title: Effects of hyperkalemia on neonatal endothelium and smooth muscle.
abstract: BACKGROUND
  Contradictory results have been reported regarding the effect of hyperkalemic cardioplegic or organ preservation solutions on endothelial and smooth muscle cells. The present study was designed to determine the effects of potassium concentrations and exposure times to hyperkalemia on endothelium-derived relaxing factor (nitric oxide) biosynthesis and release, and smooth muscle function in neonatal vessels.
  
  
  METHODS
  Aortic rings taken from neonatal rabbits were studied in organ baths at physiologic pressure. The effect of Krebs' solution containing 5, 25, 50, or 100 mmol/L potassium incubated for 45 minutes (group 1), St. Thomas' Hospital cardioplegic solution containing 16, 25, 50, or 100 mmol/L potassium for 45 minutes (group 2), and Krebs' solution containing 5 and 50 mmol/L potassium or St. Thomas' Hospital cardioplegic solution containing 16 and 50 mmol/L potassium for 135 minutes (group 3) or 270 minutes (groups 4 and 5) was examined. The rings were then washed and contracted with U46619 (30 nmol/L). The ability to release endothelium-derived relaxing factor (nitric oxide) in response to acetylcholine was tested.
  
  
  RESULTS
  The maximal relaxation induced by acetylcholine did not decrease in any group. Evidence of slight alteration of smooth muscle contraction was seen only in the rings incubated in Krebs' solution with 50 mmol/L potassium for 270 minutes (group 4) with unchanged maximal contraction and sensitivity to potassium (group 5).
  
  
  CONCLUSIONS
  We conclude that after exposure for a limited time (4 1/2 hours), hyperkalemia per se does not significantly alter the function of endothelium to release endothelium-derived relaxing factor (nitric oxide) in response to acetylcholine and only slightly alters the contraction speed of smooth muscle in the neonatal rabbit aorta.
authors.affiliation: Albert Starr Academic Center for Cardiac Surgery, St. Vincent Heart Institute, Portland, OR 97225, USA.
authors.forename: G W
authors.initials: GW
authors.lastname: He
authors.forename: C Q
authors.initials: CQ
authors.lastname: Yang
authors.forename: I M
authors.initials: IM
authors.lastname: Rebeyka
authors.forename: G J
authors.initials: GJ
authors.lastname: Wilson
mesh_terms: D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D001013:Aorta, Thoracic / Q000187:drug effects / Q000378:metabolism; D001639:Bicarbonates / Q000737:chemistry; D002122:Calcium Chloride / Q000737:chemistry; D002314:Cardioplegic Solutions / Q000737:chemistry*; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism; D005260:Female; D007552:Isotonic Solutions / Q000737:chemistry*; D008274:Magnesium / Q000737:chemistry; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000378:metabolism; D009569:Nitric Oxide / Q000096:biosynthesis*; D009926:Organ Preservation; D011188:Potassium / Q000494:pharmacology*; D011189:Potassium Chloride / Q000737:chemistry; D011450:Prostaglandin Endoperoxides, Synthetic / Q000494:pharmacology; D011817:Rabbits; D012965:Sodium Chloride / Q000737:chemistry; D013928:Thromboxane A2 / Q000031:analogs & derivatives / Q000494:pharmacology; D013997:Time Factors; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D001639:Bicarbonates; D002314:Cardioplegic Solutions; D007552:Isotonic Solutions; C051865:Krebs-Ringer solution; D011450:Prostaglandin Endoperoxides, Synthetic; C041711:St. Thomas' Hospital cardioplegic solution; D014662:Vasoconstrictor Agents; D009569:Nitric Oxide; D012965:Sodium Chloride; D013928:Thromboxane A2; D011189:Potassium Chloride; D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; D008274:Magnesium; D002122:Calcium Chloride; D000109:Acetylcholine; D011188:Potassium