A novel rat model of cardiopulmonary bypass (CPB) with cardiac arrest and precise hemodynamic assessment by conductance catheter technique

Objective: So far no small animal model of CPB with aortic cross-clamp and cardioplegic arrest exisis. We have developed an in vivo model of rat CPB with hypothermic cardiac arrest and the use of blood cardioplegia to study various fields of myocardial protection and cardiac dysfunction. Methods: CP...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Hauptverfasser: Guenzinger, R, Wildhirt, SM, Schad, H, Heimisch, W, Mendler, N, Grammer, J, Lange, R, Bauernschmitt, R
Format: Tagungsbericht
Sprache:eng
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Objective: So far no small animal model of CPB with aortic cross-clamp and cardioplegic arrest exisis. We have developed an in vivo model of rat CPB with hypothermic cardiac arrest and the use of blood cardioplegia to study various fields of myocardial protection and cardiac dysfunction. Methods: CPB was instituted in adult male Wistar rats (400–500g) for 60min at a flow rate of 120ml/kg/min, including 15min period of cooling (32°C) and rewarming (37°C). Two groups were studied: groupA (n=10) received CPB only without aortic cross clamping. In groupB (n=9) hypothermic cardiac arrest was performed for 30min with the use of blood cardioplegia. Left ventricular (LV) function was assessed by intraventricular conductance catheter measuring LV pressure and volume after hemodilution and 60min after weaning from CPB. Results: Hemodynamic data showed a significantly reduced systolic and diastolic LV function between the two groups, reflected in a decrease in ejection fraction (EF) (group A 39±3% vs. group B 22±2%), stroke work index (SWI) (groupA 7.39±0.98ml/kg/min vs. group B 3.08±0.57ml/kg/min) and dP/dtmax (group A 10498±1120mmHg/s vs. 6805±1286mmHg/s) and an increase in left ventricular relaxation time constant tau (τ) (group A 6.4±0.3ms vs. group B 7.5±0.5ms) 60min after weaning from bypass. Load-insensitive contractility parameters (i.e. endsystolic elastance (Ees), enddiastolic elastance (Eed) and preload recruitable stroke work (PRSW)) showed an impaired LV function 60min after cardioplegic arrest. Conclusion: The data show that this model is suitable to study the pathophysiology of CPB and cardioplegia. It provides a reproducible in vivo model to study clinically relevant problems linked to CPB and cardiac ischemia.
ISSN:0171-6425
1439-1902
DOI:10.1055/s-2007-967535