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.

Atrial natriuretic peptide (ANP) represents a family of related peptides originally isolated from cardiac atria that have potent natriuretic, diuretic, and vasorelaxant properties. ANP has previously been localized in neurons of the rat brain in regions subserving cardiovascular functions and fluid/electrolyte balance and has been localized in astroglia of the canine brain. To determine whether ANP is present in astrocytes of the human brain and to validate the canine model for future studies, human brain tissue was obtained from autopsy cases with no brain damage or neurological or vascular disease. Human brains were obtained less than 3 h postmortem, and anterior cingulate and striate cortices were dissected following perfusion or immersion fixation. Immunohistochemical processing utilized antibodies against the processed form of ANP (ANP IV, ANP104-128) and against rat proANP (amino terminus) and the avidin-biotin-peroxidase technique. Isolated, strongly ANP-immunoreactive protoplasmic astrocytes were observed in all layers of the cingulate and striate cortex gray matter. ANP-positive fibrous astrocytes were observed in the white matter. Additionally, distinctive immunopositive astrocytes were found both within and immediately subjacent to the glia limitans. Antibody against the prohormone stained only protoplasmic astrocytes and sublimitans astrocytes and processes. In addition to the astroglia, ANP was detected in scattered multipolar neurons in the cerebral gray matter. These results provide additional evidence for diversity of peptide localization in astrocytes and suggest roles for ANP in the local regulation of cerebral blood flow, blood-brain barrier permeability, or cerebrospinal fluid volume.

Although vasomotor activity in small pulmonary vessels has been studied extensively in the past, using the concept of resistance to flow, information on the distensibility of these vessels is very sparse. In an attempt to reduce this deficit, we adapted a theoretical method developed for small systemic vessels, to estimate distensibility of pulmonary resistance vessels in experimental animals and man. Pressure-flow data from 11 dogs and 10 human subjects (5 control subjects and 5 patients with long-standing left heart failure) were used to calculate distensibility of small pulmonary vessels. The conductance, G, was calculated from these data as the ratio of blood flow to driving pressure. The slope of the relationship between the logarithm of G1/4 and the average distending pressure (ADP) provides a graphic picture of circumferential extensibility, E, defined as percent change in radius for an infinitesimal change in ADP. Results indicate that: (1) the value of E in dogs was 1.85 +/- .40 mmHg-1 for the control state, which decreased to 1.45 +/- .43 mmHg-1 during norepinephrine administration; however, the decrease in the value was not statistically significant (p = 0.53); (2) the value of E in control human subjects was 3.38 +/- .47 mmHg-1 and the value of E in patients with left heart failure was -0.64 +/- 0.39 mmHg-1; the difference was significant (P = .0001).(ABSTRACT TRUNCATED AT 250 WORDS)

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.

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