Comparison of nitric oxide release and endothelium-derived hyperpolarizingfactor-mediated hyperpolarization between human radial and internal mammary arteries
Gw. He et Zg. Liu, Comparison of nitric oxide release and endothelium-derived hyperpolarizingfactor-mediated hyperpolarization between human radial and internal mammary arteries, CIRCULATION, 104(12), 2001, pp. I344-I349
Citations number
26
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Background-Arterial grafts for CABG have been used increasingly, and the ra
dial artery (RA) has become a preferable graft, secondary to the internal m
ammary artery (IMA). In the present study, we investigated and compared NO
release and endothelium-derived hyperpolarizing factor (EDHF)-mediated hype
rpolarization for IMA and RA.
Methods and Results-IMA and RA segments taken from CABG patients were place
d in an organ chamber. An NO-sensitive electrode (to directly measure NO re
lease) or intracellular glass microelectrode (to measure membrane potential
) was used to study NO or EDHF in response to acetylcholine (ACh) and brady
kinin (BK) before and after incubation with indomethacin (a cyclooxygenase
inhibitor), N-G-nitro-L-arginine (an NO synthase inhibitor), and oxyhemoglo
bin (an NO scavenger). The resting membrane potential of the smooth muscle
cells of IMA and RA was -58 +/-0.84 (n=61) and -61 +/-1.3 (n=46) mV, respec
tively (P=0.03). BK-induced EDHF-mediated hyperpolarization in the IMA was
significantly greater than that in RA (BK 10(-7) mol/L: -10.9 +/-1.5 [n=7]
versus -5.8 +/-0.9 [n=6] mV, P=0.04). The basal (16.8 +/-1.9 versus 11.1 +/
-1.0 nmol/L, n=12, P=0.02) and stimulated releases of NO in IMA were signif
icantly greater for BK (44.3 +/-4.0 versus 25.8 +/-3.6 nmol/L, n=8, P=0.004
) and lasting longer for ACh (9.5 +/-2.0 versus 6.6 +/-3.6 minutes, n=12, P
=0.03) than those in RA.
Conclusions-The basal and stimulated releases of NO and EDHF-mediated hyper
polarization in the IMA are significantly greater than that in the RA. The
lower capacity of NO release may contribute to the susceptibility of RA to
the perioperative vasospasm and may have an impact on the long-term graft p
atency.