title: Skeletonization of internal thoracic artery affects its innervation and reactivity.
abstract: OBJECTIVE
  The studies showing the superior characteristics of ITA graft and its impact on the clinical results of coronary artery surgery were performed with ITA harvested almost exclusively as a pedicle. This study assesses the impact of ITA skeletonization on its innervation and reactivity.
  
  
  METHODS
  Segments of skeletonized and non-skeletonized ITA were stained with antibodies against protein S-100 to look for the presence of sympathetic nerve fibers. The functional studies were performed on segments of discarded human pedicled ITA that were divided into two 3mm rings, one skeletonized and another non-skeletonized. We compared concentration-effect relationships for the contraction to norepinephrine and endothelium-dependent relaxation to acetylcholine and bradykinin, as well as endothelium-independent relaxation to sodium nitroprusside in skeletonized and non-skeletonized segments of the same ITA.
  
  
  RESULTS
  Skeletonized ITA was devoid of protein S-100 positive nerve fibers. It contracted stronger (maximal response 37.0+/-2.04 vs. 25.4+/-1.83mN (P<0.001)) and was twice as sensitive to norepinephrine: pD(2) 6.03+/-0.10 vs. 5.70+/-0.12 (P=0.035). The endothelium-dependent relaxation responses did not differ between skeletonized and non-skeletonized ITA rings. The skeletonized ITA rings appeared over 10 times more sensitive to sodium nitroprusside: pD(2) 6.66+/-0.20 vs. 5.59+/-0.37 (P=0.012)-potency ratio 11.61. The maximal responses did not differ significantly: 112.0+/-6.71 vs. 129.4+/-16.4% (P=0.33).
  
  
  CONCLUSIONS
  Skeletonization results in sympathectomy of ITA. It has no effect on endothelium-dependent relaxation but increases reactivity of ITA to norepinephrine. This augmented response to alpha-agonist is small, in comparison with over a ten-fold increase in sensitivity to sodium nitroprusside. Pedicled and skeletonized ITA are functionally significantly different vessels when studied in vitro.
authors.affiliation: 2nd Department of Cardiac Surgery, Medical University of Silesia, Ul. Ziołowa 47, 40-635 Katowice, Poland. narizol@slam.katowice.pl
authors.forename: Marek Andrzej
authors.initials: MA
authors.lastname: Deja
authors.forename: Krzysztof S
authors.initials: KS
authors.lastname: Gołba
authors.forename: Marcin
authors.initials: M
authors.lastname: Malinowski
authors.forename: Stanisław
authors.initials: S
authors.lastname: Woś
authors.forename: Maciej
authors.initials: M
authors.lastname: Kolowca
authors.forename: Jolanta
authors.initials: J
authors.lastname: Biernat
authors.forename: Maciej
authors.initials: M
authors.lastname: Kajor
authors.forename: Tomasz J
authors.initials: TJ
authors.lastname: Spyt
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D001026:Coronary Artery Bypass / Q000379:methods; D003324:Coronary Artery Disease / Q000503:physiopathology / Q000601:surgery*; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D008323:Mammary Arteries / Q000187:drug effects / Q000473:pathology* / Q000503:physiopathology / Q000637:transplantation; D009412:Nerve Fibers; D009599:Nitroprusside / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D020858:Tissue and Organ Harvesting / Q000009:adverse effects* / Q000379:methods; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D000109:Acetylcholine; D009638:Norepinephrine