Microvascular research
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Microvascular research · Jan 2005
Intravenous glycine after cecal ligation and puncture has no effect on impaired hepatic microperfusion, leukocyte adhesion, and mortality in septic rats.
Recent studies indicated that prefeeding of a glycine supplemented diet reduces the hepatic inflammatory response and liver damage in sepsis. We investigated the effect of a glycine-enriched infusion on hepatic microcirculatory disturbances and mortality in a rat model of sepsis after the onset of the disease. Male Wistar rats (240 +/- 13 g) underwent cecal ligation and puncture (CLP) or laparotomy (LAP). ⋯ Heart rate and mean arterial pressure remained stable but PBF decreased significantly in all groups 20 h after CLP. Although glycine reduces the hepatic inflammatory response and liver damage in pretreatment of septic rats, there was no effect of intravenous glycine after the onset of sepsis in our experiments. Our animal model does not support the use of glycine in patients.
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Microvascular research · Mar 2004
C1-inhibitor reduces hepatic leukocyte-endothelial interaction and the expression of VCAM-1 in LPS-induced sepsis in the rat.
Increased leukocyte-endothelial interaction (LEI) leading to hepatic microperfusion disorders is proposed as major contributor for hepatic failure during sepsis. Recently it has been demonstrated that complement inhibition by C1-inhibitor (C1-INH) is an effective treatment against microcirculatory disturbances in various diseases. The purpose of this study was to investigate the influence of C1-INH on microcirculation and LEI in the liver in a rat model of sepsis. ⋯ Our results indicate that even upon delayed treatment hepatic adhesion molecule expression and LEI can be reduced by C1-INH. The multifunctional regulator may reduce hepatic microcirculatory disturbances during sepsis under clinical conditions.
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Microvascular research · Sep 2003
Measurement of the cardiac output in small animals by thermodilution.
Cardiac output (CO) measurements based on indicator dilution, microspheres, thermodilution and ultrasonic sensors are not suitable for small animals, because of limited blood volume, high heart rates and small caliber vessels that do not allow probe placement within the heart. We developed a modified thermodilution method to measure CO in awake animals weighing less than 100 g. Under anesthesia, the animal is instrumented with a jugular vein catheter placed proximal to the subclavian vein and a temperature probe in the carotid artery with the thermocouple positioned at the aortic arch. ⋯ Cardiac index (CI=CO/weight) was 197.0 +/- 18.8 (ml/min)/kg. Repeated measurements were made. This technique allows correlating systemic flow changes to be correlated to those measured in the microcirculation of window chamber preparations.
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Microvascular research · Jul 2003
Water immersion and EMLA cause similar digit skin wrinkling and vasoconstriction.
Water immersion skin wrinkling tests limb sympathetic vasoconstrictor function. We have recently shown that water immersion wrinkling is accompanied by digit vasoconstriction and postulated that vasoconstriction is the main underlying mechanism. To test this further, we applied vasoconstrictive cream (EMLA) to the distal digit and compared the degree of skin wrinkling and digit blood flow reduction with those after water immersion. ⋯ Control using aqueous cream resulted in minimal skin wrinkling and nonsignificant reduction in digit artery flow (P = 0.170). These data further support that water immersion skin wrinkling is mediated by vasoconstriction. The EMLA cream patch test may develop into a useful screening test for hand sympathetic vasoconstrictor function.
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Microvascular research · May 2001
Histamine-induced production of interleukin-6 and interleukin-8 by human coronary artery endothelial cells is enhanced by endotoxin and tumor necrosis factor-alpha.
In this study, we tested the synergy between histamine and LPS, and histamine and TNF-alpha, on endothelial cell production of interleukin-6 (IL-6), interleukin-8 (IL-8), and monocyte chemoattractant protein-1 (MCP-1). Human coronary artery endothelial cells (HCAEC) were cultured in vitro with histamine (0.1 to 1000 microM) in the presence or absence of LPS or TNF-alpha for 24 h, and the secreted IL-6, IL-8 and MCP-1 were quantified. Unactivated HCAEC produced minimal levels of IL-6, IL-8, or MCP-1. ⋯ Electrophoretic mobility shift assays of nuclear proteins extracted from HCAEC treated with histamine and LPS, or histamine and TNF-alpha, revealed amplified translocation of NF-kappaB proteins to the nuclei. Since both LPS and TNF-alpha potentiated histamine-induced cytokine production, it is possible that these activators stimulate H-1 receptor expression and/or augment the signal transduction pathways leading to the expression of IL-6 and IL-8. These results indicate the importance of synergy between histamine and other inflammatory stimuli on endothelial cell activation and implicate their cooperative participation in vascular leak and inflammation.