**4.3. Inferior epigastric artery**

in the RA is stronger than in the IMA or the GEA [16]. The RA is more reactive than the IMA to angiotensin II and ET-1, but the endothelial function of the RA is similar to the IMA [49].

Pharmacological and non-pharmacological strategies have been evaluated to prevent RA occlusion and RA spasm. A number of pharmacological 'cocktails' have been successfully tested but there is currently no agreement on the optimal combination of agents. RA studied in vitro was found to relax fully either to GV solution or to papaverine, but the relaxation to GV solution was more rapid in onset and of longer duration than for papaverine [62]. GV (GTN +Verapamil) solution has been found to be satisfactory when is used on the RA to dilate it during harvesting and preparation and it [11,129]. It can be argued that GV solution represents the optimum agent for RA spasm when used in the perioperative period [129]. It has been suggested that a 'cocktail' of agents may be given to counteract RA spasm before transradial coronary angiography or angioplasty [130]. A combination of heparin, NTG and verapamil

Excellent long-term angiographic results have been reported with GEA [131], but its progres‐ sive loss of caliber with mobilization and its greater tendency for vasospasm compared with other arterial conduits both in in vitro testing [13] and in clinical practice [7] has limited its

Spasm of the GEA is a well-described clinical phenomenon [7] Some studies have suggested that the GEA and the IMA have similar response to NE, phenylephrine, and 5-HT [132,133], and that the IMA is more reactive to the TXA2 mimetic, U46619. On the other hand, Dignan and associates [15] have found that the GEA has a stronger contractility than the IMA and

GEA, the IMA, and the IEA and found that among arterial grafts the GEA has the highest contractility. Variation of techniques used in the studies may account for diverse results from different groups. Therefore, the above mentioned vasoconstrictors may be the spasmogenic agents for the GEA [15]. Additionally, relaxation of the GEA to SNP [15] or to endothelium-

Several vasodiators have been studied to counteract GEA spasm [81,136]. It has been demon‐ strated that papaverine, when given externally on the perivascular fat of the GEA, prevents GEA spasm for up to 2 hr [136]. In contrast, intraluminally applied papaverine does not show graft protection against NE-induced spasm. In addition, nifedipine prevents NE-induced spasm only when given intraluminally. Same study has also shown that verapamil is the most potent and versatile vasodilator with effective graft protection of up to 2 hr whether applied externally or internally and is the preferred agent for protecting against GEA spasm [136]. During intraoperative preparation of the GEA graft, GTN and papaverine to a lesser extent, used as topical vasodilators, appear to be more efficient in external application to increase the free flow of the GEA [81]. GV solution has been suggested to be suitable to treat spasm of GEA [137] GTN has a more rapid onset and verapamil has a longer action than papaverine [11].

, NE, and 5-HT. He and Yang [13,134] compared the contractility of the

seems to be associated with the best preventive outcome [130].

dependent vasodilators [134,135] appears to be similar to the IMA.

That should prevent spasm of conduit in the early postoperative hours [137].

**4.2. Gastroepiploic artery**

widespread use.

264 Artery Bypass

more reactive to K+

It has been demonstrated that there is no difference between the IEA and the IMA for some vasoconstrictors, such as ET, NE, K+ , and U46619 [48] However, a previous study showed that IEA contracted less in response to histamine, but relaxed more in response to endotheliumdependent vasodilators, compared with the IMA [138]. Different contractile responses to TXA2 and NE between the IEA and the IMA have also been reported [139]. In general, it has been argued that the contractile response of the IEA is basically similar to that of the IMA [11].

It has been demonstrated that endothelium dependent relaxation is reduced in the IEA compared with the IMA [140]. Another report has shown that the non–receptor-mediated endothelium dependent relaxation (induced by calcium ionophore A23187) in the IEA is less than in the IMA, although the receptor-mediated endothelium-dependent relaxation induced by acetylcholine is similar [48]. This decreased endothelium-dependent relaxation may be an early sign of arteriosclerosis in the IEA [48], since non– receptor-mediated endotheliumdependent relaxation is impaired.
