Alpha1-adrenergic receptor mRNA and inflammatory mediator expression in circulating leucocytes after cardiac surgery.

Vasodilation after coronary artery bypass surgery is a common complication. Inflammatory mediators influence the expression of alpha1-adrenergic receptors. Do patients requiring high doses of postoperative inotropic support have down-regulated alpha-adrenergic receptors? Is there a characteristic pattern of preoperative inflammatory mediator expression that could predict a complicated course after the operation? Forty-four patients undergoing cardiac bypass surgery with extracorporeal circulation were prospectively investigated. Five perioperative blood samples were taken (preoperative, two hours, 12 hours, 36 hours and 72 hours postoperative). The leucocyte mRNA-expression of the three alpha1-adrenergic receptor subtypes (A, B and D) and 11 different pro-inflammatory mediators were investigated with the real-time reverse transcriptase polymerase chain reaction. The patients were divided into three groups (No-noradrenaline [No-NA]= 0 microg/min, Low-noradrenaline [Low-NA]=0.1-7 microg/min, High-noradrenaline [High-NA] >7 microg/min), according to their postoperative noradrenaline requirements. Preoperatively, alpha1(A)-receptor expression was 4.9-fold (High-NA) and 18.7-fold (Low-NA) higher than the No-NA group (P=0.005) and plasma noradrenaline levels were higher in the High-NA group (P=0.005). Across all groups at 12 hours after the operation, alpha1(A) -receptor expression decreased to approximately one-fifth of preoperative levels (P=0.01); but with greater duration and magnitude of relative decrease in the High-NA group. Patients in the No-NA group had significant postoperative increases in leucocyte inflammatory mediator expression for IL-1beta, TLR4, TREM, MPO, MMP9 and TNF genes, whereas the changes in the Low-NA and High-NA groups were not significant. Low preoperative levels of noradrenaline and low expression of alpha1(A)-adrenoreceptors in leucocytes was associated with less probability of requiring noradrenaline support after cardiac surgery.

NT-pro BNP secretion and clinical endpoints in cardiac surgery intensive care patients.

The primary objective of this study was to determine the pattern of N-Terminal pro brain natriuretic peptide (NT-pro BNP) secretion pre and post cardiac surgery and then to investigate the correlation between levels of serum NT-pro BNP and postoperative clinical and biochemical endpoints. This was a prospective observational study performed at a tertiary centre in New Zealand, examining 118 adult patients undergoing cardiac surgery. Interventions included blood samples for NT-pro BNP and troponin-T taken 48 hours prior to operation and 12, 36 and 72 hours postoperatively. The plasma NT-pro BNP levels increased fourfold postoperatively, to plateau at 36 to 72 hours. Preoperative NT-pro BNP levels correlated with ventilation time (r = 0.46), length of stay in intensive care unit (r = 0.59), total perioperative noradrenaline dose (r = 0.55), but not with postoperative atrial fibrillation or mortality. Using multivariate analysis, serum NT-pro BNP levels at 36 hours were associated with increased noradrenaline dose (P = 0.001), decreased preoperative ejection fraction (EF) Group (P = 0.013) and elevated preoperative NT-pro BNP (P < 0.001). Factors not associated with NT-pro BNP levels at 36 hours include the operation type, bypass and cross-clamp times, use of milrinone and troponin-T We conclude that NT-pro BNP levels increased markedly after cardiac surgery and that high preoperative NT-pro BNP levels are associated with a slow postoperative recovery, but do not predict the occurrence of postoperative atrial fibrillation or mortality. Myocardial ischaemia is an unlikely cause of the NT-pro BNP elevation, because no correlation existed between troponin-T and NT-pro BNP levels.