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Testosterone attenuates neointima formation after coronary balloon angioplasty in male swine
Author(s) -
Bowles Doug K,
Ivey Jan,
Casati Jennifer,
Turk Jim R
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a18-c
Subject(s) - restenosis , neointima , medicine , angioplasty , cardiology , balloon , endogeny , stent
Previous studies from our lab have demonstrated that testosterone (T) 1) increases coronary smooth (CSM) muscle PKCδ both in vivo and in vitro and 2) inhibits CSM proliferation by inducing Go/G1 cell cycle arrest in a PKCδ‐dependent manner. The purpose of the present study was to determine whether endogenous T limits coronary neointimal (NI) formation following post‐angioplasty restenosis. Sexually mature, male Yucatan miniature swine were divided either left intact (IM; n =8), castrated (CM: n = 8) or castrated with T replacement (CMT; Androgel, 10 mg/day). LAD and LCX diameter was determined by coronary angiography and IVUS following intracoronary nitroglycerin. Coronary injuries were induced in both coronaries by balloon catheter overinflation (1.3x diameter; 3 x 30 sec) and animals allowed to recover for 28 days. Injured arterial sections were dissected and analyzed histologically (VVG staining). Vessels without internal elastic laminal rupture (~50% of vessels in each group) were excluded. Both intimal to medial ratio (I/M) and I/M normalized to rupture index (RI) were increased in CM, but not CMT, compared to IM. RI, medial area, and intimal/medial thickness (IMT) were not different between groups. These data support the hypothesis that endogenous T limits post‐angioplasty restenosis in males and provides direct support for a protective role for T in coronary atherosclerosis. Support: NIH HL 071574 and NASA.