Adaptation of hearts to chronic hypoxia increases tolerance to subsequent ischemia by increased nitric oxide production.

Abstract

Each year, in excess of 25,000 children undergo corrective surgery for cardiac birth defects. Advances in surgical techniques have made possible the correction of nearly all congenital cardiac defects. Timing of surgery is critically important, with early surgery desirable to promote more normal development. For example, repair of tetralogy of Fallot is now generally recommended in the first 6 to 12 months of life, and routine repair is now being advocated in the first month of life.1–7 Many children undergoing cardiac surgery in the first year of life exhibit varying degrees of cyanotic heart disease where the myocardium is chronically perfused with hypoxic blood. Understanding the mechanisms by which cyanotic congenital heart disease modifies the myocardium and how that modification impacts on protective mechanics during ischemia may provide insight into developing treatments for limiting myocardial damage during surgery.