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. 2021 May 18;2:95–109. doi: 10.1016/j.jvssci.2021.04.002

Table.

Mortality and aneurysm development rate in mice following periaortic application of CaCl2 (0.5 mol.L−1 or NaCl (0.15 mol.L−1)

Genotype Overall operative mortality (%) Causes of death (% of deaths within group) Aneurysm prevalence at 6 -weeks after injury Aneurysm prevalence at 24 weeks after injury
C57Bl/6J NaCl 9.4a - -
CaCl2 17/28 (60.7%) 10/19 (52.6%)
Tgm2–/– NaCl 3.4 - -
CaCl2 20/27 (74.1%) 17/17 (94.1%)
F13a1–/– NaCl 37.3 Bleeding 11%
Cardiac +/- thrombotic 37%
- -
CaCl2 16/26 (61.5%) -
Tgm2–/–/F13a1–/– NaCl 62.0 Bleeding 27%
Cardiac +/- thrombotic 27%
- -
CaCl2 7/19 (36.8%) -

Values are number/total number (%) unless otherwise indicated.

Aneurysm prevalence (absolute numbers and percentage) of mice developing an aneurysm (defined as aortic dilatation >50%) in each genotype group. Vessel dilatation was defined at the time of harvest at either 6 or 24 weeks after CaCl2 injury.

a

The mortality of wild-type mice undergoing CaCl2 injury or NaCl sham procedure includes the first mice operated upon during familiarization with the method. The mortality rate among Tgm2–/– mice (3.4%) more accurately reflects the incidental death rate among wild-type mice post-familiarization. Deaths post-familiarization were very high in F13a1–/– mice and Tgm2–/–/F13a1–/– mice. Other causes of death include fighting post-operation, bowel ischemia and wound complications. A large renal mass was detected in one Tgm2–/–/F13a1–/– mouse. In some cases, the cause of death was unknown.