摘要
Background： Murine model of coronary arterial inflammation has been widely accepted as an animal model of and used in Kawasaki disease （KD）. This study sought to evaluate the developmental changes of coronary arteries and cardiac function in a murine model of KD with a high-frequency ultrasound system and to provide evidence for the preparation of the model of KD. Methods： Lactobacillus case~ cell wall extract was prepared and injected into C57BL/6 mice intraperitoneally （i.p.） to induce KD. A total of 120 mice were grouped into three groups. The intravenous immunoglobulin （IVIG） treatment group was i.p. injected with IVIG （2 g/kg）, while the KD model and normal control groups were i.p. injected with 0.5 ml of phosphate buffered solution on day 5. All high-resolution echocardiography detection of mouse heart was performed by the same senior technician. Animal echocardiography was performed by measuring the coronary artery dimensions and cardiac function on days 0, 7, 14, 28, and 56 （high-resolution small animal ultrasound [Vevo770 pattem; VisualSonic, Canada] with broadband probe [RMVTM707B; frequency, 30 mHz; depth of focus, 1.2 cm]） which were measured and analyzed with Vevo770 software. Results： Pathological studies revealed focal inflammatory infiltrate asymmetrically distributed around the coronary artery trunk in the KD model group. Echocardiographic study including coronary dimension and cardiac function measurements was successfully performed in all subjects. The KD model and IVIG treatment groups showed left coronary artery dilation on days 7, 14, 28, and 56. The diameter of left coronary artery in the KD model group （0.53 ± 0.09 mm; 0.36 ± 0.07 mm; 0.34 ±0.05 mm; 0.34±0.04 mm） was significantly larger than those of 1VIG treatment group （0.22± 0.02 mm; 0.28 ± 0.03 mm; 0.26± 0.03 mm; 0.27 ±0.05 mm; 0.26 ± 0.03 mm; all P〈 0.01） and the normal control group （0.21 ±0.02 mm; 0.22 ±0.03 mm; 0.22± 0.02 mm; 0.23 ± 0.02 mm; 0.27± 0.04 mm; all P 〈 0.01） on days 7, 14, 28, and 56. No significant differences were observed in the measurements of cardiac fimction among the groups on days 0, 7, 14, 28, and 56 （all P〉 0.05）. Conclusions： Echocardiography could identify the consecutive changes of coronary artery in KD mice. Echocardiography is more convenient and direct in evaluating the coronary abnormalities in this animal model.
Background： Murine model of coronary arterial inflammation has been widely accepted as an animal model of and used in Kawasaki disease （KD）. This study sought to evaluate the developmental changes of coronary arteries and cardiac function in a murine model of KD with a high-frequency ultrasound system and to provide evidence for the preparation of the model of KD. Methods： Lactobacillus case~ cell wall extract was prepared and injected into C57BL/6 mice intraperitoneally （i.p.） to induce KD. A total of 120 mice were grouped into three groups. The intravenous immunoglobulin （IVIG） treatment group was i.p. injected with IVIG （2 g/kg）, while the KD model and normal control groups were i.p. injected with 0.5 ml of phosphate buffered solution on day 5. All high-resolution echocardiography detection of mouse heart was performed by the same senior technician. Animal echocardiography was performed by measuring the coronary artery dimensions and cardiac function on days 0, 7, 14, 28, and 56 （high-resolution small animal ultrasound [Vevo770 pattem; VisualSonic, Canada] with broadband probe [RMVTM707B; frequency, 30 mHz; depth of focus, 1.2 cm]） which were measured and analyzed with Vevo770 software. Results： Pathological studies revealed focal inflammatory infiltrate asymmetrically distributed around the coronary artery trunk in the KD model group. Echocardiographic study including coronary dimension and cardiac function measurements was successfully performed in all subjects. The KD model and IVIG treatment groups showed left coronary artery dilation on days 7, 14, 28, and 56. The diameter of left coronary artery in the KD model group （0.53 ± 0.09 mm; 0.36 ± 0.07 mm; 0.34 ±0.05 mm; 0.34±0.04 mm） was significantly larger than those of 1VIG treatment group （0.22± 0.02 mm; 0.28 ± 0.03 mm; 0.26± 0.03 mm; 0.27 ±0.05 mm; 0.26 ± 0.03 mm; all P〈 0.01） and the normal control group （0.21 ±0.02 mm; 0.22 ±0.03 mm; 0.22± 0.02 mm; 0.23 ± 0.02 mm; 0.27± 0.04 mm; all P 〈 0.01） on days 7, 14, 28, and 56. No significant differences were observed in the measurements of cardiac fimction among the groups on days 0, 7, 14, 28, and 56 （all P〉 0.05）. Conclusions： Echocardiography could identify the consecutive changes of coronary artery in KD mice. Echocardiography is more convenient and direct in evaluating the coronary abnormalities in this animal model.
