Effect of hypertension on elasticity and geometry of aortic tissue from dogs.

Inflation-extension experiments were carried out on segments of the descending thoracic aortas from 4 normotensive and 4 hypertensive dogs rendered hypertensive using either unilateral or bilateral renal artery constriction. Intravascular pressures up to 200 mm Hg and axial forces up to 200 g were used. The external diameter of the segment and the distance between two longitudinally spaced gage marks were recorded photographically at each pressure-force level combination. Dimensions in the underformed configuration were measured at the end of the inflation-extension experiment. Data were analyzed for changes in geometry and force-deformation response. Results indicate that: 1. Under sustained hypertension the wall thickness in the underformed configuration increases with a concurrent reduction in the in-situ longitudinal extension ratio. 2. This dual tissue response accomplishes substantial reductions in the circumferential and longitudinal stresses from the levels that would be reached at equivalent pressures in the absence of these geometric changes. 3. At comparable intravascular pressures the extensibility in the circumferential direction is slightly greater for the hypertensive aortas as compared to normals. However, the stress-extension ratio relationship in the circumferential direction is similar in the two groups. 4. The stress-extension ratio relationship in the longitudinal direction indicates that the hypertensive aorta is stiffer than its normotensive counterpart.

Absence of increase in left ventricular mass in dogs with bilateral renovascular hypertension.

Using sonomicrometric and indwelling pressure transducers, 16 healthy, normotensive dogs were prepared for semicontinuous monitoring of left ventricular (LV) mass, volumes, pressures, flows and wall tension (W Ten), aortic pressure (AP), total peripheral resistance (TPR), and indices of myocardial contractility. After a period of control measurements, bilateral renal artery constriction (2K-2C) was produced in 5 dogs and monitoring continued for 3 weeks or more. Mean arterial pressure (MAP) and LV end-systolic pressure (LVESP) was significantly higher (P less than 0.01) in the 2K-2C dogs compared to controls. There was no significant difference in LV mass, W Ten, or dP/dt, although TPR was 65% higher in the 2K-2C dogs. Comparable data from five dogs with single kidney hypertension (1K-1C), after 3 weeks, showed an elevated MAP and LVESP similar to the 2K-2C dogs. This group also showed a significant increase in LV mass and dP/dt (P less than 0.01), while the TPR was significantly decreased. The data suggest that the mechanism of hypertension development in the 2K-2C dog is different from that of the 1K-1C dog, and that there is evidence of increase in neuroadrenergic activity (viz, myocardial contractility) associated with the development of LV hypertrophy. The role of W Ten in the hypertrophic process was less clear from these data. Further study of these models may provide insight into the relative roles of the neuroadrenergic and volume-vasoconstriction components in the pathogenesis of hypertension and changes in LV mass.

Estimation of left ventricular mass in conscious dogs.

The short-axis area-length method for the estimation of left ventricular mass (LVM) and volume was validated in 24 formaldehyde-fixed canine hearts, using the truncated ellipsoid model. Estimates of the short-axis muscle area were highly correlated with directly measured values (R = 0.92; P less than 0.001). Similarly, LVM calculated using the area-length method showed good correlation with the actual weight of the left ventricle (LVW) (R = 0.85; P less than 0.001). When the regression equation was used, retrospectively, to correct the LVM estimates, the correlation between the actual LVW and the calculated LVM was markedly improved (R = 0.96; P less than 0.001). In awake dogs instrumented for measuring transverse and long axis ventricular dimensions using sonomicrometry, short-axis two-dimensional echocardiograms were used to convert the sonar external transverse dimensions to true diameters. The combined use of the corrected diameters and the regression equation to calculate LVM in the intact dog resulted in values that were highly correlated with the actual LVW (R = 0.95; P less than 0.001). Application of this technique for monitoring LVM in awake instrumented dogs demonstrated the method to be reproducible from day to day and to be sensitive enough to detect serial changes in mass such as during the development of left ventricular hypertrophy.