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Effect of erythrocyte stroma on reticuloendothelial system phagocytic function
The Journal of Laboratory and Clinical Medicine
|August 1, 1983
Summary
Intravenous erythrocyte stroma depresses reticuloendothelial system (RES) phagocytic function. This study found that impaired phagocytic cell function, not reduced blood flow or coagulation, likely mediates this RES depression.
Area of Science:
- Immunology
- Hematology
- Physiology
Background:
- Intravenous administration of erythrocyte stroma is known to depress reticuloendothelial system (RES) phagocytic function.
- The mechanisms underlying this RES depression remain unclear.
Purpose of the Study:
- To investigate whether decreased hepatic blood flow, coagulation system activation, or depletion of opsonic factors mediate RES depression induced by erythrocyte stroma.
- To explore the role of impaired phagocytic cell function in stroma-induced RES depression.
Main Methods:
- Erythrocyte stroma was prepared from rat erythrocytes and injected intravenously into rats at varying doses.
- Hepatic blood flow, fibrinogen levels, fibronectin levels, and hemolytic complement levels were measured.
- RES phagocytic function was assessed using a standardized test particle.
- Experiments included heparin administration, complement depletion, and preopsonization of test particles.
Main Results:
- RES depression increased with stroma doses greater than 0.3 ml/100 gm.
- Decreased hepatic blood flow and coagulation activation were observed only at the highest stroma dose (1.0 ml/100 gm).
- Neither heparin administration nor complement depletion affected stroma-induced RES depression at a dose of 0.5 ml/100 gm.
- Preopsonization of test particles did not alter the RES depression.
Conclusions:
- Decreased hepatic blood flow, coagulation activation, and opsonin depletion do not mediate the RES depression induced by a 0.5 ml/100 gm dose of erythrocyte stroma.
- Impairment of phagocytic cell function is suggested as the primary mechanism responsible for the RES depression caused by erythrocyte debris.