title: Effects of vasoconstrictors on rabbit coronary arteries exposed to iohexol with addition of electrolytes (sodium and calcium).
abstract: OBJECTIVE
  A well-known side effect of contrast media (CM) is vasodilation. Different types of CM in vitro inhibit the action of vasoconstrictors to various degrees. The nonionic CM iohexol inhibits the action less than ionic CM. In this study, the authors investigate whether the addition of electrolytes to iohexol causes less inhibition of the vasoconstrictors. Vasoconstriction dependent on potential-operated calcium channels (POCs) (potassium chloride), or receptor-operated calcium channels (ROCs) (histamine, endothelin-1, and prostaglandin F2 [PGF2 alpha]) was specifically studied.
  
  
  METHODS
  Segments of rabbit coronary arteries were mounted between two L-shaped prongs in tissue baths with buffer solution or solutions of iohexol (140 mg I/mL) with addition of different concentrations of NaCl and CaCl2. The responses of the vessels to increasing concentrations of a vasoconstrictor were examined. Concentration of vasoconstrictor versus contractile response curves were plotted, and the maximal contraction of the vasoconstrictor (Emax) and half maximal constriction were calculated.
  
  
  RESULTS
  Addition of 30 mM NaCl and 1.5 mM CaCl2 caused a vasoconstriction to KCl in iohexol almost identical to its vasoconstriction in buffer. Higher concentrations of NaCl caused decreasing Emax of all vasoconstrictors. The inhibition of the ROC-dependent vasoconstrictors could not be normalized by the addition of electrolytes.
  
  
  CONCLUSIONS
  The inhibition of the POC-dependent vasoconstrictor was caused by "ion toxicity" of iohexol. The inhibition of the ROC-dependent vasoconstrictors was caused by other mechanisms, in a manner compatible with a blocking effect on ROCs.
authors.affiliation: Department of Diagnostic Radiology, Malmö General Hospital, Sweden.
authors.forename: J
authors.initials: J
authors.lastname: Karstoft
authors.forename: L
authors.initials: L
authors.lastname: Bääth
authors.forename: I
authors.initials: I
authors.lastname: Jansen
authors.forename: L
authors.initials: L
authors.lastname: Edvinsson
mesh_terms: D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D015220:Calcium Channels / Q000502:physiology; D003331:Coronary Vessels / Q000187:drug effects* / Q000502:physiology; D015237:Dinoprost / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D016232:Endothelins / Q000494:pharmacology; D006632:Histamine / Q000494:pharmacology; D066298:In Vitro Techniques; D007472:Iohexol / Q000494:pharmacology*; D009119:Muscle Contraction / Q000187:drug effects; D011189:Potassium Chloride / Q000494:pharmacology; D011817:Rabbits; D012964:Sodium / Q000494:pharmacology*; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000037:antagonists & inhibitors / Q000494:pharmacology*
chemical_list: D015220:Calcium Channels; D016232:Endothelins; D014662:Vasoconstrictor Agents; D007472:Iohexol; D011189:Potassium Chloride; D006632:Histamine; D012964:Sodium; D015237:Dinoprost; D002118:Calcium