The influences of NO and Ach on cGMP levels in two patient populations.

Pulmonary hypertension following cardiac surgery is an important factor affecting postoperative mortality, and its mechanism has not been thoroughly clarified. Cardiopulmonary bypass (CPB) can destroy pulmonary endothelium and aggravate pulmonary hypertension. This study is designed to investigate the impacts of CPB on vascular endothelium-dependent relaxation, and the relations of CPB to pulmonary hypertension. Forty patients undergoing valve surgery were involved. According to their preoperative pulmonary arterial pressure (PAP), these patients were divided into pulmonary hypertension group (H group) and normal group (N group). The concentrations of cyclic guanosine monophosphate (cGMP) were measured at baseline conditions, after acetylcholine (Ach) injection, and during nitric oxide (NO) inhalation. Samples were taken before sternotomy and after weaning from CPB, 4 and 12 hours post-CPB. At baseline, the level of cGMP in the H group was lower than that of the N group by 33.9% before CPB. After initiating the CPB, although the level of cGMP continuously decreased in both groups until weaning from CPB (the N group decreased 33.3%, and the H group decreased 59%). At that point cGMP was higher in N group than in the H group (p < .01). The level of cGMP of both groups tended to recover 4 hours after CPB, but only the N group returned to baseline 12 hours after CPB. After injection of Ach, the level of cGMP of both groups followed the same change as in the baseline, except with different numeric value. The level of cGMP in N group rose ranging from 160.0-197.3%, while it rose ranging from 87.7-168.1% in H group. The levels of cGMP were higher in N group than those in H group at all times following injection of Ach (61.4, 173.3, 202.7, and 188.0%) (p < .01). After inhalation of NO, the level of cGMP of both groups followed the same change as the baseline. The level of cGMP in N group rose ranging from 194.8-320.5%. Although the levels of cGMP were higher in N group than those in H group (6.9, 25.3, 23.3, and 16.6%), significant differences were achieved at the 4 and 12 hour post-CPB periods (p < .05 or p < .01, respectively). It was concluded that the injury of vascular endothelial function caused by CPB was more critical in pulmonary hypertension patients.