In vitro function of porcine carotid arteries preserved in UW, HTK and Celsior solutions.
We compared the efficacy of histidine-tryptophan-ketoglutarate (HTK) and University of Wisconsin (UW) solution with Celsior solution using hypothermically-preserved porcine carotid arteries and studied the importance of different components of these solutions by preserving carotid arteries in modified HTK solutions. Excised carotid arteries were stored at 4 degrees C in 0.9% (w/v) NaCl, UW, HTK, Celsior, or a modified HTK solution for up to 14 days. Preservation-induced changes in smooth muscle cell and endothelial cell function were determined using an organ bath for isometric tension recording. Short-term preservation (1-3 days) in UW, HTK and Celsior did not significantly alter contractile and relaxation responses of arterial segments when compared to freshly-excised segments, but significantly impaired these responses in arterial segments stored in 0.9% (w/v) NaCl solution. Long-term hypothermic preservation of arterial segments (7 and 14 days) in 0.9% (w/v) NaCl and HTK solution almost completely abolished all responses, but only slightly reduced the responses of arterial segments stored in UW solution. Intermediate results were obtained for Celsior. Modifying HTK by replacement of chloride for sulfate and phosphate resulted in improved contractile and relaxation responses after long-term preservation. With respect to smooth muscle and endothelial function, UW is superior to HTK and Celsior and the absence of chloride or presence of sulfate and phosphate plays a relevant role in this in vitro model of hypothermic preservation of porcine carotid arteries.
Abrahamse
S T L
ST
Department of Surgery (Surgical Laboratory), Academic Medical Center, The University of Amsterdam, The Netherlands.
Dinant
S
S
Pfaffendorf
M
M
van Gulik
T M
TM
D000241:Adenosine / Q000494:pharmacology*; D000493:Allopurinol / Q000494:pharmacology*; D000818:Animals; D002339:Carotid Arteries / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D002470:Cell Survival / Q000187:drug effects; D004187:Disaccharides / Q000494:pharmacology*; D004573:Electrolytes / Q000494:pharmacology*; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects; D005260:Female; D005947:Glucose / Q000494:pharmacology*; D005971:Glutamates / Q000494:pharmacology*; D005978:Glutathione / Q000494:pharmacology*; D006639:Histidine / Q000494:pharmacology*; D007036:Hypothermia, Induced / Q000009:adverse effects; D066298:In Vitro Techniques; D007328:Insulin / Q000494:pharmacology*; D008297:Male; D008353:Mannitol / Q000494:pharmacology*; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D009926:Organ Preservation; D019188:Organ Preservation Solutions / Q000494:pharmacology*; D011189:Potassium Chloride / Q000494:pharmacology*; D011343:Procaine / Q000494:pharmacology*; D011887:Raffinose / Q000494:pharmacology*; D013552:Swine; D013997:Time Factors
C039984:Bretschneider cardioplegic solution; C088453:Celsior; D004187:Disaccharides; D004573:Electrolytes; D005971:Glutamates; D007328:Insulin; D019188:Organ Preservation Solutions; C055206:University of Wisconsin-lactobionate solution; D008353:Mannitol; D006639:Histidine; D011343:Procaine; D000493:Allopurinol; D011189:Potassium Chloride; D005978:Glutathione; D005947:Glucose; D000241:Adenosine; D011887:Raffinose