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Chronic hypertension is associated with hypertrophy of cerebral blood vessels. Previous studies of the mechanical properties of cerebral vessels in chronic hypertension have examined large cerebral arteries. The goals of this study were first to develop a method to examine vascular mechanics of cerebral arterioles in vivo and second to determine whether the stiffness of cerebral arterioles is altered in the presence of chronic hypertension. We calculated circumferential stress and strain of pial arterioles in age-matched, anesthetized stroke-prone spontaneously hypertensive rats (SHRSP) and in Wistar Kyoto rats (WKY) from measurements of pial arteriolar pressure, inner diameter, and wall thickness. Pial arteriolar pressure was measured with a servonull system. Smooth muscle of pial arterioles was deactivated with ethylenediaminetetraacetic acid (EDTA), and pressure-diameter relations were examined during step-wise reductions in pressure. Prior to deactivation of smooth muscle in 3-4-month-old rats, pial arteriolar pressure was greater in SHRSP than in WKY (110 +/- 4 versus 75 +/- 2 mm Hg [mean +/- SE]; p less than 0.05). Pial arteriolar diameter, which was measured at prevailing levels of pial arteriolar pressure, was less in SHRSP than in WKY (52 +/- 5 versus 63 +/- 3 microns; p less than 0.05). Following deactivation of smooth muscle, diameter of pial arterioles at 70 mm Hg of pial arteriolar pressure was similar in the two groups: 104 +/- 6 microns in SHRSP and 109 +/- 3 microns in WKY (p greater than 0.05). Wall thickness was 4.5 +/- 0.2 microns in SHRSP and 4.1 +/- 0.1 microns in WKY (p greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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Arteries exposed to sustained hypertension undergo a moderate degree of intimal thickening and a marked amount of medial thickening. Autogenous veins that are used as bypass grafts undergo similar histological changes. In this study autogenous vein grafts were used as an indirect model of arteries exposed to sustained hypertension. It was hypothesized that it is not pressure per se but rather mechanical changes brought about by exposure to increased pressures that act as a stimulus inducing histological changes. Exposure to arterial pressure increases the following nine mechanical factors: deformation in the circumferential, longitudinal, and radial directions; stresses in each of these three directions; pulsatile deformations and pulsatile stresses; and flow velocity. All of these mechanical changes occur simultaneously. Accordingly, a three-step algorithm was devised to separate each of the nine mechanical factors and correlate them with histological changes. Three sequential experimental studies were performed in 38 dogs following the algorithm. These experiments demonstrated that intimal thickening was best correlated with low flow velocity, a correlate of low shear stress, whereas medial thickening was best correlated with deformation in the circumferential direction.

Segments of dog carotid artery were studied in vitro at four longitudinal extension ratios, lambda z = 1.2, 1.4, 1.6, and 1.8, in randomized order. At each length, the pressure was elevated in steps to 200 mmHg or until the vessels buckled. Vessels were studied under control conditions and after treatment with moderate doses of degradative enzymes: 80 U/ml elastase for 90 min or 640 U/ml collagenase for 120 min. These doses were selected, following pilot studies, to degrade vessels but not to destroy them. Treatment with elastase (n = 24) reduced both longitudinal and circumferential stresses at all vessel lengths. Circumferential stress was reduced at pressures greater than 15 mmHg, the magnitude of effect increasing with both longitudinal and circumferential deformations. Longitudinal stress was reduced by a constant amount, irrespective of vessel length. Treatment with collagenase (n = 24) reduced circumferential stress when the vessels were distended by at least 60 mmHg; it did not reduce longitudinal stress. These data suggest that in intact cylindrical segments of dog carotid artery, subjected to physiological levels of strain, elastin bears a portion of both circumferential and longitudinal loads, whereas collagen bears a portion of only circumferential loads.

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The sections in this article are: Behavior of Arteries in Vivo Circumferential Properties of Arteries Relaxed Arteries Contracted Arteries Longitudinal Properties of Arteries Elastic Characteristics Intimal Shear Stresses Radial Properties of Arteries Elastic Characteristics Mechanics and Wall Nutrition Special Aspects of Vascular Mechanics Baroreceptors Arteries of Hypertensive Subjects Atherosclerotic Arteries Multidirectional Properties of Arteries Analytic Assumptions Incremental Analysis Finite‐Deformation Analysis