Preclinical evaluation of coronary vascular function after cardioplegia with HTK and different antioxidant additives.
OBJECTIVE
Due to limited resources, improvement of preservation solutions is still of great importance in cardiac transplant surgery. New additives with antioxidant properties were tested with respect to coronary function of isolated rat hearts.


METHODS
Bretschneider HTK solution containing none or an antioxidant additive (deferoxamine, trolox or LK 616) was used for 8h cold cardioplegia. After reperfusion with Krebs-Henseleit buffer (KHB), we assessed vascular dilator capacity (bradykinin, adenosine triphosphate, reactive hyperemia), myocardial function (left ventricular developed pressure, heart rate, oxygen consumption) and release of biochemical markers (aspartate aminotransferase, creatine kinase, lactate dehydrogenase, troponin, adenosine).


RESULTS
Bradykinin- and adenosine triphosphate-induced vasodilations were largely reduced in hearts stored 8h in traditional HTK as compared to unstored controls. Storage in HTK+LK 616 significantly improved bradykinin-induced vasodilation. Vasodilation toward ATP was best preserved in hearts stored in HTK+deferoxamine. Deferoxamine and trolox, both improved reactive hyperaemic response during reperfusion. Left ventricular pressure development was significantly reduced after 8h cardioplegia, but no difference existed between different cardioplegia groups. Release of biochemical markers of tissue injury was similar in all cardioplegia groups. After storage in HTK+LK 616 (100 microM), however, heart marker release was slightly augmented as compared to HTK.


CONCLUSIONS
Despite similar myocardial function and marker release, coronary vascular function after cardioplegic storage may profit by addition of iron chelators (or antioxidants) to traditional HTK solution.
Schröder
Cornelia
C
Institute of Physiology, Medical Faculty Carl Gustav Carus, TU Dresden, Germany.
Heintz
Anke
A
Pexa
Annette
A
Rauen
Ursula
U
Deussen
Andreas
A
D000255:Adenosine Triphosphate / Q000494:pharmacology; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D015415:Biomarkers / Q000032:analysis; D001920:Bradykinin / Q000494:pharmacology; D002314:Cardioplegic Solutions / Q000494:pharmacology*; D002839:Chromans / Q000494:pharmacology; D003326:Coronary Circulation / Q000187:drug effects* / Q000502:physiology; D003331:Coronary Vessels / Q000187:drug effects / Q000503:physiopathology; D003676:Deferoxamine / Q000494:pharmacology; D005947:Glucose / Q000494:pharmacology; D006324:Heart Arrest, Induced / Q000379:methods; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D008297:Male; D008353:Mannitol / Q000494:pharmacology; D015425:Myocardial Reperfusion / Q000379:methods; D009926:Organ Preservation / Q000379:methods; D019188:Organ Preservation Solutions / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D011343:Procaine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D017262:Siderophores / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology
D000975:Antioxidants; D015415:Biomarkers; C039984:Bretschneider cardioplegic solution; D002314:Cardioplegic Solutions; D002839:Chromans; D019188:Organ Preservation Solutions; D017262:Siderophores; D014665:Vasodilator Agents; D008353:Mannitol; D011343:Procaine; D011189:Potassium Chloride; D000255:Adenosine Triphosphate; D005947:Glucose; D003676:Deferoxamine; C010643:6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid; D001920:Bradykinin