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PubMed1991

Spatial disorder of collagens in the great vessels, associated with congenital heart defects.

Surgical ablation of the cardiac neural crest from the chicken embryo results in persistent truncus arteriosus (PTA) and a change in the elastic laminae of the great vessels, wherein elastin and the elastin microfibril show significant spatial disorder. The purpose of this study was to test the hypothesis that the interstitial collagens would also be disordered in the elastic laminae of chicken embryos with PTA. The birefringence characteristics of interstitial collagen were examined to evaluate spatial ordering. The results showed that collagen in the elastic laminae assumed an orderly configuration of well-defined fiber bundles in the great vessel walls of control embryos, whereas vessels from embryos with PTA lacked any distinct spatial order. Collagens type I and III were localized in the vessel walls. Type III collagen was the principal collagen of the elastic laminae, but was absent from the intima of all vessels. In the elastic laminae of vessels from control embryos, collagen type III showed well-defined fiber bundles whereas embryos with PTA had diffuse collagen type III in poorly defined laminae that were not separated by discrete layers of smooth muscle cells. Collagen type I was a minor component of the elastic laminae but formed robust pericellular fiber bundles throughout the media and intima. Collagen type I fibers appeared to be coarsened and less uniform in the vessels from embryos with PTA.

Animals↗
PubMed2006

Abundance of the long pentraxin PTX3 at sites of leukocytoclastic lesions in patients with small-vessel vasculitis.

OBJECTIVE: The prototypical tissue pentraxin PTX3 inhibits phagocytosis of late apoptotic polymorphonuclear leukocytes (PMNs) by macrophages. Levels of PTX3 parallel disease activity in small-vessel vasculitis. Small-vessel vasculitis is often characterized by leukocytoclasia, a phenomenon of accumulation of nuclear remnants from unscavenged PMNs in or near the vessel wall. We therefore hypothesized that PTX3 accumulates at sites of leukocytoclastic vasculitis and, as such, is a key factor for the induction of leukocytoclasis. METHODS: We examined skin biopsy samples from 13 patients with small-vessel vasculitis and from 4 healthy and 3 inflammatory skin disease controls. Biopsy tissues, characterized histopathologically as leukocytoclastic vasculitis, were studied for the presence of PTX3 using rabbit anti-PTX3 polyclonal antibodies. Sections were scored morphometrically for leukocytoclastic infiltrates in conjunction with PTX3 staining. Morphometric scores were expressed as percentages of staining of the total tissue area. RESULTS: Biopsy specimens from patients with leukocytoclastic vasculitis revealed an abundant up-regulation of PTX3 at sites of leukocytoclastic infiltrates. Significantly more PTX3 was found in tissues from the 13 patients with vasculitis (mean +/- SEM 48.9 +/- 6.1%) than in tissues from the 7 controls (4.5 +/- 2.7%) (P = 0.0003). PTX3 was localized around vessels, as well as spread diffusely throughout the tissue. CONCLUSION: PTX3 is abundantly present at sites of leukocytoclastic infiltrates in patients with small-vessel vasculitis, but not in controls. Since PTX3 inhibits phagocytosis of late apoptotic PMNs by macrophages and is strongly up-regulated at sites of leukocytoclastic infiltration, PTX3 is a candidate factor in the phenomenon of leukocytoclasia in small-vessel vasculitis.

C-Reactive Protein↗
PubMed2002

Expression of smooth muscle calponin in tumor vessels of human hepatocellular carcinoma and its possible association with prognosis.

BACKGROUND: Hepatocellular carcinoma (HCC) is a vascular-rich tumor. The tumor vessels in HCC were demonstrated to have alpha-smooth muscle actin positive smooth muscle cells (SMCs). However, it is unclear whether the SMCs in the wall of the tumor vessels are differentiated or undifferentiated. Basic calponin is an actin-, tropomyosin-, and calmodulin-binding protein, and expression of the calponin gene in SMCs has been recognized as one of the late stage differentiation markers of SMCs. The authors investigated the differentiation state of SMCs in tumor vessels by immunohistochemical examination of calponin in patients with HCC, and whether it is associated with the patients' prognosis. METHODS: Tumor and nontumor tissues were obtained from 75 patients with HCC who underwent radical hepatic resection. The differentiation state of the smooth muscle cells were evaluated based on the expression level of calponin, an actin-binding protein, using immunohistochemistry and reverse transcription-polymerase chain reaction analysis. The disease free survival (DFS) rates were estimated according to the Kaplan-Meier method comparing groups of patients with calponin positive and negative tumor vessels. A multivariate analysis based on the Cox proportional hazards regression model was performed to estimate whether the expression of calponin is an independent prognostic factor. RESULTS: In the 75 patients with HCC examined, 36 patients (48%) possessed calponin positive SMCs, and the remaining 39 (52%) did not. There were no significant differences in either clinical or pathologic factors between the two groups of patients. The 5- and 8-year DFS rate of the patients with calponin positive vessels were 37% and 26%, respectively. These values were significantly higher (11% and 5%) than those of patients with calponin negative vessels. Gender, TNM classification, perioperative transfusion, and calponin expression were found to be independent prognostic factors for DFS. CONCLUSIONS: Immunohistochemical examination of the calponin expression in the tumor vessels is a new and useful means to predict the prognosis of HCC patients after hepatic resection.

Aged↗
PubMed2006

Anatomic study of distally based pedicle compound flaps with nutrient vessels of the cutaneous nerves and superficial veins of the forearm.

The purpose of this study was to describe the anatomic basis for a distally based neurovenovascular pedicle compound flap, with nutrient vessels of the cutaneous nerves and superficial veins of the forearm. In this study, the origins, branches, and anastomoses of nutrient vessels of the cutaneous nerves and superficial veins of the forearm and their relationships with the blood supply of adjacent muscle, bone, and skin were assessed in 96 adult cadavers by perfusion of red gelatin into the superior limb arteries. The results showed that the nutrient vessels of cutaneous nerves and superficial veins of the forearm were found to have multiple origins, consisting of six longitudinal vascular plexuses and one transverse vascular plexus of the forearm, as follows: 1) the anterior-lateral vascular plexus from cutaneous branches of the radial artery; 2) the anterior-medialis vascular plexus from cutaneous branches of the ulnar artery; 3) the dorso-lateral vascular plexus from radial osteal and cutaneous branches; 4) the dorso-medialis vascular plexus from ulnar osteal and cutaneous branches; 5) the radial vascular plexus from osteal and cutaneous branches of the radial artery, cutaneous branches of the radial artery in the upper wrist, recurrent branches of the styloid process of the radius, and the radialis vascular plexus of cutaneous branches of the tabatière anatomique (anatomical snuffbox); and 6) the ulnar lateral vascular plexus from cutaneous branches of the ulnar artery in the upper wrist and osteal and cutaneous branches. The transverse vascular plexus is composed of dorsal branches of the ulnar and radial arteries. These perforating branches give fascial branches, cutaneous branches, periosteal branches, and nutrient vessels of cutaneous nerves and superficial veins. These results suggest that nutrient vessels of the cutaneous nerves and superficial veins of the forearm have the same origins as those of the nutrient vessels of adjacent muscles, bones, and skin of the forearm, which can be designated as five types of distally based pedicle flaps with nutrient vessels of cutaneous nerves and superficial veins of the forearm, whose rotation point is at the wrist joint. This flap can be applied to repair tissues of distal parts of the hand.

Adult↗
PubMed1994

Nitric oxide and endothelium-dependent relaxation in tracheobronchial lymph vessels.

Lymphatic smooth muscle tone and contractility are important determinants of lymph flow. Because we have shown previously that lymph vessels exhibit endothelium-dependent relaxation similar to that identified in blood vessels, we assessed the possible role of nitric oxide as an endothelium-dependent relaxant factor in lymph vessels using porcine tracheobronchial lymph vessel rings mounted in organ baths. Isometric active tension was measured and normalized as a percentage of response to 65 mM KCl-substituted perfusate. Histamine and NE elicited contraction in all vessel rings at a concentration of 10(-5) M, and we were unable to demonstrate relaxant responses to these substances even at low concentrations. In histamine- and NE-contracted vessel rings an increase in active tension was produced by NMMA (33.9 +/- 5.4 and 26.1 +/- 5%, respectively, P < 0.0001 for each), an effect that was reversed by addition of L-arginine but not by D-arginine. Endothelial disruption reversed the effects of NMMA in histamine-contracted (16.2 +/- 4.0% increase in active tension; P = N.S. vs initial histamine response) and in NE-contracted vessel rings (11.5 +/- 1.2% increase in active tension; P = N.S. vs initial NE response). The data provide evidence that nitric oxide is an endothelium-dependent relaxant factor that regulates tracheobronchial lymphatic smooth muscle tone and is released in response to administration of contractile agonists.

Animals↗
PubMed1997

Vessels supplying septa and tendons as functional shunts in perfused rat hindlimb.

An assessment was made of the relationship between vasoconstrictor-mediated changes in metabolism and the apparent flow in putative nonnutritive vessels of muscle located on tendon. Surgically isolated rat hindlimbs were perfused at constant flow while monitoring perfusion pressure and venous pO2. In addition exposed tibial tendon vessels of the biceps femoris muscle of the perfused leg were positioned either under a surface fluorometer probe to monitor signal strength when pulses of fluorescein isothiocyanate dextran were infused or over the objective lens of an inverted microscope for photography when pulses of India ink were infused. Measurements were conducted under steady state with vehicle, norepinephrine, or serotonin infused. Norepinephrine increased perfusion pressure and oxygen uptake (VO2), but decreased fluorescence signal from the tendon vessels. Photomicroscopy confirmed that the vessels had generally decreased in diameter. Serotonin also increased perfusion pressure but decreased VO2 and increased fluorescence signal from the tendon vessels. Photomicroscopy confirmed that serotonin infusion had led to a marked increase in diameter of the vessels. It is concluded that a reciprocal relationship exists between resting muscle metabolism as controlled by vasoconstrictors and flow-through muscle tendon vessels.

Animals↗
PubMed2001

Role of endogenous nitric oxide generation in the regulation of vascular tone and reactivity in small vessels as investigated in transgenic mice using synchrotron radiation microangiography.

Nitric oxide (NO) produced by endothelial NO synthase (eNOS) plays a central role in regulation of vascular tone and reactivity. The purpose of this study is to clarify the basal tone and microvascular reactivity in eNOS-overexpressing transgenic (Tg) mice in vivo with a microangiography system using monochromatic synchrotron radiation (SR). The mouse femoral artery was cannulated, nonionic contrast media was injected, and microangiography was performed in hindlimbs of mice. Serial images of the small blood vessels (diameter <200 microm) were recorded by the SR microangiography system. At basal conditions, the diameter of tibial arteries in eNOS-Tg mice was larger than that of wild-type mice (179 +/- 8 versus 132 +/- 8 microm; P < 0.01). l-NAME treatment decreased the vessel diameter and canceled the difference in vessel diameters between two genotypes. Acetylcholine- and sodium nitroprusside-induced relaxations of small vessels were significantly reduced in Tg mice compared with wild-type mice (35.0 +/- 9.4 versus 61.6 +/- 6.7%, 85.0 +/- 10.2 versus 97.3 +/- 6.7% of the maximum relaxation, respectively). Our data provide the evidence that overproduced NO from endothelium reduces vascular tone and plays a pivotal role in regulation of vascular tone in small vessels. Furthermore, the reduced NO-mediated relaxation in small vessels of eNOS-Tg mice is demonstrated for the first time in vivo. SR microangiography allows us to evaluate the reactivity in small-sized vessels and appears to be a powerful tool for assessing the microvascular circulation in vivo.

Angiography↗
PubMed1996

Arterio-venous shunting and proliferating new vessels in acute painful neuropathy of rapid glycaemic control (insulin neuritis).

Insulin neuritis, or painful neuropathy following rapid improvement in glycaemic control, is well recognised but its aetiology is unclear. An understanding of the processes involved in the genesis of acute painful neuropathy of rapid glycaemic control may give an insight into the early pathogenetic factors leading to diabetic nerve damage in general. We have identified five subjects with insulin neuritis including one who developed severe autonomic neuropathy following treatment with insulin. Subjects underwent: 1) assessment of neuropathic symptom and deficit scores; 2) quantitative sensory and electrophysiological studies and 3) sural nerve epineurial vessel photography and fluorescein angiography in vivo. The sural nerve photographs were independently graded by an ophthalmologist. All subjects with insulin neuritis presented with severe sensory symptoms but clinical examination and electrophysiological tests were normal except in the subject with the severe autonomic neuropathy in whom all the tests were abnormal. On nerve photography, there was an abundance of epineurial nutrient vessels although these showed severe abnormalities including arteriolar attenuation, tortuosity and arterio-venous shunting in all subjects. Proliferating neural 'new vessels' which bear striking similarities to those found in the retina and that were more leaky to fluorescein than normal vessels, were observed in three subjects. Venous distension and/or tortuosity was also observed in three subjects and this was most marked in the subject with severe autonomic neuropathy. This study shows that epineurial nutrient vessel anatomy is abnormal in subjects with acute painful neuropathy of rapid glycaemic control, a condition previously thought to be purely metabolic in origin. The presence of epineurial arterio-venous shunting and a fine network of vessels resembling the new vessels of the retina, may lead to a 'steal' effect rendering the endoneurium ischaemic. This process may be important in the genesis of neuropathic pain, and further supports the importance of vascular factors in the pathogenesis of diabetic neuropathy.

Acute Disease↗
PubMed1980

Photoelectric device for the recording of diameter changes of opaque and transparent blood vessels in vitro.

A new photoelectric device for measuring blood vessel diameters is described. The principle of this device consists in locating the vessel within a beam of parallel light at right angles to the beam direction, and eliminating all light striking the vessel. Thus only the light passing by the side of the vessel determines the signal strength of a photocell. The elimination of the light by the vessel due to reflection, refraction, diffraction, or scattering, is achieved with the aid of a lens and pinhole representing a spatial filter. This arrangement is effective irrespective of whether the vessel is opaque or transparent. The resolving power of the device in measuring changes of outside diameter is better than 0.5 micrometer for vessels up to 3 mm in diameter. The upper frequency limit is 300 Hz (--3 dB). The application of the method is demonstrated by two examples of measurements obtained on a small muscular artery.

Blood Pressure↗
PubMed1989

Arteriovenous malformation of the spinal cord. Three-dimensional reconstruction of the intramedullary abnormal vessels.

We report a case of spinal arteriovenous malformation (AVM) in which detailed morphological examination of the intramedullary vascular lesion was carried out employing serial section studies. The relationship of the malformation to parenchymal lesions was evaluated. An abnormal vessel at the spinomedullary transition, whose lamina elastica was partially interrupted, was suggestive of a shunt vessel. The location of the intramedullary abnormal vessels and foci of softening of the spinal cord almost overlapped in distribution. Three-dimensional reconstruction of the intramedullary abnormal vessels demonstrated marked elongation and tortuosity of the original vascular architecture and they ended in the extramedullary abnormal vessels with thickened wall. Thus, our study showed that the intramedullary abnormal vessels were the result of secondary changes subsequent to pressure and volume overload inflicted upon the spinal venous system through AVM. Compression by tortuous elongation of the intramedullary vessels is the apparent cause of the parenchymal softening. A traumatic factor in the aetiology of the AVM was also discussed, since the patient had had two preceding episodes of traffic accidents with cranial and lumbar injury. Trauma seemed to be significant factor as a trigger of symptoms.

Aged↗
PubMed1991

Morphometric investigations on intrarenal vessels of streptozotocin-diabetic rats.

We have investigated 975 different grazing sections of vessels in kidney preparations of 20 rats of the Wistar strain. Half of these genetically identical animals had an insulin-deficiency diabetes induced by injection of streptozocin. The kidneys were removed for investigation after 2 and 12 weeks duration of diabetes. The vessel cross-section, wall, lumen and endothelial surface area were determined in renal arteries, arterioles and preglomerular afferent arterioles in a blind experiment. Statistically detecteable changes were found in the diabetic vessels in the early stage of the diabetes. Preglomerular afferent arterioles showed a highly significant and increasing lumen dilatation commencing after 2 weeks. Diabetic arteries and arterioles developed narrower lumina. A significant thickening of the endothelium took place at the same time in both vessel types. All three vessel regions became smaller and had thinner walls than healthy vessels as the diabetes progressed. The findings on the afferent vessels indicate that haemodynamic effects on the glomerulus are to be expected. Familial diabetic gloermulopathy begins with a reversible hyperfiltration. However, the mechanism has not been clarified in the context of the diabetic metabolic disorder, and this change is probably the haemodynamic consequence of the substantial dilatation of the preglomerular afferent arterioles. With their renin-positive segment, these arterioles are the centre of intrarenal regulation. The increase of the capillary glomerular pressure associated with the dilatation of the preglomerular afferent arterioles is a crucial factor in the development of diabetic glomerulopathy.

Animals↗
PubMed1984

Analysis of the wall permeability of blood vessels in the rat mesentery.

The transport of fluorescent tracer molecules of various molecular weights (MW 340-300,000) within the blood vessels and through the vessel walls into the perivascular tissue of the rat mesentery was studied microscopically. Using a highly sensitive TV-tube the fluorescence intensities were transformed into video signals and recorded for subsequent analysis. The results show that small molecules, such as the water-soluble dye fluorescein-sodium ( F1Na ) (MW 340) can pass through the wall of all blood vessels with minimal delay, whereas the passage of large molecules, such as the serum proteins (MW greater than 60,000), depends very strongly on the diameter of the vessels and on the medium in which the mesentery is embedded during the observation. In this respect, no difference was registered between vessels of the arterial and of the venous part of the microcirculation. The large serum protein molecules moved through the blood vessel walls at specific leakage points. The small dye molecules, however, traversed the wall uniformly along the entire length of the blood vessel. The small-molecule behavior could be described by a passive diffusion model with a cylindrical diffusion source.

Animals↗
PubMed2005

Intracranial arterial aneurysm vasculopathies: targeting the outer vessel wall.

The pathogenesis of intracranial arterial aneurysms (AA) remains unclear, despite their clinical importance. An improved understanding of this disease is important in choosing therapeutic options. In addition to the "classical" berry-type aneurysm, there are various other types of intracranial AA such as infectious, dissecting or giant, partially-thrombosed aneurysms. From the clinician's perspective, the hypothesis that some of these intracranial AA might be due to abluminal factors has been proposed for several years. Indeed, this hypothesis and the empirical use of anti-inflammatory drugs in giant intracranial aneurysms have been confirmed by recent studies reporting that an enzyme involved in the inflammatory cascade (5-lipoxygenase or 5-LO) promotes the pathogenesis of specific aneurysms in humans. 5-LO generates different forms of leukotrienes which are potent mediators of inflammation. Adventitial inflammation leads to a weakening of the media from the abluminal part of the vessel wall due to the release of proinflammatory factors that invade the media, thereby degrading the extracellular matrix, the elastic lamina of the vascular wall, and, finally, the integrity of the vessel lumen. This in turn results in a dilation of the vessel and aneurysm formation. Moreover, neoangiogenesis of vasa vasorum is found in close proximity to 5-LO activated macrophages. In addition to this biological cascade, we argue that repeated subadventitial haemorrhages from the new vasa vasorum play an important role in aneurysm pathogenesis, due to a progressive increase in size mediated by the apposition of new layers of intramural haematoma within the vessel wall. Intracranial giant AA can therefore be regarded as a proliferative disease of the vessel wall induced by extravascular activity. Considering certain aneurysmal vasculopathies as an abluminal disease might alter current therapeutic strategies. Therapy should not only be aimed at the intraluminal repair of the artery, but also cross the vessel wall to reach the vasa vasorum. Drug-eluting stents placed proximal to the lesion and targeted to the origin of the vasa vasorum could be considered as a potential future option. "Intelligent" MRI contrast agents (i.e., macrophage marking) could be used to detect vasa vasorum proliferation and weakening of the vessel wall in vivo.

Anti-Inflammatory Agents↗
PubMed2006

Visualization of intrarenal vessels by 3.0-T MR angiography in comparison with digital subtraction angiography using renal specimens.

BACKGROUND: MRI at 3.0 T enables high-spatial resolution for renal MR angiography. OBJECTIVE: Evaluation of an arterial tree model in animal kidney specimens with comparison of digital subtraction angiography (DSA) and high-field MRI to find out the maximum spatial resolution of intrarenal vessels. It was considered that objective quantitation of angiogram quality could be achieved. MATERIALS AND METHODS: A total of 27 pig kidney specimens were examined by MR angiography (flash 3D) using a 3.0-T scanner (TRIO; Siemens, Erlangen, Germany) with an eight-channel head coil and a voxel size of 0.9x0.9x1.1 mm in the early arterial phase after implantation of a 4F catheter in the renal artery. DSA (Integris, Philips, Best, The Netherlands) was performed immediately after the MRI. With the help of semiautomated segmentation, all vessels were marked for comparison of the vessel trees. The Wilcoxon rank test was used for statistical evaluation of vessel numbers and branching depths. RESULTS: Objective comparison between DSA and MR angiography was achieved. High-field MR angiography had the ability to depict vessels up to the seventh branching on average. Significant differences in vessel delineation and counts were found from the fifth level of intrarenal branching onwards with DSA showing an advantage. CONCLUSION: High-field MRI has great potential in the detection of intrarenal arteries and is comparable to DSA in visualization of the central intrarenal vessel tree.

Angiography, Digital Subtraction↗
PubMed2002

Vessel distensibility and flow distribution in vascular trees.

In a class of model vascular trees having distensible blood vessels, we prove that flow partitioning throughout the tree remains constant, independent of the nonzero driving flow (or nonzero inlet to terminal outlet pressure difference). Underlying assumptions are: (1) every vessel in the tree exhibits the same distensibility relationship given by D/D(0) = f(P) where D is the diameter which results from distending pressure P and D(0) is the diameter of the individual vessel at zero pressure (each vessel may have its own individual D(0). The choice of f(P) includes distensibilities often used in vessel biomechanics modeling, e.g., f(P) = 1 + alpha P or f(P) = b + (1-b) exp(-c P), as well as f(P) which exhibit autoregulatory behavior. (2) Every terminal vessel in the tree is subjected to the same terminal outlet pressure. (3) Bernoulli effects are ignored. (4) Flow is nonpulsatile. (5) Blood viscosity within any individual vessel is constant. The results imply that for a vascular tree consistent with assumptions 2-5, the flow distribution calculations based on a rigid geometry, e.g., D=D(0), also gives the flow distribution when assuming the common distensibility relationships.

Lung↗
PubMed1996

[Apparent wall shear rate and leukocyte-endothelium interaction in iris blood vessels in endotoxin-induced uveitis].

UNLABELLED: Inflammatory stimuli induce the expression of adhesion molecules on leukocytes and endothelial cells. The adhesive forces between leukocytes and the vascular endothelium are antagonized by the shear stress of the flowing blood. The aim of this study was to examine how differences in the apparent wall shear rate measured in iris venules with varying caliber affect leukocyte-endothelium interaction. METHODS: The microvasculature of the iris in Lewis rats (n = 6) was examined using intravital fluorescence microscopy [2]. Blood flow was visualized with FITC-HES and leukocytes were stained with rhodamine 6G. Venules (n = 110) ranging in diameter from 20-60 microns were analysed with regard to the following parameters: Flux of leukocytes, velocity of leukocytes in the center stream, number of rolling and adherent leukocytes. The apparent wall shear rate was calculated from the center stream velocity and the vessel diameter. Animals were examined 4 h after administration of endotoxin from S. typhimurium (500 mg/kg body wt i.p.), when leukocyte-endothelium interaction is strongly enhanced. RESULTS: The flux of leukocytes, the absolute number of rolling leukocytes and the velocity of leukocytes in the center stream was higher in larger than in smaller venules. The apparent wall shear rate decreased with increasing vessel diameter. Calculated values were 806 +/- 59 s-1 for vessels 20-30 microns in diameter and 483 +/- 34 s-1 for vessels of 50-60 microns (mean +/- SEM). The number of adherent leukocytes per mm2 endothelial surface and the rolling fraction did not show significant differences between vessels with varying caliber. CONCLUSION: Although the shear rate declined with increasing vessel diameter, we could not observe an increase in rolling and adherent leukocytes. The effects of vessel diameter on leukocyte adhesion to the vascular endothelium in postcapillary iris venules are minimal.

Animals↗
PubMed2000

MRI findings of small subcortical "lacunar-like" infarction resulting from large vessel disease.

Small subcortical infarctions resulting from large-vessel disease are often observed. It is important to distinguish these from pure lacunar infarction resulting from small-vessel disease because the investigations and examinations differ. We investigated the differences on brain magnetic resonance imaging (MRI) between small subcortical "lacunar-like" infarcts resulting from large-vessel disease and pure lacunar infarcts. Thirteen subjects with small lacunar-like infarcts (size < 2 cm), resulting from large-vessel disease, and 30 subjects with lacunar infarcts (< 2 cm), without large-vessel disease were studied. We measured infarction size using a 1.5-T MRI device and evaluated silent subcortical hyperintensity lesions using the modified Scheltens' score. Large-vessel lesion was confirmed by conventional angiography, duplex carotid scan, and magnetic resonance angiography. There was no difference in the mean age of the two groups. Cerebrovascular risk factors and atherosclerotic complications were also comparable for the two groups. Progressive stroke was more common in the lacunar-like infarction group than in the lacunar infarction group (P = 0.004). Scores for periventricular hyperintensity, white matter hyperintensity, basal ganglia hyperintensity, and total subcortical hyperintensity scores were significantly higher in the lacunar infarction group than in the lacunar-like infarction group. The difference in basal ganglia hyperintensity scores was remarkable (P = 0.001). The enlargement of the perivascular space was also significantly greater in the lacunar infarction group than in the lacunar-like infarction group. These findings seem to reflect differences in the pathogenesis of infarction between the two groups. Silent subcortical hyperintensity lesions and enlargement of perivascular space are useful for between distinguishing small lacunar-like infarct resulting from large-vessel disease and pure lacunar infarction. This may have significant implications for the management of patients with lacunar-sized infarctions. It suggests that the pathogenesis of lacunar-sized infarction is variable.

Aged↗
PubMed1997

Number and size of epineurial blood vessels in normal and diseased human sural nerves.

The number and dimensions of epineurial blood vessels in normal human sural nerves have, thus far, not been determined using systematic, reproducible morphometric methods, although this nerve is most frequently used for diagnostic biopsies. Quantitative changes in epineurial blood vessels appear to be major parameters for identifying angiopathy and angiopathic peripheral neuropathy. Therefore, we examined the epineurial blood-vessel number in relation to the age of the patients and to the number and size of the nerve fascicles in each of 51 human sural nerve biopsies. The data from a control group were compared with pathological cases. We found that the number of epineurial blood vessels (normal mean: 57. 7) increased significantly (up to 196) in biopsies where there were signs of angiopathy (P</=0.01) or vasculitis (P</=0.05). The increase in the number of epineurial blood vessels usually resulted from a proliferation of capillaries. The fascicular cross-sectional area did not appear to be related to the number of epineurial blood vessels, although it increased significantly in cases with vasculitis (P</=0.05) or an axonal type of neuropathy (P</=0.05). Thus, this study shows that the number of epineurial blood vessels is a helpful parameter in verifying angiopathy and angiopathic peripheral neuropathy.

Adolescent↗