BACKGROUND: We examined the effect of 11,12-epoxyeicosatrienoic acid (EET(11,12)) added to St. Thomas' Hospital (ST) solution or University of Wisconsin (UW) solution on endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation under clinically relevant temperature and exposure time. METHODS: Porcine coronary microarteries (200 to 450 microm) were incubated with Krebs' solution (control), ST with or without EET(11,12) (300 nmol/L) at 22 degrees C for 1 hour as well as at 4 degrees C for 1 or 4 hours, and UW with or without EET(11,12) at 4 degrees C for 4 hours. The EDHF-mediated relaxation was induced by bradykinin (-10 to approximately -6.5 log M) in the precontraction evoked by U(46619) (10 nmol/L) or U(46619) (1 nmol/L) plus endothelin-1 (6 nmol/L). RESULTS: The EDHF-mediated relaxation was reduced after exposure to UW (79.7% +/- 4.6% versus 93.6% +/- 2.8%, p = 0.01) at 4 degrees C for 4 hours. One-hour exposure to ST under 22 degrees C or 4 degrees C decreased the relaxation (75.2% +/- 7.6% versus 96.7% +/- 1.6%, p < 0.05) or the sensitivity to bradykinin (-8.04 +/- 0.15 versus -8.50 +/- 0.20 log M, p < 0.05). The relaxation increased to 86.8% +/- 5.3% by addition of EET(11,12) to ST (1 hour at 22 degrees C, p < 0.05) but was unchanged when added to either ST or UW at 4 degrees C for 1 or 4 hours. CONCLUSIONS: As an additive to ST solution, EET(11,12) may partially restore EDHF-mediated endothelial function under moderate hypothermia but had no significant effect under profound hypothermia when added to either ST or UW solution. Further investigation is necessary to improve the effect.
BACKGROUND: We examined the effect of 11,12-epoxyeicosatrienoic acid (EET(11,12)) added to St. Thomas' Hospital (ST) solution or University of Wisconsin (UW) solution on endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation under clinically relevant temperature and exposure time. METHODS: Porcine coronary microarteries (200 to 450 microm) were incubated with Krebs' solution (control), ST with or without EET(11,12) (300 nmol/L) at 22 degrees C for 1 hour as well as at 4 degrees C for 1 or 4 hours, and UW with or without EET(11,12) at 4 degrees C for 4 hours. The EDHF-mediated relaxation was induced by bradykinin (-10 to approximately -6.5 log M) in the precontraction evoked by U(46619) (10 nmol/L) or U(46619) (1 nmol/L) plus endothelin-1 (6 nmol/L). RESULTS: The EDHF-mediated relaxation was reduced after exposure to UW (79.7% +/- 4.6% versus 93.6% +/- 2.8%, p = 0.01) at 4 degrees C for 4 hours. One-hour exposure to ST under 22 degrees C or 4 degrees C decreased the relaxation (75.2% +/- 7.6% versus 96.7% +/- 1.6%, p < 0.05) or the sensitivity to bradykinin (-8.04 +/- 0.15 versus -8.50 +/- 0.20 log M, p < 0.05). The relaxation increased to 86.8% +/- 5.3% by addition of EET(11,12) to ST (1 hour at 22 degrees C, p < 0.05) but was unchanged when added to either ST or UW at 4 degrees C for 1 or 4 hours. CONCLUSIONS: As an additive to ST solution, EET(11,12) may partially restore EDHF-mediated endothelial function under moderate hypothermia but had no significant effect under profound hypothermia when added to either ST or UW solution. Further investigation is necessary to improve the effect.
Authors: John D Imig; Ahmed Elmarakby; Kasem Nithipatikom; Shouzou Wei; Jorge H Capdevila; Venugopal Raju Tuniki; Bhavani Sangras; Siddam Anjaiah; Vijaya L Manthati; D Sudarshan Reddy; John R Falck Journal: Front Physiol Date: 2010-12-03 Impact factor: 4.566