The critical phase during cardiosurgical procedures is weaning the diseased heart from the ECC (extracorporeal circulation). Post-ischaemic heart failure sometimes requires the administration of inotropic and/or vasconstrictive agents. The natriuretic peptides influence pre- and after-load through their natriuretic, diuretic and vasodilating actions. To date, there are only a few reports describing the therapeutic effect of BNP (brain natriuretic peptide) administration during cardiosurgical procedures. The aim of the present study was to evaluate the effect of BNP administration following ECC in an animal model. Surgery was performed on 20 pigs using ECC. A 30-min ischaemic episode was simulated. Following de-clamping, BNP was administered to the BNP group ( n =10) by an i.v. (intravenous) bolus at 0.3 μg·kg −1 of body weight·min −1 , followed by an infusion at a rate of 0.015 μg·kg −1 of body weight·min −1 for 60 min. The animals in the control group ( n =10) received a saline solution instead of BNP. Haemodynamic and clinical chemistry parameters as well as the amount of catecholamines that were required were measured. All of the animals in the BNP group had a significantly better cardiac output and cardiac index at the end of the experiment. Seven out of 10 animals from the control group required catecholamines, whereas only one animal from the BNP group did. Creatine kinase levels were significantly lower in the BNP group. Systemic vascular resistance was markedly lower in the BNP group. In conclusion, administration of BNP is highly effective in treating post-ischaemic heart failure following ECC. Haemodynamics are greatly improved, and there is almost no need for pharmacological support.

Heparin, when administered to patients undergoing operations using cardiopulmonary bypass, induces plasma changes that gradually impair platelet macroaggregation, but heparinization of whole blood in vitro does not have this effect. The plasma changes induced by heparin in vivo continue to progress in whole blood ex vivo . Heparin releases several endothelial proteins, including lipoprotein lipase, hepatic lipase, platelet factor-4 and superoxide dismutase. These enzymes, which remain active in plasma ex vivo , may impair platelet macroaggregation after in vivo heparinization and during cardiopulmonary bypass. In the present study, proteins were added in vitro to hirudin (200units·ml -1 )-anticoagulated blood from healthy volunteers, and the platelet macroaggregatory responses to ex vivo stimulation with collagen (0.6 μ g·ml -1 ) were assessed by whole-blood impedance aggregometry. Over a 4h period, human lipoprotein lipase and human hepatic lipase reduced the platelet macroaggregatory response from 17.0±2.3 to 1.5±1.3 and 1.2±0.6Ω respectively (means±S.D.) (both P <0.01; n = 6). Other lipoprotein lipases also impaired platelet macroaggregation, but platelet factor-4 and superoxide dismutase did not. Platelet macroaggregation showed an inverse linear correlation with plasma concentrations of non-esterified fatty acids ( r 2 = 0.69; two-sided P <0.0001; n = 8), suggesting that heparin-induced lipolysis inhibits platelet macroaggregation. Lipoprotein degradation products may cause this inhibition by interfering with eicosanoids and other lipid mediators of metabolism.

1. Adrenomedullin (AM), a potent hypotensive peptide, was originally isolated from human phaeochromocytoma. Plasma AM concentrations are elevated in hypertension, heart failure and renal failure in proportion to the severity of the disease. This study was performed to investigate the pathophysiological significance of AM during cardiac surgery. 2. Serial blood samples were obtained from patients undergoing cardiac surgery and plasma AM concentrations were determined by specific radioimmunoassay. 3. Plasma AM concentrations did not increase with anaesthesia or surgery ( n = 9). Plasma AM concentrations gradually increased during cardiopulmonary bypass and after pulmonary reperfusion. After pulmonary reperfusion, plasma AM concentrations increased further. In addition, we measured plasma AM concentrations in the pulmonary vein ( n = 8) and coronary sinus ( n = 8) to examine the contribution of the lungs and heart to the increase in circulating AM concentrations after cardiopulmonary bypass. However, no significant differences were seen in plasma AM concentrations of the pulmonary vein or the coronary sinus and the aorta. Peak AM concentrations during cardiac surgery correlated with duration of surgery. Elevated plasma AM levels during and after surgery began to decline next day after surgery and returned to normal levels 7 days after surgery. 4. These results demonstrate that plasma AM concentrations increase during cardiac surgery and that the duration of surgery may be related to the changes in AM concentrations. Taken together with recent findings that vascular endothelial cells and vascular smooth muscle cells actively produce AM, these results suggest that plasma AM during cardiac surgery may act as a vasodilatory hormone.