title: Endothelial cell toxicity of solid-organ preservation solutions.
abstract: Endothelial cell damage caused by myocardial cardioplegic solutions (Bretschneider HTK and St. Thomas' Hospital No. 2) or renal and hepatic cold storage solutions (modified Collins and University of Wisconsin solution) was assessed in monolayer cultures of adult human venous endothelial cells at 4 degrees to 10 degrees C with phase-contrast microscopy. St. Thomas' Hospital solution caused the cells to contract, resulting in disruption of monolayer integrity and opening of intercellular gaps, and resulted in a 24-hour postexposure survival of 51.0% +/- 2.4%. Bretschneider HTK solution altered cellular morphology less and produced the best postexposure survival (80.2% +/- 2.6%; p less than 0.001). Although morphology was altered the least with University of Wisconsin solution, postexposure survival with this solution, which was similar to that with modified Collins solution, was superior to that with St. Thomas' (p less than 0.01) but inferior to that with Bretschneider HTK (p less than 0.05). The superior protection provided by Bretschneider HTK was due to its additives histidine, tryptophan, and KH-2-oxygluterate (p less than 0.005), and to its low chloride content (p less than 0.005). Furthermore, modifying St. Thomas' solution by decreasing its chloride content improved cell survival to 71.2% +/- 2.3% (p less than 0.001). Normothermic (37 degrees C) exposure to Bretschneider HTK, modified Collins, and University of Wisconsin solution was cytotoxic, whereas normothermic exposure to St. Thomas' cardioplegia was not. In conclusion, the preservation solution that is the least harmful to endothelial cells at hypothermia is Bretschneider HTK cardioplegic solution.
authors.affiliation: Department of Cardiothoracic Surgery, University of Cape Town, South Africa.
authors.forename: U O
authors.initials: UO
authors.lastname: von Oppell
authors.forename: S
authors.initials: S
authors.lastname: Pfeiffer
authors.forename: P
authors.initials: P
authors.lastname: Preiss
authors.forename: T
authors.initials: T
authors.lastname: Dunne
authors.forename: P
authors.initials: P
authors.lastname: Zilla
authors.forename: B
authors.initials: B
authors.lastname: Reichart
mesh_terms: D000241:Adenosine; D000328:Adult; D000493:Allopurinol; D001639:Bicarbonates / Q000633:toxicity; D002118:Calcium / Q000494:pharmacology; D002122:Calcium Chloride / Q000633:toxicity; D002314:Cardioplegic Solutions / Q000633:toxicity*; D002448:Cell Adhesion / Q000187:drug effects; D002452:Cell Count / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D002712:Chlorides / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000473:pathology* / Q000648:ultrastructure; D005947:Glucose / Q000633:toxicity; D005978:Glutathione; D006801:Humans; D006982:Hypertonic Solutions / Q000633:toxicity; D007328:Insulin; D008274:Magnesium / Q000494:pharmacology / Q000633:toxicity; D008353:Mannitol / Q000633:toxicity; D019188:Organ Preservation Solutions; D011189:Potassium Chloride / Q000633:toxicity; D011343:Procaine / Q000633:toxicity; D011887:Raffinose; D012965:Sodium Chloride / Q000633:toxicity; D012996:Solutions / Q000009:adverse effects; D013696:Temperature; D014021:Tissue Preservation
chemical_list: D001639:Bicarbonates; C039984:Bretschneider cardioplegic solution; D002314:Cardioplegic Solutions; D002712:Chlorides; C024102:Collins' solution; D006982:Hypertonic Solutions; D007328:Insulin; D019188:Organ Preservation Solutions; D012996:Solutions; C041711:St. Thomas' Hospital cardioplegic solution; C055206:University of Wisconsin-lactobionate solution; D008353:Mannitol; D012965:Sodium Chloride; D011343:Procaine; D000493:Allopurinol; D011189:Potassium Chloride; D005978:Glutathione; D008274:Magnesium; D005947:Glucose; D000241:Adenosine; D002122:Calcium Chloride; D011887:Raffinose; D002118:Calcium