Albumin augmentation improves condition of guinea pig hearts after 4 hr of cold ischemia.
BACKGROUND
Major causes of death after heart transplantation are right ventricular pump failure and, chronically, cardiac allograft vasculopathy. Traditional preservation techniques focus on immediate cardioplegia, without particularly considering vascular demands. Recently, the endothelial surface layer, composed of the endothelial glycocalyx and plasma proteins, was discovered to play a major role in vascular barrier function, edema formation, and leukocyte-to-endothelial interaction. The impact of augmenting a traditional preservation solution with plasma colloid albumin was therefore investigated.


METHODS
Guinea pig hearts underwent cold ischemic storage for 4 hr using Bretschneider's solution (histidine-tryptophan-ketoglutarate [HTK]) without and with augmentation with 1 g% human albumin. After reperfusion, intracoronary adhesion of polymorphonuclear granulocytes, edema formation, left and right heart performance of pressure-to-volume work, and glycocalyx shedding were assessed.


RESULTS
Intracoronary retention of leukocytes was doubled in the traditional group (36.4+/-6.6%), whereas it remained at basal values after albumin preservation (23.5+/-2.4%; P<0.05). Addition of albumin to HTK significantly decreased edema formation (wet to dry weight ratio 6.9+/-0.1 vs. 7.2+/-0.2; P<0.05). Although left heart performance was comparable, right heart cardiac output was doubled in hearts having received HTK containing albumin versus HTK alone (94+/-14 vs. 50+/-11 mL/min/g; P<0.05). Glycocalyx shedding was significantly reduced when the hearts were stored under albumin protection.


CONCLUSIONS
Augmenting HTK with human albumin improves endothelial integrity and heart performance after 4 hr cold ischemia, because of a marked protection of the endothelial glycocalyx. For the prevention of acute and chronic graft failure, the glycocalyx might represent a new target.
Clinic of Anesthesiology, Ludwig-Maximilians-Universitaet Muenchen, Munich, Germany. matthias.jacob@med.uni-muenchen.de
Matthias
M
Jacob
Oliver
O
Paul
Laurenz
L
Mehringer
Daniel
D
Chappell
Markus
M
Rehm
Ulrich
U
Welsch
Ingo
I
Kaczmarek
Peter
P
Conzen
Bernhard F
BF
Becker
D000818:Animals; D002302:Cardiac Output; D002448:Cell Adhesion; D003331:Coronary Vessels / Q000502:physiology / Q000503:physiopathology; D004487:Edema / Q000209:etiology; D004730:Endothelium, Vascular / Q000503:physiopathology; D005947:Glucose; D006168:Guinea Pigs; D006321:Heart / Q000187:drug effects*; D016027:Heart Transplantation / Q000009:adverse effects*; D006801:Humans; D008353:Mannitol; D023421:Models, Animal; D017202:Myocardial Ischemia / Q000188:drug therapy*; D009206:Myocardium / Q000276:immunology*; D009504:Neutrophils / Q000502:physiology; D009926:Organ Preservation / Q000379:methods; D019188:Organ Preservation Solutions; D011189:Potassium Chloride; D011343:Procaine; D012709:Serum Albumin / Q000627:therapeutic use*; D017211:Treatment Failure
C039984:Bretschneider cardioplegic solution; D019188:Organ Preservation Solutions; D012709:Serum Albumin; D008353:Mannitol; D011343:Procaine; D011189:Potassium Chloride; D005947:Glucose