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In vivo leukocyte–endothelium interactions in rat mesenteric microvessels after ischemia/reperfusion and sepsis

  • NK Nakagawa1,
  • RA Nogueira1,
  • S Sinosaki1,
  • SR Shiwa1,
  • LF Poli de Figueiredo1,
  • P Sannomiya1 and
  • M Rocha e Silva1
Critical Care20059(Suppl 2):P41

https://doi.org/10.1186/cc3585

Published: 9 June 2005

Keywords

PentobarbitalSystemic Inflammatory Response SyndromeSodium PentobarbitalHemorrhagic ShockRemarkable Event

Objective

A leukocyte–endothelium interaction is known to be a remarkable event at the beginning of systemic inflammatory response syndrome. The aim of this study was to evaluate leukocyte–endothelium interactions in superfused mesenteric postcapillary venules after hemorrhagic shock/reperfusion and cecal ligation and puncture in rats.

Methods

Thirty-six Wistar rats (200–250 g) were submitted to the following interventions: 0 hours, anesthesia with sodium pentobarbital (50 mg/kg i.p.), hemorrhagic shock (MAP ~40 mmHg lasting 1 hour) and reperfusion with lactated Ringer's solution (3 × shed blood) + 25% of the shed blood; 24 hours, anesthesia and cecal ligation and puncture; 48 hours, anesthesia, cecal resection and peritoneal lavage; and 72 hours, anesthesia and intravital microscopy of the mesentery (venule diameter, 15–25 μm).

Results

Data of leukocyte–endothelium interactions in rat mesenteric microcirculation are presented as the mean ± standard deviation (Table 1).
Table 1

Leukocyte–endothelium interactions in rat mesenteric postcapillary venules

Group

n

Rolling cells/10 min

Adherent cells/100 μm venule length

Migrated cells/5000 μm2

SHAM

4

100 ± 13

3 ± 1

2 ± 1

   + CLP

6

215 ± 25*

15 ± 1*

15 ± 1*

   + CLP + REL

3

106 ± 13

5 ± 1

5 ± 1

HS + 25%

4

215 ± 14*

14 ± 2*

16 ± 1*

   + CLP

5

219 ± 9*

20 ± 2*

16 ± 1*

   + CLP + REL

4

105 ± 12

8 ± 1

8 ± 1

HS + LR

3

175 ± 10*

12 ± 0*

13 ± 1*

   + CLP

3

207 ± 16*

16 ± 1*

16 ± 1*

   + CLP + REL

4

102 ± 12

4 ± 1

15 ± 1*

HS, hemorrhagic shock; 25%, reinfusion of 25% of the shed blood volume; LR, lactated Ringer's solution; CLP, cecal ligation and puncture; REL, cecal resection and peritoneal lavage. * P < 0.01 compared with SHAM.

Conclusions

The double-hit model (ischemia/reperfusion and sepsis) induced a severe inflammatory injury similar to sepsis alone. The inflammatory process was overcome by cecal resection and peritoneal lavage. Up to 72 hours of reperfusion with lactated Ringer's solution and 25% of the shed blood volume, inflammation is still evidenced by the increased number of migrated cells in the perivascular tissue.

Declarations

Acknowledgements

Supported by PRONEX, FAPESP and UNICID.

Authors’ Affiliations

(1)
Research Division, Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil

Copyright

© BioMed Central Ltd 2005

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