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We examined whether vascular endothelial function is impaired with deep hypothermia during cardiopulmonary bypass. Such impairment may cause the prolonged hypoperfusion of tissues or organs. Thirty adult patients were classified into three groups according to the degree of hypothermia during cardiopulmonary bypass; deep (DH: 18-20 degrees C, n = 10), moderate (MDH: 25-30 degrees C, n = 10) and mild (MLH: 32-34 degrees C, n = 10) hypothermia. A bolus dose of 100 mg acetylcholine was injected, followed by 1 mg nitroglycerine 20 min later under hypothermic cardiopulmonary bypass. Plasma concentrations of nitric oxide metabolites (NOx) and endothelin-1 were determined until the 7th post-operative day (POD). The reduction of arterial pressure after acetylcholine was the smallest in the DH group (-9 +/- 6 mmHg, p &lt; 0.01). The time to reach the maximum reduction of arterial pressure was the longest in the DH group (acetylcholine: 47.7 +/- 23.6 sec, nitroglycerine: 53.4 +/- 21.4 sec, p &lt; 0.01). NOx production was reduced until the 1st POD and then recovered. The recovery was more rapid in the MLH group than the other two groups (p &lt; 0.01). The plasma endothelin-1 did not differ among the three groups. These results suggest that endothelial function is impaired during cardiopulmonary bypass with deep hypothermia.

Impaired Endothelial Responses in Patients with Deep Hypothermic Cardiopulmonary Bypass