Abstract
Cerebral nerve injury is a critical condition in the management of patients in intensive care. Pathological conditions such as cerebral ischemia, head trauma and low oxygen can result in marked impairment of cerebral function, even if the patient's life is saved. We sometimes encounter sudden changes in a patient's condition not only during intensive care, but also during cardiac arrest in emergency situations, and transient low-oxygen and ischemic conditions accompanying with serious shock. We have been studying the mechanisms to prevent pathological conditions leading to neuronal cell death that have been exposed to such emergency conditions, and to discover therapeutic methods to minimize the neuronal damage after insult. With advances in the understanding of the mechanism of neuronal cell death, technology in intensive care for salvaging neuronal cell that are at the brink of death and for recovery of brain function has progressed. However, no breakthrough has been achieved in the development of effective therapy. Protection of the brain from terminal impairment and preservation of function will be an issue in intensive care in the 21st century. To achieve this goal, it is critical to clarify the key mechanism causing neuronal cell death. This report discusses the importance of the calcineurin/immunophilin signal transduction mechanism as a new mechanism that is involved in the induction of ischemic brain damage.
