Cellular and Vessel Wall Morphology of Cerebral Cortical Arterioles after Short-Term Diabetes in Adult Rats

Moore, Steven A.; Bohlen, H. G.; Miller, Bryan G.; Evan, Andrew P.

doi:10.1159/000158613

Cited by 33 publications

(33 citation statements)

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“…Therefore, force transmission by the muscle to the circumference of the vessel should be equally efficient in normotensive and hypertensive rats, assuming there is little or no slippage of the VSM cells relative to the vessel wall in either strain of rats. Walmsley et al , x Miller, 18 Miller and colleagues, 17 ' " and Moore et al 23 have recorded a similar arrangement for VSM 29 have shown that active muscle tone did not substantially alter the orientation of the VSM cells relative to the vessel wall. We would expect similar circumstances for vessels of hypertensive rats because their VSM cells have a normal length and wrapping arrangement (see Table 1 and Figure 1, respectively).…”

Section: Discussionmentioning

confidence: 91%

Cell and wall morphology of intestinal arterioles from 4- to 6- and 17- to 19-week-old Wistar-Kyoto and spontaneously hypertensive rats.

et al. 1987

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SUMMARY To determine whether vascular smooth muscle cells around intestinal arterioles of various sizes undergo comparable changes in spontaneously hypertensive rats, 4-to 6-week-oId (n = 10) and 17-to 19-week-old (n = 10) rats from the Wistar-Kyoto and the spontaneously hypertensive strains were used to study the external morphology of vascular smooth muscle cells by scanning electron microscopy and the vessel wall cross-sectional characteristics by light microscopy. At the tune of fixation all vascular tone had been abolished. Scanning electron microscopy analysis revealed that all Wistar-Kyoto and spontaneously hypertensive rats at a given age have spindle-shaped vascular smooth muscle cells of comparable length and longitudinal width for a given branching order of arterioles. However, normal maturation is associated with elongation and widening of the vascular smooth muscle cells. Light and sinning electron microscopy indicated that a monolayer of vascular smooth muscle cells, wrapped at almost 0 degrees to the vessel's radial axis, is maintained in adult spontaneously hypertensive rats. The radial thickness of this vascular smooth muscle cell monolayer was significantly (p< 0.025) increased for only the largest arterioles of young and adult spontaneously hypertensive rats. This radial thickening of individual vascular smooth muscle cells increased the muscular component of the wall area for the largest arterioles by about 50% in adult spontaneously hypertensive rats. Other smaller submucosal arterioles of young and adult spontaneously hypertensive rats had normal vessel wall and vascular smooth muscle cell characteristics. These data indicate that hypertrophy in the smooth muscle cell's radial dimension is the primary morphological change in intestinal arterioles of spontaneously hypertensive rats. However, the vascular smooth muscle cell hypertrophy is confined to the largest arterioles such that the remaining smaller arteriolar vessels in the spontaneously hypertensive rat retain a normal smooth muscle cell and overall wall morphology. Received March 10, 1986; accepted July 17, 1986. vasculature. Indeed, both functional and anatomical studies have shown vessel wall enlargement resulting from hyperplasia, hypertrophy, or both, to be associated with some part of the arterial or arteriolar vasculature during hypertension.

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Section: Discussionmentioning

confidence: 91%

Cell and wall morphology of intestinal arterioles from 4- to 6- and 17- to 19-week-old Wistar-Kyoto and spontaneously hypertensive rats.

et al. 1987

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“…Nonetheless, reduced microsphere entrapment by SDI treatment in diabetic rats indicates a vascular effect, albeit not directly related to nutritive blood flow. Platelet aggregation, thrombus formation and leucocyte-endothelium interactions are increased in diabetes [71,72]. It is possible that SDI treatment might decrease one or more of these factors, which could explain reduced microsphere trapping and suggests a direction for future research.…”

Section: Discussionmentioning

confidence: 99%

Comparison of the effects of inhibitors of aldose reductase and sorbitol dehydrogenase on neurovascular function, nerve conduction and tissue polyol pathway metabolites in streptozotocin-diabetic rats

et al. 1997

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Elevated polyol pathway activity has been implicated in the development of diabetic complications, including neuropathy [1]. In diabetic models, inhibitors of the first enzyme in the pathway, aldose reductase, prevent or correct nerve conduction velocity (NCV) and regeneration deficits [2][3][4][5][6][7][8][9][10][11][12][13]. Clinical trials of aldose reductase inhibitors (ARIs) have shown modest improvements in neurological symptoms, NCV, sensory measures, and an increase in nerve fibre regeneration [14-17] despite a less effective polyol pathway blockade than was found necessary for functional effects in animal studies [6,10,18].Several hypotheses have been advanced to explain the action of ARI. Some putative mechanisms are primarily dependent on the first half of the polyol pathway, conversion of glucose to sorbitol by aldose Diabetologia (1997) 40: 271-281 Comparison of the effects of inhibitors of aldose reductase and sorbitol dehydrogenase on neurovascular function, nerve conduction and tissue polyol pathway metabolites in streptozotocin-diabetic rats Summary Aldose reductase inhibitors (ARIs) attenuate diabetic complications in several tissues, including lens, retina, kidney, blood vessels, striated muscle and peripheral nerve. However, it is unclear whether their action in diabetes mellitus depends directly on inhibiting the conversion of glucose to sorbitol by aldose reductase or indirectly by reducing the sorbitol available for subsequent metabolism to fructose by sorbitol dehydrogenase. To identify the polyol pathway step most relevant to complications, particularly neuropathy, we compared the biochemical effects of a sorbitol dehydrogenase inhibitor, WAY-135 706, (250 mg ⋅ kg −1 ⋅ day −1 ) and an ARI, WAY-121 509, (10 mg ⋅ kg −1 ⋅ day −1 ) on a variety of tissues, and their effects on nerve perfusion and conduction velocity. After 6 weeks of untreated streptozotocin diabetes, rats were treated for 2 weeks. Sorbitol was elevated 2.1-32.6-fold by diabetes in lens, retina, kidney, aorta, diaphragm, erythrocytes and sciatic nerve; this was further increased (1.6-8.2-fold) by WAY-135 706 whereas WAY-121 509 caused a marked reduction. Fructose 1.6-8.0-fold elevated by diabetes in tissues other than diaphragm, was reduced by WAY-135 706 and WAY-121 509, except in the kidney. Motor and sensory nerve conduction velocities were decreased by 20.2 and 13.9 %, respectively with diabetes. These deficits were corrected by WAY-121 509, but WAY-135 706 was completely ineffective. A 48.6 % diabetes-induced deficit in sciatic nutritive endoneurial blood flow was corrected by WAY-121 509, but was unaltered by WAY-135 706. Thus, despite profound sorbitol dehydrogenase inhibition, WAY-135 706 had no beneficial effect on nerve function. The data demonstrate that aldose reductase activity, the first step in the polyol pathway, makes a markedly greater contribution to the aetiology of diabetic neurovascular and neurological dysfunction than does the second step involving sorbitol dehydrogenase. [Diabetologia (1997) 40: ...

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“…1 In diabetic humans as well as experimental animals, morphological abnormalities, including arterial endothelial cell necrosis and thickened capillary basement membranes, have been observed in small cerebral vessels. [7][8][9] Besides these morphological changes, diabetic patients have also shown impaired cerebrovascular reactivity to hypercapnia, 10,11 acetazolamide, 12 and blood pressure changes. 13,14 These vascular changes may alter cerebral blood flow (CBF) and eventually produce a stroke.…”

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confidence: 99%

Arterial Pulsatility as an Index of Cerebral Microangiopathy in Diabetes

Lee

Sohn

Baik

et al. 2000

Stroke

143

109

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Background and Purpose-This study was designed to evaluate cerebral hemodynamic changes related to diabetes mellitus (DM) with transcranial Doppler ultrasonography (TCD). Methods-We measured the flow velocities and the Gosling pulsatility index (PI) of the middle cerebral artery (MCA), extracranial internal carotid artery (ICA), and basilar artery (BA) in 56 stroke-free, normotensive patients with type 2 DM and 70 age-and gender-matched healthy volunteers. Patients were divided into 2 groups according to the presence of microvascular complications such as retinopathy, nephropathy, and neuropathy. Results-Patients showed slightly lower hematocrit and higher serum fibrinogen levels than control subjects, but other clinical profiles, including stroke risk factors except for diabetes, were comparable between patients and controls. The flow velocity of the ICA but not the MCA and BA in patients regardless of the complication was significantly higher than that in controls. The PIs of the MCA and ICA were significantly higher in patients with complication than those without complication, as well as in controls. The PI of the BA was also significantly higher, even in patients without complication, than in controls. The PIs of the MCA and ICA but not the BA were closely correlated with the duration of DM (r 2 ϭ0.46 and 0.34, respectively). Conclusions-This study defines TCD findings of diabetes-related cerebral hemodynamic changes and suggests that the PI reflects microangiopathic changes of cerebral vessels.

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Cellular and Vessel Wall Morphology of Cerebral Cortical Arterioles after Short-Term Diabetes in Adult Rats

Cited by 33 publications

References 8 publications

Cell and wall morphology of intestinal arterioles from 4- to 6- and 17- to 19-week-old Wistar-Kyoto and spontaneously hypertensive rats.

Cell and wall morphology of intestinal arterioles from 4- to 6- and 17- to 19-week-old Wistar-Kyoto and spontaneously hypertensive rats.

Comparison of the effects of inhibitors of aldose reductase and sorbitol dehydrogenase on neurovascular function, nerve conduction and tissue polyol pathway metabolites in streptozotocin-diabetic rats

Arterial Pulsatility as an Index of Cerebral Microangiopathy in Diabetes

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