ALTERATIONS IN CIRCULATING BLOOD-VOLUME DURING POLYMICROBIAL SEPSIS

Citation
P. Wang et al., ALTERATIONS IN CIRCULATING BLOOD-VOLUME DURING POLYMICROBIAL SEPSIS, Circulatory shock, 40(2), 1993, pp. 92-98
Citations number
27
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
00926213
Volume
40
Issue
2
Year of publication
1993
Pages
92 - 98
Database
ISI
SICI code
0092-6213(1993)40:2<92:AICBDP>2.0.ZU;2-U
Abstract
Although a great deal is known concerning the pathophysiology of sepsi s, it is not clear whether circulating blood volume (CBV) is altered u nder such conditions. To study this, rats were subjected to sepsis by cecal ligation and puncture (CLP). Immediately after CLP or sham opera tion, the animals received 3 ml/100 g body weight normal saline subcut aneously. CBV was determined by using in vivo indocyanine green (ICG) clearance at 2, 5, 10, or 20 hr after CLP or sham operation. This tech nique does not require any blood sampling. Serum glutamic pyruvic tran saminase (SGPT) and glutamic oxaloacetic transaminase (SGOT) were assa yed enzymatically as indicators of hepatocyte damage. Hepatic microcir culation was assessed at a selected time point (10 hr post-CLP) by usi ng laser Doppler flowmetry and colloidal carbon infusion techniques. T he results indicate that CBV, as determined by ICG clearance, remained unchanged up to 10 hr following the onset of sepsis (i.e., early seps is) but decreased significantly at 20 hr after CLP (late sepsis). Howe ver, systemic hematocrit increased significantly at 5, 10, and 20 hr a fter CLP, indicating that plasma volume decreased at those time points . This suggests that there may be limitations in accurately assessing CBV at 5 and 10 hr after CLP, i.e., during the hyperdynamic circulator y state of sepsis, using the ICG clearance method. Moreover, SGPT and SGOT levels increased significantly at 10 hr, and the levels increased further at 20 hr post-CLP. In contrast, microvascular blood flow and carbon-perfused areas in the liver were significantly increased at 10 hr post-CLP. Thus, the hepatocyte damage, which occurs in early sepsis at 1 0 hr after CLP (as demonstrated by elevated SGPT and SGOT levels ), is not due to any reduction in hepatic microcirculation, but may be due to elevated inflammatory cytokines.