High potassium contents in organ preservation solutions cause strong pulmonary vasocontraction

Abstract

Euro-Collins (ECS) and UCLA-formula organ preservation solutions induced strong vasocontraction in porcine pulmonary arteries when studied in organ baths at temperatures of 37 °C and 30 °C. At 20 °C ECS induced a 30% contraction, but at 6 °C no contraction (n = 5) or a weak contraction (n = 1) was elicited. Neither prostaglandin E 1 nor nifedipine caused any significant reduction of the vasocontraction elicited by ECS and UCLA. Krebs solution, enriched with potassium in amounts corresponding to those in ECS (115 mmol/L) or UCLA (30 mmol/L), induced vasocontraction comparing well with those induced by ECS or UCLA, indicating that it is the high potassium content that causes the vasocontraction. In a second experiment lung segments were stored at 4 °C for 9 hours in ECS, UCLA, or Krebs solution. Pulmonary arterial segments were then studied in organ baths at 37 °C. The choice of preservation solution did not significantly affect the contractile properties of potassium, noradrenaline, or the thromboxane mimic U-46619. To conclude, high potassium contents in organ preservation solutions induce strong pulmonary vasocontraction in lung temperatures greater than 20 °C but not in temperatures less than 10 °C. These vasocontractions are not significantly reduced by prostaglandin E 1 or nifedipine. We suggest that the initial preservation solution used to cool down the lungs should contain 4 mmol/L or no potassium. When the lung temperature is less than 10 °C, a second perfusion might be done, and then a high potassium content (if thought to be essential) will not cause vasocontraction.