Decreased nitric oxide products in the urine of patients undergoing cardiac surgery.

OBJECTIVE

Renal vasoconstriction has been blamed as a cause of perioperative renal dysfunction after cardiac surgery. Endothelial function is a critical determinant of vascular tonus, including vasoconstriction. The objective of this study was to establish whether the release of the endothelial vasodilator nitric oxide (NO) or NO products is altered in patients undergoing surgery with cardiopulmonary bypass in 3 different clinical conditions.

DESIGN

Observational and randomized prospective study.

SETTING

University hospital.

PARTICIPANTS

Adults and pediatric patients undergoing elective cardiac surgery with cardiopulmonary bypass.

INTERVENTIONS

Three groups of patients were studied: group 1, 10 patients undergoing elective coronary artery surgery; group 2, 20 patients undergoing elective coronary artery surgery randomized to 2 hematocrit values during cardiopulmonary bypass, high (27%) and low (23%); and group 3, 10 pediatric patients undergoing surgical repair of noncyanotic cardiac defects.

MEASUREMENTS AND MAIN RESULTS

NO products (NO2 + NO3) and cyclic guanosine monophosphate (cGMP) in urine were measured before, during hypo- and normothermic cardiopulmonary bypass, and 1 hour postoperatively. Filtration fraction was calculated. The glomerular filtration rate and effective renal plasma flow were measured with inulin and (131)I-hippuran clearances, respectively. Urinary alpha glutathione s-transferase was measured pre- and postoperatively in groups 1 and 3. NO products, as well as cGMP, decreased significantly during hypo- and normothermic cardiopulmonary bypass in all groups. This was not because of urine dilution or the degree of hemodilution. Age did not appear to alter this response. Filtration fraction decreased during cardiopulmonary bypass. Alpha glutathione s-transferase was normal pre-and postoperatively.

CONCLUSIONS

Cardiac surgery with cardiopulmonary bypass is associated with a significant decrease of NO products. In the absence of kidney damage, decreased NO products could represent a physiologic response to cardiopulmonary bypass; however, endothelial dysfunction cannot be excluded.