cell damage are not clear, possibly because extensive relevant evidence is often fragmented. However, a sequence of changes can be suggested; this cross-linked sequence is tentatively outlined in this review. The outline suggests explanations for otherwise ill-understood clinical disturbances such as the loss of inhibitory control in damaged cells and the well documented reduction of cellular ATP. Loss of control may be due to reduced synthesis of control proteins and the reduced ATP concentration may be due to increased energy consumption.
Harkness
R A
RA
Pediatrisk Forskningsinstitutt, Universitetet i Oslo, Norway.
D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D017209:Apoptosis; D001923:Brain Chemistry; D002545:Brain Ischemia / Q000150:complications / Q000378:metabolism*; D015687:Cell Hypoxia / Q000502:physiology; D002547:Cerebral Palsy / Q000209:etiology; D006360:Heat-Shock Proteins / Q000502:physiology; D006801:Humans; D002534:Hypoxia, Brain / Q000150:complications / Q000378:metabolism*; D013997:Time Factors
D006360:Heat-Shock Proteins; D000255:Adenosine Triphosphate