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Liver and spleen phagocytic clearance of blood-borne microparticulate tissue debris
and products of intravascular coagulation after trauma and surgical injury is an important
mechanism to limit the deposition of debris in the pulmonary vascular bed. Plasma
fibronectin (pFn) modulates this clearance process. We evaluated the effect of a localized
preripheral ischemia and reperfusion injury on liver and spleen phagocytic function.
Male rats (250 to 350 g) underwent 4 hours of tourniquet-induced bilateral hindlimb
ischemia, followed by 18 hours of reperfusion after release of the tourniquet. Rats
subjected to ether anesthesia alone or anesthesia followed by groin incision without
ischemia were the control and sham groups, respectively. Reticulo-endothelial (RE)
phagocytic function was assessed at 15 minutes and 18 hours after the start of reperfusion
by the in vivo liver and spleen removal of blood-borne iodine 125 (125I)-test microparticles, which were coated with gelatin (denatured collagen) to enhance
their interaction with pFn. Liver and spleen particle uptake in control and sham rats
was similar. In contrast, after 4 hours of ischemic injury with 15 minutes of reperfusion,
we observed a 30% to 40% decrease (p<0.05) in liver and spleen particle uptake as
compared with sham controls with partial restoration of this removal mechanism by
18 hours. This depression in liver and spleen phagocytic function was associated with
a significant (p<0.05) increase in the deposition of the 124I-test particles in the lung. RE depression was not due to a deficiency of pFn; indeed,
a marked elevation (588±12 μg/mL versus 1,083 ±40 μg/mL) of pFn was observed by immunoassay
over the 18-hour reperfusion interval. Comparative bioassay of humoral (opsonic) versus
cellular (Kupffer's cell) activity revealed that Kupffer's cells in livers from controls
or ischemia-reperfusion rats exhibited normal phagocytic function when incubated in
plasma harvested from either control or 4-hour ischemic rats. The opsonic activity
of plasma harvested after ischemia and reperfusion was also more than adequate, consistent
with the immunoassay analysis. Thus, the impaired liver and spleen clearance mechanism
after peripheral ischemia and reperfusion injury did not appear to be due to either
a macrophage cellular deficit or a lack of pFn. This clearance depression may be mediated
by splanchnic malperfusion, which is known to develop after peripheral ischemia and
reperfusion and associated soft tissue injury.
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Article info
Footnotes
*This study was supported by Grant NIH-GM-21447 from the National Institute of General Medical Sciences.
**Presented at the 20th Annual Meeting of the Society for ClinicalVascular Surgery, Orlando, Florida, March 25–29, 1992.
Identification
Copyright
© 1992 Reed Publishing USA. Published by Elsevier Inc.
