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  • Title: Hepatic microvascular regulatory mechanisms. VII. Effects of endoportally-infused endotoxin on microcirculation and mast cells in rats.
    Author: Unger LS, Reilly FD.
    Journal: Microcirc Endothelium Lymphatics; 1986; 3(1):47-74. PubMed ID: 3547067.
    Abstract:
    Changes in hepatic microvasculature and systemic arterial blood pressure were measured for 1 hr in anesthetized male Sprague-Dawley rats receiving an endoportal injection of 15 mg/kg b.w. Boivin-extracted E. coli endotoxin (026:B6) or sterile saline solution as a control. Image shearing and videodensimetric methods were used to quantify internal diameters (D) and cellular velocities (V) and to calculate relative rates of volumetric blood flow (Q) at the inlet of periportal and the outlet of centrilobular sinusoids. Determination of the number of Falck-Hillarp-positive mast cells was made in 8 microns sections of liver at the light microscopic level. Endotoxin produced a mild hypotensive response by 20 min after which time rats remained normotensive. In vivo microscopy of transilluminated livers revealed adherence of platelets and mononuclear leukocytes to the microvascular wall between 15 to 30 min post-endotoxin infusion and constriction at 50 and 60 min of centrilobular sinusoids but not that of the other microvascular segments. A significant increase in cellular velocity was observed within 5 min at the inlet of periportal sinusoids. This response was accompanied by constriction at both the inlet and outlet of periportal and centrilobular sinusoids, respectively. After 1 hr, endotoxin- treated livers demonstrated a 26% decrease in the number of fluorescent serotonin-containing mast cells. However, no change in hepatic lobular perfusion or in volumetric flow rate was observed during this period. Given these results, it is postulated that volumetric flow rate within hepatic lobules is maintained during the first hr after endotoxin infusion by modulation of microvascular internal diameters in response to changes in cellular blood flow velocity, and mast cell mediators such as serotonin trigger hepatic microvascular autoregulation following the administration of endotoxin.
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