Table II.

Murine aorta relaxation and contraction analyses

	Max relaxation to MCh		Max relaxation to SNP		Max contraction to KCl		Max contraction to PE
	Δ	CI	Δ	CI	Δ	CI	Δ	CI
Krebs-HEPES with 1.8 mmol/L Ca	34	0.84 to 68.00	8	−13 to 30	4	−0.44 to 8.10	3	−1.6 to 8.0
Krebs-HEPES with 2.5 mmol/L Ca	40	9.2 to 70.0	−5	−29 to 20	4	−0.57 to 8.40	1	−3.7 to 5.8
Opti-MEM at 4°C	53	15 to 90	6	−21 to 33	6	−0.13 to 11.00	4	−2.5 to 10.1
Opti-MEM at 37°C	18	−14 to 50	−13	−36 to 10	−1	−5.2 to 3.4	−2	−7.0 to 2.2
WI	1	−29 to 32	0	−22 to 22	1	−3.3 to 6.2	1	−4.2 to 5.9

CI, Confidence interval; HEPES, 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid; MEM, minimal essential medium.

Maximum endothelial-dependent relaxation to methacholine (MCh) and maximum endothelial-independent relaxation to sodium nitroprusside (SNP). Maximum arterial contraction stimulated with potassium chloride (KCl) and maximum arterial contraction stimulated with phenylephrine (PE). Delta (Δ) denotes the change of parameter compared with a fresh condition with confidence intervals listed alongside. Wisconsin at 4 °C and Opti-MEM at 37 °C demonstrate intact endothelial-dependent relaxation, while aortas preserved in Krebs-HEPES with 1.8 mmol/L calcium and 2.5 mmol/L calcium as well as Opti-MEM at 4 °C exhibited significantly depressed endothelium-dependent relaxation function. Endothelial-independent relaxation and arterial contraction were not affected by storage conditions. Total of six descending thoracic aortas (3 males and 3 females). Statistical testing with one-way analysis of variance. Significance defined as P < .05 and significant values bolded.