¹⁸F‑fluorodeoxyglucose positron emission tomography for the detection of inflammatory lesions of the arterial vessel walls in Wistar rats

Abstract

The present study aimed to evaluate the use of 18 F-fluorodeoxyglucose ( 18 F-FDG) positron emission tomography (PET) for detection of high-fat and high-salt diet-induced inflammatory lesions of the arterial vessel walls in Wistar rats. A total of 20 healthy, 8-week-old, male Wistar rats were randomly assigned to the high-fat diet group and the normal diet group. After 16 and 24 weeks of feeding, Wistar rats in the normal diet group and the high-fat diet group (five rats in each group) were injected with 18 F-FDG through the tail vein at a dose of 1 mCi/kg after fasting for 12 h. After 1 h, the rats were anesthetized with 2% isoflurane, followed by micro-PET imaging with a 10-min image capture duration and immunohistochemical staining. The standardized uptake values (SUVs) of 18 F-FDG were significantly higher in the iliac artery in the high-fat diet group compared with those in the normal diet group at 16 weeks (1.53±0.08 vs. 1.04±0.03; P<0.05) and at 24 weeks (1.96±0.17 vs. 1.12±0.07; P<0.05). The SUVs of 18 F-FDG were also significantly greater in the abdominal aorta in the high-fat diet group compared with those in the normal diet group at 16 weeks (1.35±0.08 vs. 1.02±0.02; P<0.05) and at 24 weeks (1.54±0.09 vs. 1.04±0.02; P<0.05). In addition, the SUVs of 18 F-FDG in the iliac artery and abdominal aorta were significantly higher at 24 weeks compared with those at 16 weeks in the high-fat diet group (P<0.05). As determined by immunohistochemistry, the percentage of CD68-positive cells in the total number of cells per unit area in each group was 3.20±1.80% in the 24-week normal diet group, 4.70±2.02% in the 16-week high-fat diet group and 6.94±2.02% in the 24-week high-fat diet group; the percentage of CD68-positive cells in the high-fat diet group at 24 weeks was significantly higher than that in the high-fat diet group at 16 weeks and in the normal diet group at 24 weeks (P<0.05). In conclusion, 18 F-FDG PET is a noninvasive imaging tool that can continuously monitor inflammatory lesions of the arterial vessel walls in Wistar rats. Further improvement of the Wistar rat atherosclerosis model may provide data to support the early assessment of and intervention in atherosclerosis.

Recent Advances in Cardiovascular Diseases Research Using Animal Models and PET Radioisotope Tracers

“…Genetic modification tools provide access to multiple knock-in and knockout (KO/KI) mice that mimic spontaneous and induced CVD models. Table 2 lists the strains and how a given pathophysiological condition can be induced or monitored in rodents for in vivo cardiovascular studies [37][38][39][40][41][42][43][44][45][46].…”

“…ApoE −/− mice display delayed lipoprotein clearance and develop dyslipoproteinemia, hypercholesterolemia and atherosclerotic lesions even when fed normal chow [37,38] LDRL −/− mice fed normal chow develop atherosclerosis gradually, can be accelerated on a high-fat diet, hyperlipidemia with human-like profile [37,39] OPG −/− mice exhibit an unexpected increase in vascular calcification in the aorta and renal arteries [40] Lewis rats immunisation with porcine cardiac myosin fraction [41,42] C3H mice (Harlan) viral myocarditis with Coxsackie virus B3 (CVB3) [43] Myocardial infarction and perfusion C57BL/6J mice coronary artery ligation [44] Ischemia-reperfusion Sprague Dawley rats development of an ischemia-reperfusion injury, temporal coronary artery ligation for 30 min followed by a 120 min reperfusion [45,46] The occlusion of the lumen of the artery can lead to the most fatal symptoms. Modelling of the myocardial infarction is based on permanent or temporary (with the reperfusion event) ligation of the left coronary artery.…”

“…ApoE −/− rats developed early atherosclerotic lesions, and the calcification were detected with [ 18 F]-NaF in pulmonary arteries, but the glucose-based radiotracer could not show the increased metabolic activity of immune cells in pulmonary arteries, but it was visible in the aortic arch. With Wistar rats, Shen's group showed the accumulation of the compound in other vessels, such as the iliac artery and the abdominal aorta, after 16 and 24 weeks of feeding with a high-fat diet [39].…”

Cigarette Smoke Exposure, but Not High Fat Diet, is Able to Induce Atherosclerosis in Wild-Type Rats

“…18 The thoracic aortic tissue was paraffin embedded and stained hematoxylin-eosin (HE) before IMT ratio was measured microscopically using calibrated Image-J software. 19 The abdominal aortic tissue was immediately prepared for fresh frozen section before stained by oil red O. The number of foam cells was calculated microscopically from average 8 field of views from these preparations.…”