Does β2-adrenergic stimulation attenuate fluid extravasation during hypothermic cardiopulmonary bypass? An experimental study in pigs.
OBJECTIVE
Hypothermic cardiopulmonary bypass (CPB) is associated with increased fluid filtration, edema formation and, occasionally, organ dysfunction. Cold-induced reduction in endothelial barrier function may play a role. β(2)-adrenergic activation elevates cellular cyclic adenosine monophosphate (cAMP) which maintains endothelial barrier properties. In this study, we tested whether β-adrenergic stimulation could influence the increase in fluid extravasation observed during hypothermic CPB.


METHODS
Fourteen pigs randomly received terbutaline infusion (T-group) (n=7) or a control infusion (C-group) (n=7). All animals were given 60 min of normothermic CPB, followed by 90 min of hypothermic CPB. Fluid input and losses, plasma volume, colloid osmotic pressures (plasma, interstitial fluid), hematocrit, serum proteins and total tissue water content were measured and the fluid extravasation rates (FER) calculated.


METHODS
by SPSS. Values presented as mean ± SD. Repeated measure analysis of variance was performed and a t-test used when appropriate.


RESULTS
The commencement of normothermic CPB resulted in a 20% hemodilution, with an abrupt increase in fluid requirements during the first 10 min. FER increased from 0.18 (0.06) pre-bypass to 0.78 (0.27) ml/kg/min (T-group) (p=0.002) and from 0.16 (0.05) to 0.93 (0.26) ml/kg/min (C-group) (p<0.001) with no between-group differences. Thereafter, FER stabilized at a level of 0.32 (0.13) and 0.27 (0.14) ml/kg/min in the T-group and C-group, respectively. After the start of cooling, FER increased in the T-group to 0.55 (0.12) ml/kg/min (P=0.046) and in the C-group to 0.54 (0.13) ml/kg/min (P=0.006), with no between-group differences (P=0.738).


CONCLUSIONS
In the present experimental study, we were unable to demonstrate any clinically relevant modulating effect of terbutaline on fluid extravasation during hypothermic cardiopulmonary bypass.
Department of Anesthesia and Intensive Care, Haukeland University Hospital, Bergen, Norway.
P
P
Husby
H K
HK
Brekke
A
A
Mongstad
M
M
Farstad
O
O
Haugen
V L
VL
Kvalheim
D058666:Adrenergic beta-2 Receptor Agonists / Q000494:pharmacology*; D000818:Animals; D001826:Body Fluids / Q000378:metabolism; D002199:Capillary Permeability / Q000187:drug effects; D002315:Cardiopulmonary Bypass / Q000009:adverse effects / Q000379:methods*; D004487:Edema / Q000378:metabolism; D045604:Extracellular Fluid / Q000378:metabolism; D005119:Extravasation of Diagnostic and Therapeutic Materials / Q000188:drug therapy* / Q000209:etiology; D005260:Female; D006438:Hemodilution; D007036:Hypothermia, Induced / Q000009:adverse effects / Q000379:methods*; D008297:Male; D023421:Models, Animal; D010953:Plasma Volume / Q000502:physiology; D011897:Random Allocation; D018343:Receptors, Adrenergic, beta-2 / Q000378:metabolism*; D013552:Swine; D013726:Terbutaline / Q000494:pharmacology*
D058666:Adrenergic beta-2 Receptor Agonists; D018343:Receptors, Adrenergic, beta-2; D013726:Terbutaline