Bp. Booth et al., EFFECT OF TEMPERATURE ON GLYCERYL TRINITRATE INDUCED RELAXATION OF RABBIT AORTA, Canadian journal of physiology and pharmacology, 71(8), 1993, pp. 629-632
It has previously been shown that the vasodilatory response to glycery
l trinitrate (GTN) was decreased during hypothermic cardiopulmonary by
pass. The purpose of these experiments was to determine the effect of
temperature on GTN-induced relaxation and on GTN biotransformation in
rabbit aorta. It was determined that the EC(50) of GTN on rabbit aorti
c rings (RARs) was increased significantly from 1.8 x 10(-8) M at 37 d
egrees C to 3.4 x 10(-8) M at 27 degrees C (p < 0.05). The production
of NO by rabbit aortic strips (RASs) was significantly less at 27 degr
ees C compared with 37 degrees C after 80 min, being 9.62 x 10(-11) +/
- 13.2 x 10(-11) mol NO/g wet wt. RASs compared with 5.71 x 10(-10) +/
- 9.43 x 10(-11) mol NO/g wet wt. RASs, respectively (p < 0.05), after
80 min incubation. There was no difference in the amount of glyceryl-
1,2-dinitrate (1,2-GDN) produced from GTN at the two temperatures. The
ED(20) for NO-induced relaxation of RARs increased from 3.46 x 10(-10
) +/- 2.24 x 10(-10) mol at 37 degrees C to 1.01 x 10(-9) +/- 4.51 x 1
0(-10) mol at 27 degrees C (p < 0.05). These data indicate that the bi
otransformation of GTN and the release of NO were impaired by hypother
mia, and that this, as well as a decrease in the tissue response to NO
at 27 degrees C, explains the decrease in GTN activity at reduced bod
y temperatures.