Long-term follow-up of low-risk patients undergoing simple cardiac surgery demonstrates a more than 10% higher mortality when receiving perioperative RBC transfusion. Even transfusion of 1-2 units seems to carry a risk of that magnitude.

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Background. The cerebral effect of clamping following normothermic regional perfusion (NRP) in donation after circulatory death (DCD) remains unknown. We investigated the effect of cerebral reperfusion during NRP and the preventive effect of clamping on brain function in a porcine model. Methods. In 16 pigs, intracranial physiological parameters were recorded, including pressure, cerebral blood perfusion (CBF), temperature, and oxygen. Additionally, electroencephalography (EEG) and somatosensory evoked potentials (SSEPs) were used to assess brain function. The animals were cannulated for the heart-lung machine, and baseline measurements were performed before withdrawal from life support. After 8 min of mechanical asystole, the animals were randomly allocated to clamp (n = 8) or nonclamp (n = 8) of the aortic arch vessels. After 30 min of NRP, the animals were monitored for 3 h after weaning (AW). Results. Intracranial measurements of CBF, oxygen, and temperature indicated successful occlusion of the arch vessels following NRP and AW in the clamp group versus the nonclamp group. In the clamp group, EEG was isoelectric and SSEPs were absent AW in all pigs. In the nonclamp group, EEG activity was observed in all 8 pigs, whereas SSEPs were observed in 6 of 8 pigs. Additionally, agonal respiratory movements in the form of gasping were observed in 6 of 8 pigs in the nonclamp group. Conclusions. Reperfusion of the brain during NRP led to a return of brain activity. Conversely, clamping of the arch vessels halted cerebral circulation, ensuring the permanent cessation of brain function and maintaining the determination of death in DCD.

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Acute neonatal pulmonary hypertension is associated with increased activation of the endogenous endothelin pathway. We investigated the role of selective endothelin-A receptor blockade using i.v. BQ-123 in a piglet model of meconium aspiration syndrome. Meconium aspiration was induced in 18 anesthetized piglets. Six controls received no further intervention. Six piglets received 1 mg/kg BQ-123 at 120 min, with the addition of 20 ppm inhaled nitric oxide at 240 min. Six commenced nitric oxide therapy at 120 min, and were given i.v. BQ-123 at 240 min. The total study duration was 360 min. Meconium aspiration resulted in acute pulmonary hypertension and elevated endothelin-1 levels in all animals. There were no changes in pulmonary hemodynamics or endothelin-1 levels beyond 120 min in controls. In the group receiving BQ-123 first, this agent alone reduced the pulmonary artery pressure and pulmonary vascular resistance, and the subsequent addition of inhaled nitric oxide further reduced pulmonary artery pressure. In the group first receiving nitric oxide alone, this reduced the pulmonary artery pressure, and the addition of BQ-123 resulted in a fall in pulmonary vascular resistance. Endothelin-1 levels increased with both agents. BQ-123 was found to be a highly effective pulmonary vasodilator and augmented the effects of nitric oxide in this model of acute pulmonary hypertension. Abbreviations PPHN, persistent pulmonary hypertension of the newborn PVR, pulmonary vascular resistance ET, endothelin iNO, inhaled nitric oxide PPHN occurs when there is a failure of the normal rapid fall in PVR and increase in pulmonary blood flow with the onset of respiration at birth (1). Meconium aspiration syndrome is the single most common cause of PPHN, and can result in significant morbidity and mortality in term and near-term infants (2).The normal transition from the high-resistance fetal circulation to the low-resistance postnatal pulmonary circulation is associated with activation of the endogenous vasodilator nitric oxide-cyclic guanosine 5'-monophosphate pathway, and reduced release of the potent pulmonary vasoconstrictor, ET (3). The ET-1 isopeptide is a 21-amino acid polypeptide (4) that is produced within the pulmonary endothelium by the cleavage of its precursor, pro-ET (big ET), by ET converting enzyme. ET-1 is released by the vascular endothelium, and produces its effects through its interaction with at least two receptor subtypes-the A and B receptors, located on the vascular smooth muscle and endothelium. The pulmonary vasoconstrictor effects of ET-1 result mainly from activation of the G-proteincoupled smooth muscle A receptor, whereas stimulation of the endothelial ET-B receptor has been shown to result in vasodilatation (5). ET-1 is present in high levels at birth, with a gradual fall during the early neonatal period in healthy individuals (6). Elevated ET-1 levels have been demonstrated in animal models of meconium aspiration (7), in neonates with PPHN (3,8,9), and in older children (10) and adults (11) with pulmo...