The morphometry of consecutive segments in cerebral arteries of normotensive and spontaneously hypertensive rats.

Abstract

313SUMMARY The media cross-sectional area, the media thickness, the internal radius and the ratio between media thickness and internal radius were determined in consecutive sections of extraparenchymal cerebral arteries of 7-and 12-month-old normotensive and spontaneously hypertensive rats. The study included intracranial pial and basal arteries as well as extracranial cervical arteries. In the chronically hypertensive rats the media to radius ratio was consistently higher than in normotensive rats over the entire calibre spectrum investigated (radius 5-400 /im). The increase of the ratio in the extracranial arteries of the hypertensive rats was exclusively due to a thicker media. In the basal intracranial arteries the increase of ratio was due to a thicker media and/or a smaller internal radius in 7-and 12-month-old rats with moderate hypertension (mean arterial pressure, MAP 171 ± 8 and 177 ± 7 mm Hg respectively). In 7-month-old rats with severe hypertension (MAP 204 ± 1 1 mm Hg) the increase of ratio was mainly due to a smaller internal radius. The observed structural alterations are likely to be of hemodynamic importance. Stroke Vol 16, No 2, 1985 THE JAPANESE STRAIN of spontaneously hypertensive rats (SHR) 1 and its stroke-prone substrain (SHRSP) 2 are extensively used in experimental hypertension research. Hemodynamic studies indicate similarities to primary hypertension in man.3 Compared to normotensive rats the cerebrovascular resistance is enhanced. Thus, in most conscious SHRSP with markedly increased blood pressure the cerebral blood flow is not altered.4 SHR are also less prone to develop bloodbrain barrier dysfunction in response to an abrupt rise in blood pressure than normotensive rats, 5 " 8 i.e. the microvessels are better protected against overdistension.The heightened cerebrovascular resistance in SHR may be functional and/or structural. 9 To what extent the various calibre segments of the cerebral arterial tree are involved is debated.10 " Intravital studies on the main cortical surface branches of the middle cerebral artery, monitored through a closed cranial window by the aid of a multichannel videoangiometer, have demonstrated significantly smaller luminal diameters in SHR compared to normotensive Wistar Kyoto rats (WKY) at rest as well as during dilatation.12 This is in agreement with an earlier study indicating a higher resistance in the relaxed cerebrovascular bed in SHR than in WKY. 13In the smallest pial 14 "16 and intraparenchymal arteries 17 of SHR and SHRSP, morphometric measurements have shown increased media or wall thickness to radius ratios. Little is known about more proximal parts of the cerebral vasculature in SHR and SHRSP, although it has been reported that the diameters of the Received September 19, 1983; revision # 3 accepted October 10, 1984. arteries in the circle of Willis do not differ significantly from controls. 18 In the present study we investigated the entire calibre spectrum of the extraparenchymal cerebral arteries of WKY, SHR and SHRSP at standardiz...

Cerebral glucose utilization and blood flow in adult spontaneously hypertensive rats.

“…A similar set of morphological differences between adult SHR and WKY rats has been reported for pial arteries. 15 The finding of virtually identical LCBF rates in 26-30-week-old SHR and WKY rats for 29 of 31 brain areas is, therefore, compatible with the morphological and physiological observations of others.…”

In Vivo X-Ray Angiography in the Mouse Brain Using Synchrotron Radiation

“…The diameters of the cerebral arteries have been reported in rats, as measured by conventional histology or by the endocasting method using scanning electron microscopy. 3,16 Demonstration of cerebral vessels by endocasting method in mice has never been performed. Comparing between angiography and corrosion casting (or conventional histological study), we consider that the casting method contains many artifacts (eg, lack of pulsatile flow that is related to physiological shear stress on the endothelial cells, and tissue shrinkage and smooth muscle contraction attributable to fixation procedure).…”

“…In rats, a different histology regarding the cerebral arteries has been observed between normotensive rats and spontaneously hypertensive rats. [1][2][3] In mice, the cerebrovascular anatomy is different between C57BL/6J and SV129. SV129 mice have markedly less severe histological damage than C57BL/6J mice with the same ischemic manipulation.…”

Spatial features of focal infarction after hydralazine treatment in stroke-prone spontaneously hypertensive rats.

“…As early as 15 days after birth, BP is elevated in SHR compared with normotensive rats, and medial hypertrophy is evident in cerebral vascular beds at this very early age.2' Protection against infarction could depend upon reversal or attenuation of vascular structural changes that are produced secondary to increased systolic BP,15 elevated pulse pressure,22 or even changes unrelated to high BP.9Y'5 Reversal of medial hypertrophy, [16][17][18]21,23 recovery from endothelial dysfunction,24 and prevention or reversal of "remodeling" of vessels into smaller vessels17 all require time, and complete normalization may never occur after BP reduction. Furthermore, the hypotensive action of hydralazine could reduce perfusion downstream to fully dilated but structurally narrowed anastomoses,'3'14,25 thereby making flow pressure dependent in collateral-dependent tissue.26 Thus, the amount and location of tissue protected by hydralazine after MCA occlusion in SHRSP is probably determined more by flow reserve in the anastomoses and downstream driving pressure within cortical penetrating arterioles than by NMDA receptor blockade from ketamine.…”