Impedance recordings to determine change in extracellular volume in the brain following cardiac arrest in broiler chickens

The present study describes a method to determine the onset and development of brain damage in broiler chickens. Exsanguination disrupts the brain metabolism and causes the brain to become ischemic. Energy-requiring systems in the cell membrane fail, which results in an ionic shift over the membrane, accompanied by a water influx into the cell. This cellular edema decreases the extracellular volume of brain tissue. In mammals, this brain damage has been measured by recording brain impedance. We adapted this approach for use with poultry. Five to six-week-old commercial broilers were equipped with impedance recording electrodes in the striatum area of the brain. Cardiac arrest was induced by means of an intravenous injection of MgCl2 and brain impedance was recorded for 30 min. The resulting curves showed a high similarity to those obtained in rats. No effects of 12 h antemortem feed deprivation on the size and rate of change in brain impedance could be found. Both in anesthetized and conscious birds, a change in brain impedance was found. We conclude that brain impedance can be used to determine the development of ischemic brain damage in broiler chickens.     

Validation of the in vivo intravascular ultrasound measurement of in-stent neointimal hyperplasia volumes

OBJECTIVES: This study was undertaken to validate the in vivo intravascular ultrasound (IVUS) measurement of in-stent neointimal hyperplasia (IH) volumes. BACKGROUND: Because stents reduce restenosis compared to balloon angioplasty, stent use has increased significantly. As a result, in-stent restenosis is now an important clinical problem. Serial IVUS studies have shown that in-stent restenosis is secondary to intimal hyperplasia. To evaluate strategies to reduce in-stent restenosis, accurate measurement of in-stent neointimal tissue is important. METHODS: Using a porcine coronary artery model of in-stent restenosis, single Palmaz-Schatz stents were implanted into 16 animals with a stent:artery ratio of 1.3:1. Intravascular ultrasound imaging was performed at 1 month, immediately prior to animal sacrifice. In vivo IVUS and ex vivo histomorphometric measurements included stent, lumen and IH areas; IH volumes were calculated with Simpson's rule. RESULTS: Intravascular ultrasound measurements of IH (30.4+/-11.0 mm3) volumes correlated strongly with histomorphometric measurements (26.7+/-8.5 mm3, r=0.965, p < 0.0001). The difference between the IVUS and the histomorphometric measurements of IVUS volume was 4.1+/-2.7 mm3 or 15.8+/-11% (standard error of the estimate=0.7). Both histomorphometry and IVUS showed that IH was concentric and uniformly distributed over the length of the stent. Intravascular ultrasound detected neointimal thickening of < or =0.2 mm in 5 of 16 stents. Sample size calculations based on the IVUS measurement of IH volumes showed that 12 stented lesions/arm would be required to show a 50% reduction in IVUS-measured IH volume and 44 stented lesions/arm would be required to show a 25% reduction in IH volume. CONCLUSION: In vivo IVUS measurement of IH volumes correlated strongly with ex vivo histomorphometry. Using volumetric IVUS end points, small sample sizes should be necessary to demonstrate effectiveness of strategies to reduce in-stent restenosis.     

Distinct tumor necrosis factor-alpha responses in alveolar and peritoneal macrophages are associated with local levels of endotoxin

Tumor necrosis factor alpha (TNF-alpha) responses of alveolar macrophages (AMs) and peritoneal macrophages (PMs) were studied in rats after intravenous injection of lipopolysaccharide (LPS). High levels of plasma TNF-alpha, increased pulmonary myeloperoxidase activity, and leukopenia occurred within 2 h after LPS injection. Alveolar spaces exhibited a strict compartment property, as manifested by only slightly increased LPS and TNF-alpha levels in alveolar lavage fluid and an unchanged capacity of AMs to produce TNF-alpha. By contrast, the peritoneal cavity had greatly increased local LPS and TNF-alpha levels and a diminished PMs TNF-alpha response to LPS. The amount of LPS in the alveolar spaces was less than 0.2% of the level in peritoneal fluid. These results indicate that activation of resident macrophages is dependent on the amounts of local LPS and, in addition, suggest that resident AMs neither participate in the plasma TNF-alpha response nor contribute to neutrophil sequestration in the lung during the early stages of endotoxemia.