Whole-body ionizing irradiation increases aortic stiffness and stiffness senstivitiy to high blood pressure in rats

Objective: The cardiovascular effects of ionizing radiation are mediated through inflammatory mechanisms affecting endothelial function and arterial extracellular matrix (ECM) leading to alteration of arterial stiffness and pulse wave velocity (PWV). This study aims to determine the effects of X-radiation on aortic PWV in rats and and change in sensitivity of PWV to MP. Methods: Male Sprague-Dawley rats (14 weeks) were exposed to a single high-dose of high-energy X-ray (source: LINAC, 6 MV) at 0 (control) or 5 Gy (irradiated). Between 0 to 24 hours, 24 to 48 hours and 3 weeks following irradiation, rats were anaesthetized (1.3 g/kg, urethane) and beat-to-beat aortic PWV and MP measured invasively using two 1.3 F high fidelity pressure sensors. MP was increased and decreased over the range of 60–150 mmHg with intravenous infusion of phenylephrine (0.2 mg/kg/min) and sodium nitroprusside (0.05 mg/kg/min) respectively. Results: Mean aortic PWV in irradiated rats measured within 24 hours post-irradiation was 5.08 ± 0.15 m/s (n = 6), a 14% increase compared to the control group (4.44 ± 0.11 m/s; n = 6; P < 0.05). No significant difference was observed between PWV in the irradiated group measured in the 24–48 hour period post-irradiation and control or 3 weeks post radiation. PWV-MP sensitivity (m/sec/10mmHg) determined from the slope of the PWV-MP curves was similar for both control (0.10 ± 0.01 (SE)) and irradiated rats (0.11 ± 0.01) for the low pressure range (MP 60–100 mmHg) but significantly different for the high pressure range (100–150 mmHg) only for the first 24 hour period (control 0.27 ± 0.02; irradiation: 0.37 ± 0.03; p < 0.05). Conclusions: Findings indicate an acute and marked increase in aortic stiffness and pressure dependency of aortic stiffness due to radiation at mean pressure values above normal resting pressure in rats. This may be related to differential effects of radiation induced inflammation-mediated mechanisms on active (cellular and molecular) and passive (ECM) components involved in regulation of arterial stiffness.