Hypertonic cardiopulmonary bypass primes and endothelial damage.

Hypertonic hyperosmolar primes, consisting of NaCl with an osmolarity of 2300 mOsmol/L, has emerged as a possible advance in cardiac surgery, because of the decrease in end organ edema and increased function, particularly of the heart and lungs, that is associated with its use (1–6). Because the osmolarity of the prime is non-physiologic, endothelial damage/aberrant function may ensue. Endothelial activation, damage, and loss can result in neutrophil adhesion and complement and coagulation activation caused by direct contact of the blood components with the underlying exposed basement membrane (7). Complement and coagulation activation can result in systemic inflammatory response syndrome (SIRS), which manifests in a varied clinical picture from barely detectable to multiple organ failure. In the long term, acute endothelial damage may predispose to platelet aggregation and cholesterol influx, which can be the initiating events in the atheroma cascade, leading to accelerated graft failure (8,9). Increasingly greater proportions of patients undergoing cardiopulmonary bypass (CPB) are elderly. Higher plasma concentrations of the measured adhesion molecules in elderly critically ill patients indicate that elderly patients are more prone than younger patients to a more pronounced activation and damage of the endothelium (10). Under normal conditions, the body’s osmolarity is ˜280 mOsmol/L. On initiation of bypass, the pump prime, 2300 mOsmol/L, is in direct contact with the endothelium. After complete mixing with the blood volume, the blood’s osmolarity is ˜630 mOsmol/L. After whole body water distribution, the whole body osmolarity will have fallen to ˜320–350 mOsmol/L. Thus, use of a hyperosmolar prime (2300 mOsmol/L) exposes vascular endothelium to a nonphysiologic osmolarity for an extended period of time.