Heart preservation in HTK solution: role of coronary vasculature in recovery of cardiac function.
BACKGROUND
Poor myocardial tolerance to prolonged cold ischemia remains a major concern in heart transplantation. In this study, we estimated superiority of Histidine-Tryptophan-Ketoglutarate (HTK) over University of Wisconsin (UW) as a cardiac preservation solution.


METHODS
Isolated rat hearts were mounted on a Langendorff apparatus to estimate the baseline cardiac function. The hearts were arrested and stored at 4 degrees C in UW and HTK solution for 8 hours, and then reperfused. The aortic flow, coronary flow, cardiac output, rate pressure product, and left ventricular dp/dt in the HTK group recovered significantly more than the UW group. The values of myocardial total adenine nucleotides and the adenosine triphosphate to adenosine diphosphate ratio were higher in the HTK than in the UW group. We also examined coronary vascular responsiveness using left coronary arteries dissected from the rat hearts before flushing, before storage, after storage, and after reperfusion.


RESULTS
The maximal relaxation response to acetylcholine was significantly higher in the HTK than in the UW group after reperfusion, although there were no significant differences at each stage before reperfusion. In addition, the endothelium-independent relaxation response to sodium nitroprusside in the HTK group was also well preserved after reperfusion.


CONCLUSIONS
These results indicate that HTK is superior to UW solution for cardiac preservation. HTK protects coronary vasculature during preservation, which together with reperfusion might lead to improved functional cardiac recovery following preservation.
Saitoh
Y
Y
First Department of Surgery, Shimane Medical University, Izumo, Japan.
Hashimoto
M
M
Ku
K
K
Kin
S
S
Nosaka
S
S
Masumura
S
S
Nakayama
K
K
D000241:Adenosine / Q000627:therapeutic use; D000244:Adenosine Diphosphate / Q000032:analysis; D000255:Adenosine Triphosphate / Q000032:analysis; D000493:Allopurinol / Q000627:therapeutic use; D000818:Animals; D001011:Aorta / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D002314:Cardioplegic Solutions / Q000627:therapeutic use*; D003080:Cold Temperature; D003331:Coronary Vessels / Q000187:drug effects / Q000502:physiology*; D005947:Glucose / Q000627:therapeutic use; D005978:Glutathione / Q000627:therapeutic use; D006324:Heart Arrest, Induced / Q000379:methods; D006339:Heart Rate / Q000502:physiology; D016027:Heart Transplantation / Q000502:physiology*; D006982:Hypertonic Solutions / Q000627:therapeutic use*; D007328:Insulin / Q000627:therapeutic use; D008297:Male; D008353:Mannitol / Q000627:therapeutic use; D009200:Myocardial Contraction / Q000502:physiology; D009206:Myocardium / Q000737:chemistry; D009599:Nitroprusside / Q000494:pharmacology; D009926:Organ Preservation; D019188:Organ Preservation Solutions / Q000627:therapeutic use*; D011189:Potassium Chloride / Q000627:therapeutic use; D011343:Procaine / Q000627:therapeutic use; D011887:Raffinose / Q000627:therapeutic use; D051381:Rats; D017208:Rats, Wistar; D020127:Recovery of Function; D012039:Regional Blood Flow / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology; D016277:Ventricular Function, Left / Q000502:physiology; D017725:Ventricular Pressure / Q000502:physiology
C039984:Bretschneider cardioplegic solution; D002314:Cardioplegic Solutions; D006982:Hypertonic Solutions; D007328:Insulin; D019188:Organ Preservation Solutions; C055206:University of Wisconsin-lactobionate solution; D014665:Vasodilator Agents; D009599:Nitroprusside; D008353:Mannitol; D011343:Procaine; D000244:Adenosine Diphosphate; D000493:Allopurinol; D011189:Potassium Chloride; D000255:Adenosine Triphosphate; D005978:Glutathione; D005947:Glucose; D000241:Adenosine; D011887:Raffinose