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Volume 204, Issue 2, Pages 225-235 (February 2007)


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Perfluorocarbon in Microcirculation During Ischemia Reperfusion

Pedro Cabrales, PhDCorresponding Author Information, Amy G. Tsai, PhD, Marcos Intaglietta, PhD

Received 5 June 2006; received in revised form 23 August 2006; accepted 8 November 2006. published online 04 January 2007.

Background

The effects of perfluorocarbon (PFC) emulsions administered at a nonhemodiluting dose were studied in the hamster window chamber model to determine the difference in ischemia-reperfusion injury associated with PFC delivery before and after an ischemic episode.

Study design

Ischemia was induced by compressing the periphery of the window chamber for 1 hour. Vessel diameter, red blood cell velocity, rolling and adherent leukocytes, and functional capillary density (FCD) were assessed by intravital microscopy. The animals received an infusion (10% blood volume) of PFC emulsion or equivalent volumes of saline, before or after ischemia. Two groups were studied in each experimental protocol: A, infusion after ischemia; and B, infusion before ischemia, where a fraction of the infused material stagnated in the ischemic zone during the occlusion time. Measurements were made before induced ischemia and at 0.5, 2, and 24 hours of reperfusion.

Results

Animals treated with PFC after ischemia had substantially decreased leukocytes rolling and sticking in postcapillary venules and recovered functional capillary density and blood flow when compared with saline-treated controls. Conversely, administration of PFC before ischemia considerably reduced functional capillary density and increased leukocyte activation after reperfusion.

Conclusions

Results indicate that PFC without stagnation within an ischemic zone attenuates postischemic reperfusion injury of striated skin muscle, presumably through the reduction of leukocyte-endothelial cell interactions. Accordingly, PFC effects on ischemia-reperfusion injury are determined mainly by the time of administration relative to the ischemic episodes.

 La Jolla Bioengineering Institute, La Jolla, CA.

 Department of Bioengineering, University of California, San Diego, La Jolla, CA.

Corresponding Author InformationCorrespondence address: Pedro Cabrales, PhD, La Jolla Bioengineering Institute, 505 Coast Blvd South Suite #405, La Jolla, CA 92037.

 Competing Interests Declared: None.

Supported by NIH grants R01-HL76182 to AGT, R24-64395, R01-62354 and R01-62318 to MI.

PII: S1072-7515(06)01707-8

doi:10.1016/j.jamcollsurg.2006.11.007


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