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(American Journal of Pathology. 2007;170:505-517.)
© 2007 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2007.060433

Impairment of Functional Capillary Density but Not Oxygen Delivery in the Hamster Window Chamber during Severe Experimental Malaria

Judith Martini*, Irene Gramaglia{dagger}, Marcos Intaglietta*{dagger} and Henri C. van der Heyde{dagger}

From the Department of Bioengineering,* University of California, San Diego; and the La Jolla Bioengineering Institute,{dagger} La Jolla, California

Microcirculatory changes and tissue oxygenation were investigated during Plasmodium berghei-induced severe malaria in the hamster window chamber model, which allows chronic, noninvasive investigation of the microvasculature in an awake animal. The main finding was that functional capillary density, a parameter reflecting tissue viability independent of tissue oxygenation, was reduced early during the course of disease and continued to decline to ~20% of baseline of uninfected controls on day 10 after infection. Parasitized red blood cells and leukocytes adhered to arterioles and venules but did not affect overall blood flow, and there was little evidence of complete obstruction of blood flow. According to the sequestration hypothesis, obstruction of blood flow by adherent parasitized erythrocytes is the cause of tissue hypoxia and, eventually, cell death in severe malaria. Tissue oxygen tensions were lower on day 10 of infection when the animals were moribund compared with uninfected controls, but this level was markedly higher than the lethal threshold. No necrotic cells labeled with propidium iodide were detected in moribund animals on day 10 after infection. We therefore conclude that loss of functional capillaries rather than tissue hypoxia is a major lethal event in severe malaria.






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Copyright © 2007 by the American Society for Investigative Pathology.