Microcirculatory effects of local and remote ischemic preconditioning in supraceliac aortic clamping.
BACKGROUND
Supraceliac aortic clamping in major vascular procedures promotes splanchnic ischemia and reperfusion (I/R) injury that may induce endothelial dysfunction, widespread inflammation, multiorgan dysfunction, and death. We tested the hypothesis that local or remote ischemic preconditioning (IPC) may be protective against injury after supraceliac aortic clamping through the modulation of mesenteric leukocyte-endothelial interactions, as evaluated with intravital microscopy and expression of adhesion molecules.


METHODS
Fifty-six male Wistar rats (weight, 190 to 250 g), were divided into four groups of 14 rats each: control-sham surgery without aortic occlusion; I/R through supraceliac aortic occlusion for 20 minutes, followed by 120 minutes of reperfusion; local IPC through supraceliac aortic occlusion for two cycles of 5 minutes of ischemia and 5 minutes of reperfusion, followed by the same protocol of the IR group; remote IPC through infrarenal aortic occlusion for two cycles of 10 minutes of ischemia and 10 minutes of reperfusion, followed by the same protocol of the IR group. Seven animals per group were used to evaluate in vivo leukocyte-endothelial interactions in postcapillary venules with intravital microscopy and another seven animals per group were used to collect mesentery samples for immunohistochemistry demonstration of adhesion molecules expression.


RESULTS
Supraceliac aortic occlusion increased the number of rolling leukocytes with slower velocities and increased the number of adherent leukocytes to the venular surface and leukocyte migration to the interstitium. The expression of P-selectin, E-selectin, and intercellular adhesion molecule-1 was also increased significantly after I/R. Local or remote IPC reduced the leukocyte recruitment in vivo and normalized the expression of adhesion molecules.


CONCLUSIONS
Local or remote IPC reduces endothelial dysfunction on mesenteric microcirculation caused by I/R injury after supraceliac aortic clamping.
Erling
Nilon
N
Department of Surgery, Federal University of São Paulo, São Paulo, SP, Brazil. nilonjr@gmail.com
Nakagawa
Naomi Kondo
NK
Costa Cruz
José Walber Miranda
JW
Zanoni
Fernando Luiz
FL
Baptista-Silva
José Carlos Costa
JC
Sannomiya
Paulina
P
Poli-de-Figueiredo
Luiz Francisco
LF
D000818:Animals; D001011:Aorta / Q000601:surgery*; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D003250:Constriction; D019040:E-Selectin / Q000378:metabolism; D042783:Endothelial Cells / Q000276:immunology*; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D019194:Ischemic Preconditioning / Q000379:methods*; D036904:Leukocyte Rolling; D007962:Leukocytes / Q000276:immunology; D008297:Male; D008833:Microcirculation; D018715:Microscopy, Video; D019007:P-Selectin / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000209:etiology / Q000276:immunology / Q000503:physiopathology / Q000517:prevention & control*; D013152:Splanchnic Circulation; D013997:Time Factors; D014656:Vascular Surgical Procedures / Q000009:adverse effects*; D014699:Venules / Q000276:immunology / Q000503:physiopathology
D015815:Cell Adhesion Molecules; D019040:E-Selectin; D019007:P-Selectin; D018799:Intercellular Adhesion Molecule-1