. Author manuscript; available in PMC: 2008 Dec 8.

Published in final edited form as: J Med Chem. 2005 Dec 29;48(26):8103–8107. doi: 10.1021/jm050726b

Table 2.

Recovery of left ventricular function in a mouse heart model of ischemia/reperfusion.^a

Parameter	Vehicle^b	Compound 5^c	Significance
LVDP^d	8.5 ± 5.3	26.0 ± 4.8	t=7.1, P < 0.0001
+dP/dt^d	6.3 ± 3.9	21.1 ± 4.9	t=7.4, P < 0.0001
-dP/dt^d	8.2 ± 3.7	24.6 ± 7	t=7.22, P < 0.0001
HR^d	37.1 ± 32.6	93.8 ± 19.3	t=4.1, P < 0.0005
% necrosis	23.4 ± 7.8	15.0 ± 6.9	t=2.32, P^e=0.029

Values were obtained after 35 global ischemia followed by reperfusion.

DMSO, n = 16.

A concentration of 30 nM 2 (initially dissolved in DMSO) was used, n = 6. During buffer perfusion of heart via the side port, the spontaneous heart rate dropped by 24 ± 8.2% (SEM) due to a decrease in the perfusion pressure. Perfusion of buffer containing 30 nM 2 was associated with a larger decrease in the heart rate of 57 ± 6.7%, likely because of a negative inotropic effect of 2.

% of baseline prior to ischemia/reperfusion.

Two-tailed.