PVSS Home

Peripheral Vascular Surgery Society

 

 

Abstract

#27 MURINE MODEL OF INTIMAL HYPERPLASIA: FEMORAL ARTERY ENDOVASCULAR INJURY

Ernane D. Reis, MD, Merce Roque, MD, Wen X. Zhang, MD, John Fallon, MD, PhD, Hubert Weinberg, MD, Juan J. Badimon, PhD, Mark B. Taubman, MD, and Larry H. Hollier, MD

Mount Sinai School of Medicine New York, NY

The development of intimal hyperplasia (IH) following arterial injury is one of the most investigated problems in cqrdiovascular disease. Although genetically modified mice are now available to study endogenous molecules regulating IH, to date there has been no reliable way to effectively induce intimal injury and IH in the mouse. We developed a new method of endovascular injury and evaluated intimal formation in C57 and FVB mice, two strains commonly used for the generation of genetically modified mice.

Methods: Thirty-eight mice of the C57BL/6 and FVB strains, 4 to 6 months old, were studied. The common femoral artery was injured by passage of a modified endodontic broach through an incision in the superficial femoral artery. Two weeks after injury, arterial segments were harvested for histological and morphometrical analysis.

Results: Operative mortality was 5%. Occlusive thrombus was found in 10 arteries, 3 in the C57 and 7 in the FVB group. Severe damage of the arterial wall with necrosis was found in 3 arteries. Two arteries appeared non-injured and had no IH. The remainining arteries (n-21) had IH. The table below shows the morphometric data of this latter group (mean ± SEM):

 

C57BL/6 (n = 10) FVB (n = 11)

Gender M (n = 6) F (n = 4) M (n = 5) F (n = 6)

%stenosis 27 ± 7 42 ± 8 23 ± 4 22 ± 5

Intimal area (µm2) 13,036 ± 3,256 17,789 ± 3,266 18,941 ± 3,755 13,211 ± 2,190

Intima/media ratio 0.9 ± 0.2 1.1 ± 0.2 1.2 ± 0.2 0.9 ± 0.4

Statistical analysis shoed no significant strain- or gender-related morphometric differences.

Conclusions: This method of endovascular injury induces IH in C57BL/6 and FVB mice. Our data suggest that response-to-injury is similar for male and female mice of these two strains. This technique is suitable for use in mouse models of human cardiovascular disease to examine the molecular and genetic mechanisms of vascular pathobiology.

 

Return to Master Program

Return to Homepage 

Last updated January 10, 1999