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PubMedDate not supplied

Developmental biology of the vascular smooth muscle cell: building a multilayered vessel wall.

The assembly of the vessel wall from its cellular and extracellular matrix components is a critical process in the development and maturation of the cardiovascular system. However, fundamental questions concerning the origin of vessel wall cells and the mechanisms that regulate their development and differentiation remain unanswered. The initial step of vessel wall morphogenesis is formation of a primary vascular network, comprised of nascent endothelial cell tubes, via the processes of vasculogenesis and angiogenesis. Subsequently, primordial vascular smooth muscle cells (VSMCs) are recruited to the endothelium to form a multilayered vessel wall. During the course of development and maturation, the VSMC plays diverse roles: it is a biosynthetic, proliferative, and contractile component of the vessel wall. Although the field of vascular development has blossomed in the past decade, the molecules and mechanisms that regulate this developmental pathway are not well defined. The focus of this review is on those facets of VSMC development important for transforming a nascent endothelial tube into a multilayered structure. We discuss the primordial VSMC with particular attention to its purported origins, the components of the extracellular milieu that contribute to its development, and the contribution of embryonic hemodynamics to vessel wall assembly.

Animals↗

PubMedDate not supplied

A new computerized biomechanical perfusion model for ex vivo study of fluid mechanical forces in intact conduit vessels.

We have developed a new computerized biomechanical ex vivo perfusion system for intact conduit vessels in which a wide range of combinations of intraluminal pressure, fluid flow and shear stress could be set and maintained at target levels in mammalian conduit vessels under controlled metabolic conditions. Mean wall shear stress is calculated using the formula: Accuracy of the wall shear stress calculation was validated by ultrasonographic imaging of the vessel radius. In a series of simulation experiments, the hemodynamic homeostasis functions of the system were challenged by generating a wide range of vascular resistance in artificial vessels and by pharmacologically induced changes in vascular tone in intact human vessels. Despite rapid changes in vessel resistance, shear stress and pressure, or flow and pressure were maintained well at target levels. Shear- and pressure-stimulated production of the vasodilator prostaglandin E2 (PGE2) was used to validate the biological relevance of the model. PGE2 release was significantly more stimulated by high (25 dyn/cm2) compared to low (<4 dyn/cm2) shear (ANOVA, p = 0.012). High compared to low intraluminal pressure depressed the production of PGE2 (ANOVA, p = 0.019). In summary, the computerized perfusion model appears to offer new possibilities of investigating the complex interplay between fluid mechanics and the vascular wall.

Algorithms↗

PubMed1984

Formation of a direct arterial blood supply to the anterior pituitary gland following complete or partial interruption of the hypophyseal portal vessels.

If regions of the anterior pituitary gland received systemic blood via a direct arterial blood supply these regions would escape hypothalamic regulation and thus be a sequela in endocrine disorders. Since, in the untreated rat, all of the blood supply to the anterior pituitary gland is via the hypophyseal portal vessels, we hypothesized that partial interruption of the portal vessels could provoke the establishment of a direct arterial blood supply (arteriogenesis). We utilized the injection of polystyrene microspheres (15 or 9 micron diameter) into the left ventricle of the heart to test this hypothesis. Microspheres are trapped in the first capillary plexus they reach since they are too large to traverse the capillaries. No microspheres reached the anterior pituitary gland of control rats, a finding consistent with the fact that the anterior pituitary gland receives all of its blood supply via the hypophyseal portal blood vessels. Microspheres were observed in the primary portal capillary plexus in the infundibulum (median eminence), infundibular stalk (pituitary stalk), and infundibular process (pars nervosa), the first capillary plexus which they reached. A lesion of the medial basal hypothalamus (MBH) which destroyed the long portal vessels did not result in arteriogenesis since few, if any, microspheres were observed in the anterior pituitary gland. We confirmed, using vascular casts, that these lesions resulted in the long-term destruction of the primary portal capillaries in the infundibulum and of the long portal vessels. In MBH-lesioned animals it appears that all of the blood supply of the anterior pituitary gland is via short portal vessels arising from the infundibular stem and process.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Direct measurement of blood pressure within the long hypophysial portal blood vessels.

The microvascular pressures that perfuse the anterior pituitary gland with blood were not known. We now report the direct measurement of these pressures in the urethane-anesthetized rat. The infundibular stalk and ventral surface of the anterior pituitary gland were surgically exposed via a parapharyngeal approach and a micropressure transducer inserted into the lumen of hypophysial portal vessels under direct microscopic observation. A Weiderhielm-type servo-controlled pressure system was used to record the pressures. Continuous pressure recordings up to 30 min in duration were made in long hypophysial portal vessels ranging in diameter from 10 to 50 micron in adult, female Sprague-Dawley rats. The mean pressure recorded from these vessels was 4.0 cm H2O (2.7 mm Hg). A small increase in systemic pressure produced by a rapid saline infusion into a cannulated femoral vein resulted in a mirrored but much greater magnitude increase in pressure to the hypophysial portal vessels. This finding suggests that pressure within the portal vessels is in some instances closely coupled to systemic blood pressure. The low pressures recorded in hypophysial portal vessels correlate well with pressures measured in the hepatic portal vasculature. The porosity of fenestrated capillaries surrounding anterior pituitary cells is hemodynamically essential, since the low hydrostatic pressures alone would be inappropriate for rapid and thorough exchange.

Animals↗

PubMed2002

Opposing functions of the Ets factors NERF and ELF-1 during chicken blood vessel development.

OBJECTIVE: The purpose of this study was to evaluate the role of the Ets factor NERF in the regulation of the Tie1 and Tie2 genes during chicken blood vessel development. METHODS AND RESULTS: We have isolated the full-length cDNA for the chicken homologue of the human Ets factor NERF2 (cNERF2). Northern blot analysis and in situ hybridization demonstrate that cNERF2 is enriched in the developing blood vessels of the chicken chorioallantoic membrane. Interestingly, cNERF2 functions as a competitive inhibitor of a highly related Ets factor cELF-1, which we have previously shown to be enriched in chicken blood vessel development. Although in vitro-translated cELF-1 and cNERF2 can bind equally well to conserved Ets binding sites in the promoters of the Tie1 and Tie2 genes, cELF-1 preferentially binds to the Ets sites in these promoters during early stages of chicken blood vessel development, suggesting that cNERF may bind during later stages of blood vessel development and vascular remodeling. CONCLUSIONS: cNERF2 is enriched during embryonic and extraembryonic blood vessel development in the chicken and facilitates tight control of Tie1 and Tie2 gene regulation.

Animals↗

PubMed2000

Protein-tyrosine phosphatases in the vessel wall: differential expression after acute arterial injury.

Many protein-tyrosine phosphatases (PTPases) have now been identified, but little is known about PTPase expression and regulation in vascular tissue and in vascular disease. Polymerase chain reaction (PCR) amplification and cDNA fingerprinting of PTPase catalytic domains, combined with random sequencing of PCR product libraries, identified 18 (8 receptor-like and 10 cytosolic) PTPases in the rat carotid artery and revealed differential expression of 5 of these PTPases during neointima formation after balloon catheter injury. In situ hybridization was used to localize mRNA expression in vessel cross sections for the 5 differentially expressed PTPases. This revealed that for 3 PTPases (SHP1, CD45, and PTPbeta), differential transcript abundance was due to appearance/loss of the cell types by which they were expressed (leukocytes for SHP1 and CD45, endothelial cells for PTPbeta). However, mRNA expression of 2 PTPases (PTPL1 and PTP1B) was specifically upregulated by proliferating and migrating smooth muscle cells (SMCs) in characteristic temporal and regional patterns in response to vessel damage. Quantitative PCR analysis showed that PTP1B and PTPL1 were induced approximately 30-fold and approximately 60-fold, respectively, by 2 weeks after injury in the damaged vessels compared with the uninjured vessels. PTP1B was rapidly upregulated in the media after vessel injury and remained highly expressed in the developing neointima. By contrast, PTPL1 expression did not increase dramatically until the SMCs had migrated into the intima. The differential expression of PTP1B and PTPL1 by SMCs after injury suggests roles for these PTPases in the regulation of vessel wall remodeling.

Animals↗

PubMed2000

A randomized trial comparing stenting with balloon angioplasty in small vessels in patients with symptomatic coronary artery disease. ISAR-SMART Study Investigators. Intracoronary Stenting or Angioplasty for Restenosis Reduction in Small Arteries.

BACKGROUND: More than 30% of the lesions currently treated with interventional approaches are situated in vessels smaller in size than those representing an established indication for stenting. The objective of this randomized trial was to assess whether compared with PTCA, stenting of small coronary vessels is associated with a reduction of restenosis. METHODS AND RESULTS: Patients with symptomatic coronary artery disease with lesions situated in native coronary vessels between 2 and 2.8 mm in size were randomly assigned to be treated with either stenting (n=204) or PTCA (n=200). Adjunct therapy consisted of abciximab, ticlopidine, and aspirin. Repeat angiography at 6-month follow-up was performed in 83% of the patients. The primary end point of the study was the incidence of angiographic restenosis (>/=50% diameter stenosis) at follow-up; adverse clinical events, such as death, myocardial infarction, stroke, or target vessel revascularization, were assessed as secondary end points. After 7 months, there were no significant differences in the infarct-free survival rates between the 2 study groups: 96.6% for stent patients, and 97.0% for PTCA patients (P:=0. 80). Target vessel revascularization was needed in 20.1% of the stent patients and 16.5% of the PTCA patients (P:=0.35). The primary end point of angiographic restenosis was found in 35.7% of the stent patients and 37.4% of the PTCA patients (P:=0.74). The net lumen gain observed at follow-up was identical (0.76+/-0.78 in the stent group versus 0.76+/-0.63 mm in the PTCA group, P:=0.93). CONCLUSIONS: Stenting and PTCA are associated with equally favorable results when used for treating lesions in small coronary vessels.

Abciximab↗

PubMed1983

Computerized image analysis for quantitative measurement of vessel diameter from cineangiograms.

Subjective estimates of the angiographic severity of coronary artery stenoses show variability and inaccuracy. We therefore tested the accuracy of a newly developed computerized image analysis system for quantitating vessel diameter from cineangiograms. Fourteen cylindrical phantoms of known diameter were filled with contrast medium and filmed over a wide range of clinically relevant radiographic conditions in order to develop regression equations that related computer-derived to anatomic diameters. Computer measurements of vessel diameter were unaffected by vessel size, magnification, focal spot size, thickness of scattering medium, kilovolt peak, or location within the radiographic field, but a correction factor was necessary for a small but significant (p less than .01) linear dependence on contrast medium concentration. The accuracy of computerized vessel diameter measurements ranged between +/- 59 and +/- 137 mu for all conditions except for rapid vessel motion and contrast medium concentrations of 50% or less meglumine diatrizoate (Renografin 76), both of which resulted in reduced accuracy as well as in the inability to locate lumen edges of vessels less than 1 mm in diameter.

Cineangiography↗

PubMed1997

Restenosis rates in diabetic patients: a comparison of coronary stenting and balloon angioplasty in native coronary vessels.

BACKGROUND: Diabetes is a major risk factor for restenosis after coronary balloon angioplasty. Recent studies have shown that coronary stenting significantly reduces restenosis compared with balloon angioplasty alone. However, limited information is available on the effect of coronary stenting in diabetic patients. METHODS AND RESULTS: We designed this study to analyze the effect of diabetes on restenosis in patients treated with either balloon angioplasty or coronary stenting who were enrolled in a 6-month angiographic follow-up program. Three hundred consecutive patients, 19% of whom were diabetics, who underwent coronary stent implantation during a single-vessel procedure on native coronary vessels and who had 6-month angiographic follow-up constituted the study group (stent group). Three hundred consecutive patients who underwent 6-month angiographic follow-up after single-vessel conventional balloon angioplasty served as control patients (balloon group). Preprocedural, postprocedural, and follow-up angiograms were analyzed with quantitative angiography. In the balloon group, the restenosis rate was almost twofold higher in diabetic than in nondiabetic patients (63% versus 36%; P=.0002) owing to both a greater late loss (0.79+/-0.70 versus 0.41+/-0.61 mm, respectively; P<.0001) and a higher rate of late vessel occlusion (14% versus 3%, respectively; P<.001). In the stent group, restenosis rates were similar in diabetics and nondiabetics (25% versus 27%, respectively). Furthermore, in the stent group, late loss (0.77+/-0.65 versus 0.79+/-0.57 mm, respectively) and the rate of late vessel occlusion (2% versus 1%, respectively) did not differ significantly between diabetic and nondiabetic patients. CONCLUSIONS: Although diabetics have increased rates of restenosis and late vessel occlusion after simple balloon angioplasty, they have the same improved outcome with coronary stenting that has been documented in nondiabetic patients.

Aged↗

PubMed1998

Vessel dilator enhances sodium and water excretion and has beneficial hemodynamic effects in persons with congestive heart failure.

BACKGROUND: Vessel dilator, a 37-amino acid peptide hormone synthesized in the heart, enhances urine flow 4- to 12-fold and sodium excretion 3- to 6-fold in healthy humans. The present investigation was designed to determine whether vessel dilator might have similar beneficial effects in persons with congestive heart failure (CHF). METHODS AND RESULTS: Vessel dilator (100 ng/kg body weight per minute) given intravenously for 60 minutes to NYHA class III CHF subjects increased urine flow 2- to 13-fold, which was still increased (P<0.001) 3 hours after its infusion was stopped. Vessel dilator enhanced sodium excretion 3- to 4-fold in CHF subjects (P<0.01), which was still significantly (P<0.01) elevated 3 hours after infusion. Vessel dilator decreased systemic vascular resistance 24%, pulmonary vascular resistance 25%, pulmonary capillary wedge pressure 33%, and central venous pressure 27% while increasing cardiac output 34%, cardiac index 35%, and stroke volume index 24% without significantly affecting heart rate or pulmonary artery pressure in the CHF subjects. The control CHF patients did not have any changes in the above parameters. CONCLUSIONS: These results indicate that vessel dilator has significant beneficial diuretic, natriuretic, and hemodynamic properties in humans with congestive heart failure.

Adult↗

PubMed1992

Reactivity of small blood vessels in hypertension: relation with structural changes. State of the art lecture.

Small blood vessels, particularly small arteries of 150-300 microns in lumen diameter and larger arterioles of 50-150 microns in lumen diameter, are the most important location of the arterial bed that undergoes changes resulting in the increased peripheral resistance that characterizes elevated blood pressure. This article reviews these morphological and functional alterations of small blood vessels. Study of mesenteric small arteries with a lumen diameter of 220-260 microns revealed consistently a reduced external and lumen diameter in renal and deoxycorticosterone acetate-salt hypertensive rats early in the evolution of hypertension. The media of the vessel wall was significantly thickened in the hypertensive rats, and the media/lumen ratio was increased. Although the tension that developed in response to different vasoconstrictors was not elevated or was even decreased in hypertensive rats, exaggerated transmural pressures resulted in the isolated blood vessels as a consequence of the law of Laplace because of the narrowed lumen. Similar findings were obtained in small resistance arteries from subcutaneous gluteal biopsies of hypertensive humans. In arterioles, on the other hand, decreases in the density of blood vessels (rarefaction) and in vasomotion amplitude may play a more important role than reductions in lumen diameter. As a consequence of the design of small resistance blood vessels and as a result of functional and structural alterations, which may be primary to or a consequence of high blood pressure, the pressor effect of vasoconstrictors is amplified and interacts with other factors to contribute to the maintenance of elevated blood pressure even if the intrinsic response of vascular smooth muscle to these agents is not exaggerated.

Humans↗

PubMedDate not supplied

Effect of chronic hypertension and sympathetic denervation on wall/lumen ratio of cerebral vessels.

The purposes of this study were to determine whether 1) cerebral vessels undergo hypertrophy during chronic hypertension and 2) sympathetic nerves contribute to cerebral vascular changes in chronic hypertension. Morphometric studies were undertaken in stroke-prone spontaneously hypertensive rats (SP-SHR) and normotensive Wistar-Kyoto (WKY) rats. Unilateral superior cervical ganglionectomy was performed in the SP-SHR at 8 weeks of age. When the rats were approximately 13 months old, they were killed and the brain was fixed with formalin at a perfusion pressure of 80% of the rat's systolic pressure. Wall/lumen ratio was measured in approximately 1200 arteries and arterioles. In parenchymal, but not pial, cerebral vessels there was pronounced vascular hypertrophy in SP-SHR: wall/lumen ratio was 0.08 in WKY and 0.14 in SP-SHR (p < 0.05). Sympathetic denervation attenuated the development of vascular hypertrophy in SP-SHR: wall/lumen ratio was 0.14 in the innervated parenchymal vessels, and 0.10 in denervated vessels (p < 0.05). We conclude that cerebral vessels undergo hypertrophy in stroke-prone SHR and speculate that vascular hypertrophy may protect cerebral vessels by reducing wall stress in chronic hypertension. Sympathetic nerves appear to exert a trophic effect on cerebral vascular muscle in chronic hypertension.

Animals↗

PubMed1985

Differences in norepinephrine activation and diltiazem inhibition of calcium channels in isolated rabbit aorta and mesenteric resistance vessels.

The mechanisms of norepinephrine stimulation of calcium ion entry in isolated rabbit aorta and mesenteric resistance vessels were studied through measurements of effects on calcium-45 influx, tension, and membrane potential. The resistance vessels were considerably less sensitive to norepinephrine than the aorta. The aorta exhibited complex dose-response curves for norepinephrine-stimulated calcium influx and contraction, whereas these were simple in the arterioles. Both vessels were depolarized with increasing concentrations of potassium. Norepinephrine did not depolarize the aorta, whereas it did depolarize the mesenteric resistance vessels. This result supports the contention that norepinephrine opens receptor-operated channels to induce calcium entry in the aorta, while it may activate potential sensitive calcium channels in the mesenteric resistance vessels. However, the maximum depolarization with norepinephrine (10(-4) M) in the arterioles was completely blocked by 10(-5) M diltiazem, whereas that induced by 80 mM potassium was unaltered by the diltiazem. Furthermore, 10(-4) M norepinephrine was able to stimulate virtually the same contraction and calcium influx in 80 mM potassium-depolarized arterioles as in normal polarized tissues. These results are consistent with norepinephrine opening of receptor-operated channels to allow calcium entry in the rabbit mesenteric resistance vessels. That the behavior of norepinephrine-activated channels in the aorta is more complex than in the arterioles is further illustrated by a dramatically decreasing sensitivity of norepinephrine-stimulated calcium influx to diltiazem with increasing norepinephrine in the aorta but not in the arterioles.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Evidence for increased media thickness, increased neuronal amine uptake, and depressed excitation--contraction coupling in isolated resistance vessels from essential hypertensives.

The functional and morphologic characteristics of isolated subcutaneous resistance vessels (about 170 micron i.d.) from 15 untreated subjects with essential hypertension and 15 matched controls were examined. The vessels from the hypertensives had a 29% increase in the media-thickness-to-lumen-diameter ratio. The maximal force development to noradrenaline (NA) expressed as active pressure (an estimate of the pressure the vessels could have contracted against in vivo) was 30% higher in vessels from the hypertensives, while active media stress (force per square unit of smooth muscle) and sensitivity to NA was not significantly different. Increased active pressure, as well as unaltered active media stress and sensitivity, was seen for vasopressin, serotonin, angiotensin II, and K+. There was, however, an enhanced leftward shift of the NA sensitivity with cocaine (an inhibitor of the neuronal amine pump) in vessels from the hypertensives [pD2(+cocaine) and pD2(-cocaine) were 0.185 +/- 0.53) and 0.040 +/- 0.044, hypertensives and normotensives, respectively, p less than 0.05] suggesting an abnormality of presynaptic function in essential hypertension. Furthermore, the calcium sensitivity was depressed (pD2 was 4.197 +/- 0.050 and 4.381 +/- 0.068, hypertensives and normotensives, respectively, p less than 0.05), and the rate of relaxation was faster (p less than 0.05) in vessels from hypertensives, suggesting that excitation-contraction coupling might be depressed. The results suggest that the increased pressor response in essential hypertension can, to a large extent, be explained by altered vascular structure, while smooth muscle function is either unchanged or possibly depressed.

Arteries↗

PubMed1999

Analysis of CO2 vasomotor reactivity and vessel diameter changes by simultaneous venous and arterial Doppler recordings.

BACKGROUND AND PURPOSE: The use of flow velocity changes in the middle cerebral artery (MCA) measured by Doppler techniques as an index of corresponding cerebral blood flow (CBF) changes is based on the assumption that the insonated arterial diameter remains stable. The postulate of unchanging vessel calibers during CBF changes, however, is still under debate. We performed simultaneous measurements of arterial and venous blood flow velocities by transcranial Doppler ultrasound during various stages of hypercapnia to analyze diameter changes in the insonated vessels by comparing differences in the vasomotor reactivity. METHODS: Simultaneous Doppler recordings of 1 MCA and of a contralateral venous vessel thought to represent the sphenoparietal sinus (SPS) were carried out with a pair of 2-MHz range-gated transducers in 16 young healthy subjects during variations of end-tidal PaCO2. RESULTS: During hypercapnia the mean blood flow velocity of the MCA rose from 62. 5+/-10.2 to a maximum of 99+/-12.2 cm/s (vasomotor reactivity of 60. 1+/-17.3%). The corresponding values in the SPS were significantly higher (P<0.001), revealing a rise from 17.8+/-5.7 to 34.9+/-14.3 cm/s (vasomotor reactivity of 91.4+/-25.9%). Exponential and linear regression analyses revealed an identical high correlation (r2=0.97 and 0.98 for the MCA and SPS, respectively). Slopes were 0.034+/-0. 01 on the arterial and 0.048+/-0.01 on the venous side. The CO2 reactivity (percentage per mm Hg, EtCO2) was found to be 4.5+/-1%/mm Hg in the MCA and 6.8+/-1.5%/mm Hg in the SPS. This difference indicates a vasodilation of the MCA in comparison to the venous vessel. CONCLUSIONS: We have demonstrated a different reaction pattern between intracranial venous and arterial vessels related to end-tidal CO2. Relating the flow velocities to the square of the vessel diameter and assuming a global rise of CBF and not extensible sinus walls, our results indicate that the MCA undergoes a vasodilation of 9.5+/-7% in maximal hypercapnia.

Adult↗

PubMed2006

Lumen loss in the first year in saphenous vein grafts is predominantly a result of negative remodeling of the whole vessel rather than a result of changes in wall thickness.

BACKGROUND: The use of saphenous vein grafts (SVG) in coronary artery bypass surgery is established but little is known of SVG remodeling during the first year in vivo. METHODS AND RESULTS: The feasibility of measuring total vessel diameter (lumen plus wall), lumen diameter, and wall thickness by a novel computed tomography (CT) method was established in phantom model tubes (r=0.98 for lumen diameter and r=0.98 for wall thickness) and in an initial clinical study of 14 patients correlating CT and intravascular ultrasound measurements of SVG (r=0.88 for total vessel diameter, r=0.85 for lumen diameter and r=0.89 for wall thickness). In a separate group of 42 patients (aged 66+/-10 years; 36 male, 6 female) undergoing coronary artery bypass grafting, SVG total vessel diameter, lumen diameter, and wall thickness were determined prospectively with multi-slice CT angiography at 1 and 12 months postoperatively. Mean total vessel diameter decreased from 5.95+/-0.83 mm to 5.39+/-0.87 mm, P<0.001 (range, -39% to +8% change). Twenty-six patients (62%) had a decrease of SVG vessel diameter (negative remodeling) >5%. Mean lumen diameter decreased from 3.69+/-0.66 mm to 3.36+/-0.68 mm, P<0.001, (range, -40 to +11% change). Surprisingly, mean wall thickness decreased from 1.14+/-0.27 mm to 1.01+/-0.21 mm (P<0.001; range, -48 to +33% change). CONCLUSIONS: Lumen loss in SVG between postoperative months 1 and 12 is predominantly caused by negative remodeling of the whole vessel rather than to changes in wall thickness. Therapies targeting negative remodeling may be required for optimal maintenance of SVG lumen in the first postoperative year.

Adrenergic beta-Antagonists↗

PubMed1987

Articular cartilage blood vessels in swine osteochondrosis.

Perfusion studies in swine with early lesions of osteochondrosis demonstrated that lamellar areas of chondrocyte necrosis within reserve zones of growth areas occurred only in regions of nonperfused articular cartilage. Articular cartilage with a similar anatomical location was perfused in some animals. Occasionally, nonperfused articular cartilage showed vascular alterations within cartilage canals without evidence of significant perivascular or lamellar necrosis. By light microscopy, some vessels within or adjacent to nonperfused articular cartilage had normal morphology; however, ultrastructural abnormalities were found in some vessels of all cartilage canals adjacent to necrotic cartilage lamella. Minimal alterations were in the few cartilage canal vessels that appeared normal by light microscopy, and the surrounding chondrocytes showed only minimal alterations. Early cartilage canal alterations were seen in the endothelium of cartilage canal capillaries, and ultrastructural changes in these vessels were similar to those described with experimentally induced, direct vascular injury. Vascular injury was followed by leakage of plasma and cells into the interstitial space of the cartilage canal. Necrosis of the vessel wall and interstitial tissue caused the cartilage canals to appear empty or to be filled with fibrin-like material. Although the vascular changes could be considered as part of the normal process of cartilage maturation and cartilage canal chondrification, observations suggest that in domestic swine the attendant cartilage necrosis and chondrolysis is exuberant. It is suggested that alterations in cartilage canal vessels play a major role in the pathogenesis of articular cartilage lesions that are found in osteochondrosis of swine.

Animals↗

PubMed2001

Physiological levels of beta-amyloid induce cerebral vessel dysfunction and reduce endothelial nitric oxide production.

beta-amyloid (A beta), the major component of senile plaques in Alzheimer's disease (AD), normally circulates in the blood at nanomolar levels but is elevated in AD. Previous studies have found that high concentrations (10(-5)-10(-4) M) of A beta result in neuronal cell death. Here we show that physiological levels of soluble A beta can induce dysfunction in perfused rat cerebral vessels and in cultured endothelial cells. At concentrations of 10(-9)-10(-6) M, A beta induced a significant concentration-dependent reduction of NO production in endothelial cells. At 10(-8) M, A beta significantly decreased the sensitivity of cerebral vessels to acetylcholine (ACh), an endothelium dependent vasodilator. At 10(-7) M and higher concentrations, A beta significantly reduced the maximum response of vessels to ACh, and induced significant endothelial cell death. A beta (10(-9)-10(-5) M) did not cause any detectable change in nitric oxide synthase levels. The results suggest that a modest increase in the concentration of A beta above its normal physiological level in the circulation, as found in the early stages of AD, results in decreased NO production and vessel sensitivity to endothelium-dependent vasodilation that could lead to constricted blood vessels and ischemia in the surrounding tissue. Further increases in A beta concentration, which may occur in the later stages of AD, result in cell death and decreased maximum vasodilator response of cerebral vessels.

Acetylcholine↗