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Volume 3 Supplement 2

International Symposium on the Pathophysiology of Cardiopulmonary Bypass

  • Meeting abstract
  • Open Access

Is there a capillary leak after cardiopulmonary bypass in pigs?

  • 1,
  • 1,
  • 1,
  • 2,
  • 2,
  • 1,
  • 1 and
  • 1
Critical Care19993 (Suppl 2) :P15

https://doi.org/10.1186/cc326

  • Published:

Keywords

  • Cardiopulmonary Bypass
  • Evans Blue
  • Leukocyte Infiltration
  • Colloid Osmotic Pressure
  • Plasma Protein Concentration

Objectives

Systemic inflammatory response to cardiopulmonary bypass (CPB) is claimed to cause capillary leakage, which has not yet been demonstrated in a standardized animal model.

Methods

Twenty-six pigs were subjected to 120 min CPB (90 min cardioplegic cardiac arrest, 30 min reperfusion). Left ventricular (LV) power during ejection (= CO × AoP/ejection time) was calculated. Blood samples (before CPB, at 90 min, 120 min CPB and every 30 min until 5 h after CPB) were analyzed for the receptor antagonist IL-1ra, leukocytes, the leukocyte neutral proteinase inhibitor (LNPI to assess leukocyte activation), and plasma protein concentration (PP). Half-life of intravenously injected Evans Blue and intravascular protein content (IVP) were measured before and 3.5 h after CPB. Histologic samples of the LV-wall and septum were assessed for leukocyte infiltration.

Results

LV-power was markedly reduced after CPB. Leukocytes, LNPI and IL-1ra were significantly upregulated following CPB and a marked leukocyte infiltration to the subendocardium of the LV was present 5 h after CPB. PP was reduced by the crystalloid primed CPB, it increased after CPB, but did not reach the pre-CPB level. IVP was reduced after CPB. Half-life of intravenously injected Evans Blue was not affected by CPB.

Conclusion

In the present model CPB was followed by depression of left ventricular function and a systemic inflammatory response. An increase in microvascular permeability to plasma proteins, however, was absent after 120 min of CPB including 90 min of myocardial ischemia. Fluid shift from the intra- to extravascular compartment occurred due to an increased microvascular effective filtration pressure. This is a result of reduced plasma colloid osmotic pressure due to hemodilution and, in part, to protein loss to the foreign surfaces of the CPB-system.

Authors’ Affiliations

(1)
Deutsches Herzzentrum München, Klinik für Herz- und Gefäβchirurgie, Lazarettstr. 36, München, 80636, Germany
(2)
Abteilung für klin. Chemie u. klin. Biochemie, München, Germany

Copyright

© Current Science Ltd 1999

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