Redistribution of regional blood flow and oxygen delivery in experimental cyanotic heart disease in newborn lambs.

Abstract

Redistribution of regional blood flow is an important compensatory response to acute hypoxemia which preserves oxygen delivery to the most vital organs. It is not known if this change in blood flow persists when hypoxemia is prolonged, as occurs in cyanotic congenital heart disease. Chronic hypoxemia was produced in newborn lambs by creating pulmonary stenosis and an atrial septal defect. Oxygen saturation was maintained at 60-70% of control for 2 wk. Distribution of cardiac output was then measured with radionuclide-labeled microspheres. As compared with control, chronic hypoxemia did not alter total cardiac output. Regional blood flow was redistributed, however, the pattern of this redistribution was different from that seen during acute hypoxemia. Myocardial and cerebral blood flows, which increase during acute hypoxemia, return to control levels during chronic hypoxemia. Renal, splenic, gastrointestinal, carcass, and skin blood flows remain decreased. Hemoglobin gradually increases so that after 2 wk of hypoxemia total systemic oxygen delivery returns toward control. However, oxygen delivery to all organs except the heart and brain is reduced. Thus, although cardiac output and total systemic oxygen delivery return toward normal during chronic hypoxemia, these measurements may not reflect important regional variations in blood flow and oxygen delivery. Decreased oxygen and substrate delivery to the gastrointestinal tract, liver, and carcass may account for the alterations of metabolism and growth seen in the newborn with cyanotic congenital heart disease.