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Perivascular tissue of internal thoracic artery releases potent nitric oxide and prostacyclin-independent anticontractile factor

Marcin Malinowski^a, Marek A. Deja^a,_*, Krzysztof S. Goba^b, Tomasz Roleder^b, Jolanta Biernat^b, Stanisaw Wo^a

^a 2nd Department of Cardiac Surgery, Medical University of Silesia, Katowice, Poland
^b 2nd Department of Cardiology, Medical University of Silesia, Katowice, Poland

Received 24 August 2007; received in revised form 15 November 2007; accepted 18 November 2007.

^_* Corresponding author. Address: 2nd Department of Cardiac Surgery, Medical University of Silesia, Ziolowa 47, 40-635 Katowice, Poland. Tel.: +48 32 2526093; fax: +48 32 2526093. (Email: mdeja{at}slam.katowice.pl).

Objective: It has been recently suggested that perivascular tissue (PVT) releases hypothetic adipocyte- or adventitia-derived relaxing factor. The aim of the study was to assess anticontractile properties of perivascular tissue of human internal thoracic artery (ITA) and to check if this activity is nitric oxide (NO)- or proctacyclin-dependent. We also analyzed the influence of pleural adipose tissue on ITA reactivity. Methods: Human ITA rings were studied in vitro. First, skeletonized and pedicled ITA reactivity to serotonin and angiotensin II was compared. In subsequent experiments fragments of ITA were skeletonized and divided into two preparations. One was incubated alone, the other together with PVT or pleural adipose tissue floating freely in the bath. First, concentration–response curves to either serotonin or angiotensin II were constructed. Tissue was then transferred from one bath to the other and concentration–response curves were reconstructed. The same protocol was applied with the inhibition of NO synthase with L-NMMA (10^–4 M) and cyclooxygenase with indomethacin (10^–5 M). Results: Skeletonization augmented contractile response to serotonin (E _max 16.6 ± 1.85 mN vs 43.8 ± 3.87 mN; pedicled vs skeletonized ITA, respectively; p < 0.001) and angiotensin II (E _max 10.9 ± 1.07 mN vs 26.6 ± 1.45 mN, respectively; p < 0.001). PVT presence in the bath caused decrease of E _max from 40.8 ± 5.01 to 20.1 ± 2.69 mN for serotonin; p < 0.001 and from 31.4 ± 3.75 to 13.0 ± 1.60 mN for angiotensin II, p < 0.001 (PVT(–) vs PVT(+), respectively). PVT did not change ITA sensitivity (EC₅₀) to serotonin or angiotensin II. Pleural adipose tissue did not change the contractile response of ITA to serotonin (E _max 37.2 ± 4.95 mN vs 36.3 ± 4.83 mN, pleural fat + and pleural fat–, respectively; p = 0.9). NO and prostacyclin inhibition failed to abolish anticontractile properties of perivascular tissue. PVT with cyclooxygenase and NO synthase inhibition decreased E _max of serotonin from 46.6 ± 3.03 to 28.2 ± 4.02 mN, p < 0.001 and E _max of angiotensin II from 27.2 ± 2.00 to 16.4 ± 2.10 mN, p < 0.001. Conclusions: Perivascular tissue of ITA releases potent, soluble, nitric oxide and prostacyclin-independent anticontractile factor. The pleural adipose tissue does not influence ITA reactivity to vasoconstrictors. Preservation of perivascular tissue may protect against vasospasm of ITA graft in clinical settings.

Key Words: Internal thoracic artery • ADRF • Perivascular tissue • Adventitia • Pleural adipose tissue

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