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Low-grade intravascular coagulation and reticuloendothelial function.

J E Kaplan, T M Saba

The American Journal of Physiology

|April 1, 1978

Summary

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Intravascular coagulation transiently impairs reticuloendothelial (RE) system function, reducing Kupffer cell activity. This RE dysfunction during coagulation requires further investigation for its underlying mechanisms.

Area of Science:

Physiology
Immunology
Hematology

Background:

The reticuloendothelial (RE) system, primarily composed of Kupffer cells in the liver, plays a crucial role in clearing circulating particles.
Intravascular coagulation is a complex process involving blood clot formation within vessels, potentially impacting organ function.

Purpose of the Study:

To investigate the effect of experimentally induced intravascular coagulation on the stability and function of the reticuloendothelial system.
To determine how coagulation influences Kupffer cell activity and colloid clearance.

Main Methods:

Intravascular coagulation was induced in male rats via intraperitoneal injection of bovine thrombin.
Reticuloendothelial function was assessed by measuring the vascular clearance of a radiolabeled test colloid (131I-labeled).

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Hepatic, lung, and marrow colloid localization was quantified, and hepatic blood flow was monitored.

Main Results:

Thrombin injection caused a transient depression (0.5-2 hours) in the phagocytic index (K), indicating reduced RE function.
The decrease in vascular clearance was mainly attributed to reduced Kupffer cell clearance in the liver, with increased colloid localization in the lungs and marrow.
While hepatic blood flow decreased at certain time points, sinusoidal flow remained normal during maximal RE impairment.

Conclusions:

Experimentally induced intravascular coagulation leads to a temporary dysfunction of the reticuloendothelial system.
The observed RE dysfunction is linked to altered Kupffer cell activity and colloid distribution, but the precise mechanism requires further elucidation.