Volume 7 Supplement 2

23rd International Symposium on Intensive Care and Emergency Medicine

Open Access

Extrapancreatic microcirculatory injury in acute experimental pancreatitis in the rat

  • H Freise1,
  • LG Fischer1,
  • V Hlouschek1,
  • MM Lerch1,
  • H Van Aken1 and
  • A Sielenkaemper1
Critical Care20037(Suppl 2):P212

https://doi.org/10.1186/cc2101

Published: 3 March 2003

Background

The clinical course of acute pancreatitis is determined by acute lung injury, systemic inflammatory response syndrome and septic complications. Microcirculatory dysfunction in both the intestinal and the pulmonary vessels might be partly responsible for this process.

Methods

Fourteen male Sprague–Dawley rats were randomly assigned to two groups: acute pancreatitis (AP) was induced by IV infusion of 10 μg/kg cerulein; control rats (CON) received saline infusion. Four hours later, intravital microscopy of the distal ileum mucosa was performed. In six villi, the intercapillary area of all capillaries (ICA total) and of continuously perfused capillaries only (ICA cont) was measured. Terminal arteriolar flow was calculated from arteriolar diameter and plasma flow velocity. In a second set of experiments, pulmonary endothelial function was assessed in isolated perfused lungs (IPL) in 10 rats using the same study design and treatment. After 4 hours of treatment, IPL was established (flow 16 ml/min, hematocrit 10%). After stabilization, endothelium-independent (hypoxic pulmonary vasoconstriction, 3% O2 [HPV]) as well as endothelial-dependent (bradykinin 6 μg [BK]) responses were determined as differences in pulmonary arterial pressure. Statistical analysis included ANOVA and the Student–Newman–Keuls test.

Results

Acute pancreatitis significantly increased the ICA total, thereby indicating a loss in capillary perfusion. HPV after AP was not different from control. In contrast, BK induced pulmonary vasoconstriction after AP compared with control (* P < 0.05 vs control).

Conclusion

During AP, the mucosal microcirculation showed increased arteriolar blood flow and decreased capillary perfusion, indicating increased intramucosal shunt. This may lead to critical mucosal hypoxia. Furthermore, pulmonary vascular reactivity was altered in AP. Mechanisms of AP-induced extrapancreatic microvascular injury need to be further investigated to develop treatment options in the prevention of severe AP-related complications.

Table 1

 

ICA total (μm2)

ICA cont (μm2)

Diameter (μm)

Velocity (μm/s)

Flow (nl/s)

Δ PAP HPV (mmHg)

Δ PAP BK (mmHg)

AP

874 ± 79

1355 ± 148*

7.0 ± 1.4

729 ± 64*

3.58 ± 0.31*

7.17 ± 1.89

1.5 ± 0.43*

CON

773 ± 45

932 ± 46

7.6 ± 1.1

541 ± 50

2.61 ± 0.31

9.63 ± 1.91

0.57 ± 0.3

Authors’ Affiliations

(1)
Department of Anaestheseiology and Intensive Care, University Hospital of Muenster

Copyright

© BioMed Central Ltd 2003

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