Search

Objectives: The influence of carotid artery occlusion (10, 30 and 60 min) on regulatory mechanisms implicated in the vasorelaxant responses of isolated glandular branch of rabbit facial artery to acetylcholine (ACh) and vasoactive intestinal polypeptide (VIP) was examined. Design: In organ bath studies with arterial rings precontracted with phenylephrine (1 mu M), before and after carotid artery occlusion, changes in isometric tension were recorded. Results: Endothelium-dependent vasorelaxation by ACh and endothelium-independent vasorelaxation by VIP were significantly reduced, started from 30 and 10 mm of carotid occlusion, respectively. Inhibitory effect of indomethacin on ACh vasorelaxation was enhanced whilst effect of N-G-nitro-L-arginine reduced, started from 30 min of carotid occlusion. Sodium nitroprusside-induced vasorelaxation was not changed after carotid occlusion. Inhibition of VIP vasorelaxation by L-N-omega-nitroarginine-2,4-L-diaminobutyric-amide, was reduced, started from 30 min of carotid occlusion. Forskolin enhanced VIP-induced vasorelaxation in control rings but this effect was reduced started from 30 min of occlusion. In the presence of VIP, vasorelaxant effect of ACh was increased; the increase was reduced, started from 10 min of carotid occlusion. Conclusions: The present investigation provides evidence for the decreased responsiveness to both, ACh-endothelium-dependent and VIP-endothelium-independent vasorelaxation in rabbit facial artery after carotid occlusion. In addition, the data suggest that ischaemia alters contribution of endothelial nitric oxide (eNO) and prostaglandin to ACh, and vascular smooth muscle's cAMP and neuronal NO to VIP vasorelaxant effects.

Free and pedicled flaps are frequently used in reconstruction of the lower two-thirds of the face. For these reconstructions, the submandibular facial vessels are extensively used as a receptor site. In this anatomic study, we investigate if the facial vessels in the nasolabial fold can be used as a receptor site as well. In 13 human cadavers, the facial artery and vein were dissected in the nasolabial fold in the same way as would be done during surgery. The case of dissection and length, diameter, and location of the vessels were analyzed. The average length of the dissected artery was 28 mm (+/- 11 standard deviations [SD]) and of the dissected vein, 19 mm (+/- 6 SD). The mean diameter of the artery was 1.5 mm (+/- 0.4 SD) and 2.5 mm (+/- 0.8 SD) for the vein. In 85% of the sides, both vessels were suitable to use as a microsurgical receptor site. The easy access and the measured diameter of the facial vessels in the nasolabial fold make it a potential site for microsurgical anastomosis.

The aim was to examine the influence of the endothelium on acetylcholine (ACh) and vasoactive intestinal polypeptide (VIP) functional responses in the isolated glandular branch of rabbit facial artery precontracted with phenylephrine as well as the potential contribution of nitric oxide (NO) and prostanoids in the ACh- and VIP-induced effects. Acetylcholine caused endothelium-dependent and VIP endothelium-independent relaxations of facial artery. The effect of ACh was partly inhibited by N-G -monomethyl-L-arginine (L-NMMA, a non-selective NO synthase inhibitor) or by indomethacin (a cyclooxygenase inhibitor) while being completely blocked after concomitant addition of L-NMMA and indomethacin. The relaxation of the facial artery caused by ACh was unaffected by 65 mm KCl. The VIP-induced vasodilation was potentiated by forskolin (an adenylate cyclase stimulator) and partly reduced by L-NMMA or S-methyl-L-thiocitrulline (L-SMTC, a neuronal NO synthase inhibitor), whereas it was unaffected by indomethacin. These results suggest that ACh effects on the rabbit facial artery are mediated through release of endothelium-derived NO and cyclooxygenase products, while the effect of VIP is most probably mediated by an increase of cyclic adenosine 3',5'-monophosphate (cAMP) in vascular smooth muscles and by VIP-induced release of NO from perivascular nerve fibers.

The aim was to examine the influence of the endothelium on acetylcholine (ACh) and vasoactive intestinal polypeptide (VIP) functional responses in the isolated glandular branch of rabbit facial artery precontracted with phenylephrine as well as the potential contribution of nitric oxide (NO) and prostanoids in the ACh- and VIP-induced effects. Acetylcholine caused endothelium-dependent and VIP endothelium-independent relaxations of facial artery. The effect of ACh was partly inhibited by NG-monomethyl-l-arginine (l-NMMA, a non-selective NO synthase inhibitor) or by indomethacin (a cyclooxygenase inhibitor) while being completely blocked after concomitant addition of l-NMMA and indomethacin. The relaxation of the facial artery caused by ACh was unaffected by 65 mm KCl. The VIP-induced vasodilation was potentiated by forskolin (an adenylate cyclase stimulator) and partly reduced by l-NMMA or S-methyl-l-thiocitrulline (l-SMTC, a neuronal NO synthase inhibitor), whereas it was unaffected by indomethacin. These results suggest that ACh effects on the rabbit facial artery are mediated through release of endothelium-derived NO and cyclooxygenase products, while the effect of VIP is most probably mediated by an increase of cyclic adenosine 3',5'-monophosphate (cAMP) in vascular smooth muscles and by VIP-induced release of NO from perivascular nerve fibers.