P-091: Age and hypertension strongly reduce aortic visco-elastic properties in rats at basal and matched blood pressure levels - 12/02/16
L'âge et l'hypertension réduisent de manière synergique les propriétés visco-élastiques aortiques chez le rat
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Résumé |
Background |
Age and hypertension are major causes of aortic stiffening, a cardiovascular risk factor for heart and kidney damage. Long term hypertension induces vascular remodeling, thus accelerating vascular aging. The aged Spontaneously Hypertensive Rat (SHR) is a recognized surrogate for human cardiovascular pathology however discrepancies appear in existing studies of arterial stiffness depending on the age, anaesthesia, artery, strain, protocols and techniques used.
Abstract P-091 - Figure
Abstract P-091 - Figure
Methods |
We performed experiments using a robust aortic visco-elasticity analysis via echotracking in 20 week (n=6) and 80 week old SHR (n=8), with age matched normotensive Wistar Kyoto rats (WKY, n=6;6) at basal and matched levels of blood pressure (BP). After anesthesia with pentobarbital, abdominal aortic diameter and pressure were recorded and BP was decreased by clonidine i.v.
Results |
At basal BP, aortic pulse distension, compliance, distensibility (AD) and wall viscosity (AWV) were reduced and stiffness index increased with age and hypertension and further augmented with age + hypertension. Following BP matching at 130 and 100mmHg, there was no difference between 20w SHR and WKY but importantly the age effect was maintained in both WKY and SHR and accentuated by hypertension in old rats. At 130mmHg, AD=24.2±1 in 20w WKY, 19.7±1.4 in 20w SHR, 12.4±1.3 in 80w WKY and 6.1±0.7 in 80w SHR; AWV=58±5, 54±7, 29±1 and 10±2 in the same groups. At 130mmHg this is also exemplified by the alteration of the aortic distension waveform shown in the figure below and its area under the curve (AUC) adjusted to heart rate.
Conclusions |
In conclusion stiffening due to age is clearly shown here in both WKY and SHR as well as a synergistic effect of age and hypertension. This technique and model will allow new studies on the mechanisms responsible for aortic stiffening and a test-bed for drug intervention.
Le texte complet de cet article est disponible en PDF.Vol 64 - N° S1
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