Vascular alterations in response to air desiccation injury in the carotid artery of the C3H/HeJ mouse.
The purpose of this study was to develop a model of vascular injury in 8-week-old C3H/HeJ mice (weight, 25 to 30 g) by using air desiccation. The carotid arteries were excised 1 to 8 weeks postinjury and evaluated by Verhoeff's stain and immunocytochemistry. In the first group of mice studied (n = 107), neointimal formation occurred and peaked at Day 14. In addition, medial cell division (measured by bromodeoxyuridine labeling) peaked at Day 3, whereas intimal cell proliferation increased gradually throughout the experimental period of 21 days. In addition, extensive thrombus formation occurred within 3 days after injury. The next experiment involved 124 mice and evaluated the effect of anticoagulants on the neointimal and thrombotic response. Mice received aspirin, heparin, or vehicle-only time-release pellets. Both anticoagulants significantly decreased the neointimal and thrombotic responses. The results of this study validate our animal model as being consistent with the Response to Injury Hypothesis of atherogenesis.
Madras
Diane E
DE
College Misericoridia, Dallas, Pennsylvania, USA.
Delcarpio
Joseph B
JB
Saladino
Charles F
CF
Barbee
R Wayne
RW
D000388:Air; D000818:Animals; D000925:Anticoagulants / Q000008:administration & dosage; D001241:Aspirin / Q000008:administration & dosage; D002339:Carotid Arteries / Q000473:pathology*; D003890:Desiccation; D006493:Heparin / Q000008:administration & dosage; D007150:Immunohistochemistry; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D023421:Models, Animal; D014677:Pharmaceutical Vehicles
D000925:Anticoagulants; D014677:Pharmaceutical Vehicles; D006493:Heparin; D001241:Aspirin