Key result
Older spontaneously hypertensive rats exhibited significantly faster pulse wave velocity compared to younger rats (13.2 vs. 8.0 m/sec, p < 0.001) under isoflurane anesthesia.
Why the study?
Does Doppler PWV correlate with invasively determined EaI in assessing arterial stiffness in isoflurane-anesthetized spontaneously hypertensive rats?
Does Doppler PWV correlate with invasively determined EaI in assessing arterial stiffness in isoflurane-anesthetized spontaneously hypertensive rats?
Absolute Event Rate: 13.2% vs 8%
p-value: p=<0.001
Doppler-derived pulse wave velocity provides a reproducible, non-invasive in vivo assessment of arterial stiffness that correlates with invasive arterial elastance in isoflurane-anesthetized spontaneously hypertensive rats.
Supports age-related stiffening in hypertensive rat models; leaves open clinical translation of Doppler PWV without human validation.
BACKGROUND: Rodent models are increasingly used to study the development and progression of arterial stiffness. Both the non-invasive Doppler derived Pulse Wave Velocity (PWV) and the invasively determined arterial elastance index (EaI) have been used to assess arterial stiffness in rats and mice, but the need for anesthetic agents to make these in vivo estimates may limit their utility. Thus, we sought to determine: 1) if known differences in arterial stiffness in spontaneously hypertensive rats (SHR) are detectable by PWV and EaI measurements when made under isoflurane anesthesia, and 2) if these two uniquely acquired assessments of arterial elasticity correlate. METHODS: We obtained PWV and EaI measurements in isoflurane anesthetized young and old SHRs, which are known to have significant differences in arterial stiffness. Doppler pulse waves were recorded from carotid and iliac arteries and the distance (D) between probe applantation sites was recorded. Simultaneously, an EKG was obtained, and the time intervals between the R-wave of the EKG to the foot of the Doppler waveforms were measured and averaged over three cardiac cycles. Pulse-transit time (T) of the carotid to iliac artery was determined, and PWV was calculated as Distance (D)/Time (T), where D = the distance from the carotid to the iliac notch and T = (R to iliac foot) - (R to carotid foot). EaI was subsequently determined from pressure volumes loops obtained via left ventricle catheterization. RESULTS: PWV and EaI were found to be significantly faster in the older rats (13.2 ± 2.0 vs. 8.0 ± 0.8 m/sec, p < 0.001; 120 ± 20 vs. 97 ± 16 mmHg/μl/g, p <0.05). Bland-Altman analyses of intra- and inter-observer measures demonstrate a statistically significant relationship between readings (p < 0.0001). PWV and EaI measurements were found to be significantly and positively correlated with a correlation coefficient of 0.53 (p < 0.05). CONCLUSION: Our study suggests that isoflurane administration does not limit Doppler PWV or EaI measures in their ability to provide accurate, in vivo assessments of relative arterial stiffness in isoflurane anesthetised SHR rats. Furthermore, PWV data obtained in these rats correlate well with invasively determined EaI.
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Morgan et al. (2014) studied Arterial stiffness in hypertension (n=20). Older age (32 weeks) vs. Younger age (12 weeks) was evaluated on Pulse Wave Velocity (PWV) in m/sec (p=<0.001). Older spontaneously hypertensive rats exhibited significantly faster pulse wave velocity compared to younger rats (13.2 vs. 8.0 m/sec, p < 0.001) under isoflurane anesthesia.
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