Noninvasive vessel-selective perfusion imaging with intravenous myocardial contrast echocardiography

Background Intravenous myocardial contrast echocardiography (MCE) cannot identify each perfusion area of coronary vessels separately. However, by destroying microbubbles passing through a specific vessel using high-power ultrasound during intravenous MCE, vessel-selective perfusion imaging (VSPI) may be feasible. Methods In 10 open-chest dogs, intermittent short-axis images were obtained during contrast agent infusion using an ultrasound system. For VSPI, a probe coupled to another ultrasound machine was placed on the proximal left circumflex coronary artery (LCx). High-power ultrasound pulses were transmitted to destroy bubbles passing through the LCx. A negative contrast area on VSPI was considered to represent the perfusion area of the LCx (LCx-VSPI). A negative contrast area on conventional MCE during LCx occlusion and a region without staining by Evans blue dye were used as gold standards for defining the LCx perfusion area. LCx-VSPI was compared with a negative contrast area on conventional MCE during LCx occlusion and a region without staining by Evans blue dye. Results Despite lack of LCx occlusion, high-power destructive pulses produced a definite area of negative contrast on the LCx region. Decreased power of ultrasound pulses resulted in disappearance of the negative contrast area. An excellent relationship was demonstrated between both LCx-VSPI and a negative contrast area on conventional MCE during LCx occlusion (r = 0.93, P < .0001), and LCx-VSPI and a region without staining by Evans blue dye (r = 0.92, P = .0002). Conclusion: VSPI during intravenous MCE may be feasible for noninvasive assessment of perfusion areas associated with specific vessels.Asanuma T, Fujihara T, Otani K, Miki A, Ishikura F, Beppu S. Noninvasive vessel-selective perfusion imaging with intravenous myocardial contrast echocardiography. J Am Soc Echocardiogr. 2004 Jun;17(6):654-8. doi: 10.1016/j.echo.2004.03.011

Cytokine expression in human dermal fibroblasts stimulated with eosinophil cationic protein measured by protein array

[Background] : Eosinophil cationic protein (ECP) was reported previously to be involved in allergic inflammation with cytotoxic activity. On the other hand, recent studies showed that ECP did not induce cell death but inhibited the growth of cancer-derived cells. Our previous study indicated that human ECP enhanced differentiation of rat neonatal cardiomyocytes and stress fiber formation in Balb/c 3T3 mouse fibroblasts, while the effects of human ECP on human fibroblasts are unknown. [Objective] : The present study was performed to determine the effects of human ECP on cytokine expression in human fibroblasts by protein array. [Methods] : The effects of recombinant human ECP (rhECP) on normal human dermal fibroblasts (NHDF) were examined by assaying cell growth. Furthermore, cytokine expression of NHDF stimulated by ECP, which could influence cell growth, was evaluated by protein array. [Results] : ECP was not cytotoxic but enhanced the growth of NHDF. The peak rhECP concentration that enhanced the cell counts by 1.56-fold was 100 ng/mL, which was significantly different from cultures without ECP stimulation (ANOVA/Scheffe’s test, P < 0.05). Array analyses indicated that ciliary neurotrophic factor (CNTF), neutrophilactivating peptide (NAP)-2, and neurotrophin (NT)-3 were significantly upregulated in NHDF stimulated with 100 ng/mL ECP compared to those without stimulation. [Conclusion] : ECP is not cytotoxic but enhances the growth of NHDF. CNTF, NAP-2, and NT-3 were suggested to be involved in enhancing the growth of NHDF. These findings will contribute to determination of the role of ECP in allergic inflammation. (Asian Pac J Allergy Immunol 2013;31:271-6