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OBJECTIVES Non-heart-beating donation (NHBD) has the potential to increase the number of patients treated with lung transplantation. Our study investigated, in a simulated clinical situation in the uncontrolled NHBD setting, whether or not heparin administration after death affects the donor lung function. METHODS Twelve Swedish domestic pigs underwent ventricular fibrillation and were left untouched for 7 min followed by cardiopulmonary resuscitation with mechanical compressions for 20 min. The animals were declared dead after a ‘hands-off’ period of 10 min and randomized to heparin (300 IU/kg) or placebo given into a central venous catheter. In the animals receiving heparin, 2 more minutes of chest compression followed. Intrapleural cooling was initiated 1 h after death, and prevailed for 2 h. Ex vivo lung perfusion (EVLP) was performed with the Vivoline® system. Lung function was evaluated with blood gases at different oxygen levels, pulmonary vascular resistance (PVR), wet/dry weight ratio, macroscopic appearance and histology. RESULTS During EVLP, there were no significant differences between groups in PaO2 or PVR at any investigated FiO2 level (1.0, 0.5 or 0.21). At FiO2 1.0 the PaO2 in the heparin group was 64 ± 2 (range 57–73) kPa and in the non-heparin group 63 ± 4 (range 51–71) kPa. The values for PVR were 592 ± 90 (range 402–1007) and 647 ± 97 (range 426–1044), respectively. There was no significant difference between groups in wet/dry ratio or histology. CONCLUSIONS The use of heparin is of no obvious benefit to the donor lungs in the uncontrolled NHBD situation. The exclusion of heparin will simplify lung donation from NHBDs. [ABSTRACT FROM AUTHOR]

Background: Optimal manual closed chest compressions are difficult to give. A mechanical compression/ decompression device, named LUCAS, is programmed to give compression according to the latest international guidelines (2005) for cardiopulmonary resuscitation (CPR). The aim of the present study was to compare manual CPR with LUCAS-CPR. Methods: 30 kg pigs were anesthetized and intubated. After a base-line period and five minutes of ventricular fibrillation, manual CPR (n = 8) or LUCAS-CPR (n = 8) was started and run for 20 minutes. Professional paramedics gave manual chest compression's alternating in 2-minute periods. Ventilation, one breath for each 10 compressions, was given to all animals. Defibrillation and, if needed, adrenaline were given to obtain a return of spontaneous circulation (ROSC). Results: The mean coronary perfusion pressure was significantly (p < 0.01) higher in the mechanical group, around 20 mmHg, compared to around 5 mmHg in the manual group. In the manual group 54 rib fractures occurred compared to 33 in the LUCAS group (p < 0.01). In the manual group one severe liver injury and one pressure pneumothorax were also seen. All 8 pigs in the mechanical group achieved ROSC, as compared with 3 pigs in the manual group. Conclusions: LUCAS-CPR gave significantly higher coronary perfusion pressure and significantly fewer rib fractures than manual CPR in this porcine model. [ABSTRACT FROM AUTHOR]

A pharmacological characterization of the postjunctional α-adrenoceptors in human superficial epigastric artery and vein was performed, using several α-adrenoceptor subtype selective agonists, and the antagonists prazosin (α1) and rauwolscine (α22). In the arteries prazosin fulfilled the criteria for a competitive antagonism in concentrations 10-9-10-7 M, giving a pA2-value of 9.17 in the Schild plot. Rauwolscine in concentrations 10-8-10-6 M caused less pronounced but significant dextral shifts of the noradrenaline (NA) concentration-response curves. In the veins rauwolscine behaved like a competitive antagonist (10--10-6 M). The pA2-value was 9.16. Prazosin 10-9 M displaced the NA concentration-response curve, but higher concentrations (10-8 and 10-7 M) caused no further displacement. Prazosin reduced the Emax-values in the veins. In the arteries the rank order of potency for the agonists was: cirazoline (α1)>NA>naphazoline (α2) > guanfacine (α2) > phenylephrine (α1). The intrinsic activities of clonidine (α2), ST 587 (α1), B-HT 920 (α2) and B-HT 933 (α2) were too low to allow meaningful comparisons to be made. The rank order of potency in the veins was: NA > clonidine (α2) > naphazoline (α2) > guanfacine (α2) > phenylephrine (α1) > B-HT 920 (α2) > cirazoline (α1) > B-HT 933 (α2). The intrinsic activity of ST 587 was low. Only two pEC50-values could be determined for clonidine in the arteries and these were higher than the pEC50-values for clonidine in the veins. Phenylephrine, naphazoline and guanfacine were equipotent in both types of vessel. Cirazoline was 135 times more potent and NA was 3 times less potent in the arteries than in the veins. The data suggest that the rank order of potency of subtype selective agonists cannot be used for characterization of the α-adrenoceptors in human superficial epigastric arteries and veins. Antagonists on the other hand, give distinct satisfactory information. In the arteries α1-adrenoceptors predominate, but a population of α2-adrenoceptors cannot be excluded in some patients. In the veins α2-adrenoceptors predominate, but a small population of α1-adrenoceptors can be demonstrated. [ABSTRACT FROM AUTHOR]

Excitability and contraction of cardiac muscle from brain‐dead donors critically influence the success of heart transplantation. Membrane physiology, Ca2+‐handling, and force production of cardiac muscle and the contractile properties of coronary arteries were studied in hearts of brain‐dead pigs. Cardiac muscle and vascular function after 12 h brain death (decapitation between C2 and C3) were compared with properties of fresh tissue. In both isolated cardiomyocytes (whole‐cell patch clamp) and trabecular muscle (conventional microelectrodes), action potential duration was shorter in brain dead, compared to controls. Cellular shortening and Ca2+ transients were attenuated in the brain dead, and linked to lower mRNA expression of L‐type calcium channels and a slightly lower ICa,L, current, as well as to a lower expression of phospholamban. The current–voltage relationship and the current above the equilibrium potential of the inward K+ (IK1) channel were altered in the brain‐dead group, associated with lower mRNA expression of the Kir2.2 channel. Delayed K+ currents were detected (IKr, IKs) and were not different between groups. The transient outward K+ current (Ito) was not observed in the pig heart. Coronary arteries exhibited increased contractility and sensitivity to the thromboxane analogue (U46619), and unaltered endothelial relaxation. In conclusion, brain death involves changes in cardiac cellular excitation which might lower contractility after transplantation. Changes in the inward rectifier K+ channel can be associated with an increased risk for arrhythmia. Increased reactivity of coronary arteries may lead to increased risk of vascular spasm, although endothelial relaxant function was well preserved. [ABSTRACT FROM AUTHOR]