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Updated: Sep 20, 2026
Assessing Therapeutic Angiogenesis in a Murine Model of Hindlimb Ischemia
Published on: June 8, 2019
Endovascular irradiation impairs vascular functional responses in noninjured pig coronary arteries
Jinsheng Li1, Hector De Leon, Bunken Ebato
1American Cardiovascular Research Institute, 3155 Northwoods Place, Norcross, GA 30071, USA. jli@acrionline.org
Purpose:
To assess the effects of endovascular irradiation on vascular structure and function in pig coronary arteries in the absence of vascular injury.
Methods And Materials:
Vasomotor responses to contractions of KCl and prostaglandin F2alpha (PGF2alpha), relaxations to endothelium-dependent (substance P, A23187) and -independent (sodium nitroprusside, SNP) agents; endothelial morphology and superoxide anion (02*-) production were investigated in control (naive), sham and irradiated (20 Gy, 32P) arteries 1 month after irradiation.
Results:
Contractions to KCl and PGF2alpha in the presence of L-NAME were significantly decreased, relaxations to substance P and A23187 were abolished and SNP-induced relaxation was potentiated in irradiated arteries compared to naive and sham-treated vessels. Scanning electron microscopy (SEM) revealed enlarged endothelial cells (ECs) exhibiting surface microvilli. O2*- production was significantly increased in irradiated vessels (437.0 +/- 37.3 vs. 126.0 +/- 11.6 RLU/s/mg tissue, P < .01).
Conclusions:
One month after brachytherapy, normal pig coronary arteries showed abnormal vascular reactivity, altered endothelial morphology and increased production of O2*-. Lack of relaxation to substance P and A23187 reflects ionizing radiation-mediated damage to ECs, whereas potentiation of relaxation to SNP suggests additional deleterious effects on medial smooth muscle cells (SMCs). Increased O2*- production might have contributed to endothelial dysfunction by scavenging nitric oxide (NO).
