Table 2. Effect of acute HET0016 treatment on eicosanoid levels in the cortex and subcortical areas at 5 minutes after ROSC from 12 minutes of CA.

Analyte	CA (12 minutes)
	Cortex		Subcortical region
	Vehicle	HET0016	Vehicle	HET0016
20-HETE	8.06±1.33	1.99±0.20a	6.44±0.89	3.18±0.22a
15-HETE	473±118	352±42.2	495±125	336±78
12-HETE	3698±725	2953±251	3932±965	2753±539
8,9-EET	6.24±1.03	5.66±1.02	5.62±0.76	6.82±0.84
11,12-EET	4.32±0.57	4.39±0.41	3.56±0.40	4.70±0.63
14,15-EET	6.93±0.93	6.55±0.76	5.65±0.83	6.64±0.52
5,6-DHETE	0.64±0.09	0.67±0.05	0.98±0.07	0.93±0.09
8,9-DHETE	1.89±0.25	2.00±0.29	2.56±0.28	2.08±0.36
11,12-DHETE	1.82±0.13	1.54±0.13	2.09±0.17	2.00±0.18
14,15-DHETE	2.88±0.42	2.15±0.16	3.09±0.16	2.29±0.08

Abbreviations: CA, cardiac arrest; EET, epoxyeicosatrienoic acid; DHETE, dihydroxyeicosatrienoic acid; HET0016, N-hydroxy-N'-(4-n-butyl-2-methylphenyl)formamidine; HETE, hydroxyeicosatetraenoic acid; ROSC, return of spontaneous circulation.

Eicosanoid levels (pmoL/g tissue) at 5 minutes after ROSC were compared with the vehicle-treated group. HET0016 inhibited 20-HETE levels in the cortex and subcortical region at 5 minutes after ROSC compared with vehicle treatment and did not change the levels of other metabolites, indicating the specificity of HET0016 inhibition for 20-HETE.

^aP<0.05 HET0016 versus vehicle.