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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Stress-strain diagrams of standardizised longitudinal and transversal stripes of the thoracic aorta of 125 male Sprague-Dawley rats aged 9, 15, 24 and 30 months were recorded by an electromechanical instrument. The stripes were subjected to three successive extension-relaxation cycles. The relaxation curves of the third cycle were approximated to the functions y = a + bx and y = cxd (longitudinal stripes) and y = mxf and y = gxh (transversal stripes) respectively. The parameters could be interpreted as measures for structural and functional properties of elastic and collagenous fibers. The age changes of the curve parameters led to the following conclusions concerning age-dependent functional alterations of the aorta: The emphasis can be placed upon the increasing resistance counteracting the extension occuring with great stroke volumes. This may lead to the reduction of the capacity of the air chamber with great stroke volumes. These phenomena seem to be mainly caused by an increase of the pitch of the spiral of the collagenic fiber and the increase of the amount and/or the stability of the collagen. Age-related alterations of the elastin and of the net structure formed by the fibers influence also the distensibility at smaller extensions but seem to be less important. Therefore, the structural alterations of the aorta with age will affect the function in the first place at large stroke volumes and not be very obvious at a basic heart performance.
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PMID:[Tensibility measurements on the rat's aorta III. Analysis of longitudinal and transversal extension as related to age (authors transl)]. 2 73

Static elastic properties were obtained from pressure, volume, and length measurements of 34 isolated human cerebral arteries from 23 circles of Willis of patients aged 23-76 years. No significant difference in initial or final elastance was observed with age or branch in the circle of Willis. Twenty-four of the arteries from 18 circles of Willis were then subjected to transmural pressures of 200-300 mm Hg for periods of less than or equal to 5 minutes and the elastic properties restudied. In general, this had little effect on the arteries except for a significant increase in the initial radius for the less than or equal to 40 year age group. In the less than or equal to 40 year group, female arteries tended to show a greater increase in initial elastance than the males. Histological studies to look for elastin fragmentation in the intima were inconclusive.
Stroke
PMID:Effects of high static pressures on human cerebral arteries in vitro. 84 92

Treatment of chronic hypertension with cilazapril, but not hydralazine, attenuates changes in distensibility of cerebral arterioles that occur in stroke-prone spontaneously hypertensive rats (SHRSPs). In this study, effects of antihypertensive treatment on composition of cerebral arterioles was determined in SHRSPs. Cilazapril (45 mg/kg/day), an angiotensin converting enzyme (ACE) inhibitor, or hydralazine (18 mg/kg/day) was begun when rats were 3 months of age. Both cilazapril and hydralazine reduced systolic arterial pressure in SHRSPs (from 199 +/- 6 to 122 +/- 7 mm Hg for cilazapril versus 143 +/- 5 mm Hg for hydralazine [mean +/- SEM]; p less than 0.05). Cerebral arterioles were fixed in vivo, and the cross-sectional area of the vessel wall was measured histologically. In SHRSPs, both cilazapril and hydralazine reduced cross-sectional area of the vessel wall to values obtained in Wistar-Kyoto (WKY) rats. Thus, both cilazapril and hydralazine prevented hypertrophy of cerebral arterioles in SHRSPs. Composition of the arteriolar wall was determined with point counting stereology. Cerebral arterioles in SHRSPs contained significantly more smooth muscle and elastin than in WKY rats (1,294 +/- 157 versus 853 +/- 88 microns2, respectively, for smooth muscle and 148 +/- 13 versus 108 +/- 7 microns2, respectively, for elastin (120 +/- 8 microns2) in cerebral arterioles in SHRSPs was similar to that in WKY rats. Treatment with hydralazine was effective in preventing increases in elastin (128 +/- 14 microns2) and in attenuating increases in smooth muscle (1,008 +/- 18 microns2). The ratio of nondistensible (collagen, basement membrane) to distensible (smooth muscle, elastin, endothelium) components was greater in SHRSPs than in WKY rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of antihypertensive treatment on composition of cerebral arterioles. 183 21

This study examined effects of local reductions in mean and pulse pressures on cerebral arterioles in normotensive Wistar-Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP). WKY and SHRSP underwent clipping of one carotid artery at 1 month of age. At 10-12 months of age, mechanics of pial arterioles were examined in vivo in anesthetized rats. Bilateral craniotomies were performed to expose pial arterioles in the sham and clipped cerebral hemispheres. Stress-strain relations were calculated from measurements of pial arteriolar pressure (servo null), diameter, and cross-sectional area of the arteriolar wall. Point counting stereology was used to quantitate individual components in the arteriolar wall. Before deactivation of smooth muscle with EDTA, mean (Pm) and pulse (Pp) pressures were significantly less (p less than 0.05) in clipped than in sham arterioles in WKY (Pm, 63 +/- 2 versus 73 +/- 2 mm Hg; Pp, 23 +/- 3 versus 30 +/- 3 mm Hg) and SHRSP (Pm, 94 +/- 4 versus 110 +/- 4 mm Hg; Pp, 27 +/- 2 versus 38 +/- 3 mm Hg). Cross-sectional area of the arteriolar wall was less (p less than 0.05) in clipped than in sham arterioles in both groups of rats (1,403 +/- 125 versus 1,683 +/- 125 microns2 in WKY; 1,436 +/- 72 versus 1,926 +/- 134 microns2 in SHRSP). There was a correlation between cross-sectional area of the vessel wall and pulse pressure (r2 = 0.66), but not mean pressure (r2 = 0.09). During maximal dilatation with EDTA, the stress-strain curve was shifted to the left in clipped arterioles of SHRSP, but not of WKY, which indicates that carotid clipping in SHRSP reduces passive distensibility of cerebral arterioles. The proportion of distensible components in the vessel wall (smooth muscle, elastin, and endothelium) was reduced in clipped arterioles in SHRSP, but not in WKY. These findings suggest that 1) vascular hypertrophy of cerebral arterioles is related more closely to pulse pressure than to mean pressure, and 2) reduction of pial arteriolar pressure completely prevents cerebral vascular hypertrophy and attenuates increases in passive distensibility of cerebral arterioles in SHRSP.
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PMID:Effects of local reduction in pressure on distensibility and composition of cerebral arterioles. 199 42

The degradation of elastin during various pathological processes such as emphysema or arteriosclerosis was demonstrated by several investigators. In the present work, we adapted an ELISA technique for the determination of elastin peptide (EP) levels in human sera and plasma, in healthy and arteriosclerotic subjects. This test makes use of human aorta elastin hydrolyzed by a chemical procedure (kappa-elastin) instead of EP produced by pancreatic or leukocyte elastase. Polyclonal antibodies to this antigen were obtained in rabbits. The indirect ELISA procedure is sensitive, specific and reproducible. No correlation could be demonstrated between EP level and anti-EP antibody concentration of IgG or IgM types determined in the same serum samples. These antibodies did not interfere with EP determinations. EP concentration did not change with age in control subjects. In obliterative arteriosclerosis of the legs and in type IIb hyperlipoproteinemia, EP levels showed a marked increase, while in hypertension, ischemic heart disease and diabetes mellitus, the increase was moderate. In stroke, only slight changes were observed. In type IV hyperlipoproteinemia, EP levels were lower than in controls.
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PMID:Determination of elastin peptides in normal and arteriosclerotic human sera by ELISA. 213 61

In an attempt to clarify the developmental mechanism of cerebral aneurysms, we studied the elastic skeleton of experimentally induced cerebral aneurysms in rats under scanning electron microscopy after hot formic acid extraction followed by freeze-drying. We produced cerebral aneurysms in 19 rats by unilaterally ligating the common carotid artery, inducing renal hypertension, and feeding beta-aminopropionitrile fumarate. The first noted change was the loss of folds protruding from the internal elastic lamina. Morphologic changes of the internal elastic lamina, considered to be primarily responsible for aneurysmal formation, occurred after the loss or disintegration of the elastic skeleton of first the intima, then the media. In large aneurysms with thick domes, we found proliferation of elastic lamellae that may reduce the risk of rupture. It seems probable that the complex elastic skeleton of the arterial wall may account for the mechanical properties of the artery and that growth of an aneurysm occurs due to disintegration of the elastic skeleton and not simply to rupture of the internal elastic lamina. We believe that such changes in the elastic skeleton are a property of the functional state of the cells that produce elastin.
Stroke 1990 Dec
PMID:Elastic skeleton of intracranial cerebral aneurysms in rats. 226 79

1. The goals of this study were to examine the effects of chronic sympathetic denervation on the mechanics and composition of cerebral arterioles in normotensive Wistar Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP). 2. We used an in vivo method to examine the mechanics of pial arterioles in 10- to 12-month-old, anaesthetized WKY and SHRSP that had undergone unilateral removal of the superior cervical ganglion at 1 month of age. Bilateral craniotomies were performed in each rat to expose pial arterioles in the innervated and denervated cerebral hemispheres. Arterioles were deactivated with EDTA. Incremental distensibility and stress-strain relationships were calculated from measurements of pial arteriolar pressure (servo null), diameter and cross-sectional area of the arteriolar wall. Point counting stereology was used to quantify volume density and cross-sectional area of individual components in the arteriolar wall. 3. Chronic sympathetic denervation reduced cross-sectional area of the arteriolar wall by 16 +/- 2% (mean +/- S.E. of mean; P less than 0.05) in WKY and 44 +/- 3% in SHRSP. During maximal dilatation with EDTA, incremental distensibility was reduced and the stress-strain curve was shifted to the left in denervated arterioles of SHRSP, but not WKY. These findings indicate that sympathetic denervation in SHRSP attenuates the development of hypertrophy in pial arterioles and reduces arteriolar distensibility. The ratio of non-distensible (collagen and basement membrane) to distensible (smooth muscle, elastin and endothelium) components was reduced in denervated arterioles in SHRSP, but not WKY. 4. Thus, sympathetic nerves have trophic effects on cerebral arterioles in WKY and, to a greater degree, in SHRSP. Sympathetic nerves also contribute to increases in distensibility of cerebral arterioles in SHRSP, but not WKY. The increase in arteriolar distensibility is accompanied by a disproportionate increase in the more compliant elements of cerebral arterioles.
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PMID:Effect of sympathetic nerves on composition and distensibility of cerebral arterioles in rats. 260 46

We adapted a highly sensitive and reproducible ELISA technique for the determination of anti-elastin peptide antibodies of IgG type AEAb-IgG) and IgM type AEAb-IgM) in human sera. The determination was performed in the sera of 265 normal and diseased persons. The pathologies studied included obliterative arteriosclerosis of the legs, ischemic heart disease, stroke, diabetes mellitus, type IIb and IV hyperlipoproteinemia and hypertension. No clearcut correlation could be found between AEAb and age. In contrast, in arteriosclerotic patients and especially in obliterative arteriosclerosis of the legs and ischemic heart disease, the concentration of AEAb-IgG was significantly increased. The AEAb-IgM showed no change in the studied diseases. Both types of AEAb were decreased in type IV hyperlipoproteinemia. Anti-elastin antibodies may be involved in the pathomechanisms of the above diseases and the determination of antibody concentrations may be of some help in obliterative arteriosclerotic diseases.
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PMID:Determination of anti-elastin peptide antibodies in normal and arteriosclerotic human sera by ELISA. 264 31

In the caudal and renal arteries of the male Wistar rat, interruptions in the internal elastic lamina (IEL) form spontaneously with age. beta-aminopropionitrile (BAPN), which is an inhibitor of the enzyme lysyl oxidase implicated in the synthesis of elastin, is able to induce in the young Wistar rat interruptions in the IEL which are morphologically very similar to those which form spontaneously. The spontaneously hypertensive strain (SHR), together with the Stroke-Prone spontaneously hypertensive substrain (SHR-SP) which is susceptible to cerebrovascular accidents early in life, have been selected from the Wistar strain. We have compared the incidence of IEL interruptions in caudal and renal arteries from SHR-SP aged 12 and 23 weeks with that observed in age-matched SHR. In addition, we have studied the effect of BAPN, administered from weaning during two weeks, on the formation of interruptions in the IEL in the caudal artery of SHR-SP, SHR and normotensive Wistar and WKY rats. Interruptions in the IEL were quantified by light microscopy on longitudinal semi-thin sections. Results showed that, in the caudal and renal arteries of SHR-SP, the number of interruptions in the IEL which form spontaneously was greater than in SHR. Moreover, BAPN administered between the age of 3 and 5 weeks led to the premature formation of a higher level of interruptions in the IEL in SHR-SP than in the 3 other strains of rat. The SHR was the strain which developed the least.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Formation of disruptions of the internal elastica lamina, spontaneous and BAPN induced, in arteries of stroke-prone spontaneously hypertensive rats]. 311 72

It was demonstrated recently that, in contrast to large cerebral arteries, distensibility of cerebral arterioles is increased in stroke-prone spontaneously hypertensive rats (SHRSP). The goals of this study were to examine composition of normal cerebral arterioles, and to determine whether chronic hypertension alters relative composition of the arteriolar wall. Pial arterioles in normotensive Wistar Kyoto rats contain large amounts of smooth muscle, small amounts of elastin and basement membrane, and very little collagen. Hypertrophy of pial arterioles in SHRSP is characterized by increases in the elastic components, smooth muscle and elastin. The stiffer components, collagen and basement membrane either did not change or decreased. It is concluded that cerebral arterioles contain proportionately more smooth muscle and less collagen than large arteries, and that hypertrophy of cerebral arterioles in SHRSP is accompanied by a relative increase in the more elastic components of the arteriolar wall, which probably contributes to the increase in arteriolar distensibility.
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PMID:Composition and mechanics of cerebral arterioles in hypertensive rats. 320 16


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