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Evaluation of restenosis in major vessels and side branches.

OBJECTIVES: The indications for concurrent intervention for stenosis of a side branch during the treatment for stenosis of the main vessel were investigated using quantitative coronary angiography. METHODS: The retrospective study included 451 patients treated for a stenotic main vessel incorporating a side branch, who underwent follow-up angiography within 6 months. Patients were divided into Group I with the side branch treated by coronary angioplasty, and Group II with the side branch left untreated. Quantitative coronary angiography was used to measure the minimum luminal diameter (MLD) and percentage diameter stenosis (%DS) of the main vessel and the side branch. RESULTS: The MLD of the side branch after treatment was larger in Group I (1.4 +/- 0.1 mm) than in Group II (0.7 +/- 0.1 mm), and the %DS of the side branch after treatment was smaller in Group I (34 +/- 3%) than in Group II (63 +/- 2%). These differences decreased at follow-up to 1.1 +/- 0.1 mm, 48 +/- 2% in Group I; 0.9 +/- 0.04 mm, 46 +/- 2% in Group II, respectively. The MLD and %DS of the side branch at follow-up in Groups I and II were affected by the presence of main vessel restenosis[Restenosis(+): 0.9 +/- 0.1 mm, 57 +/- 4%; restenosis(-): 1.2 +/- 0.1 mm (p < 0.05), 43 +/- 3% (p < 0.05) in Group I; Restenosis(+): 0.9 +/- 0.1 mm, 51 +/- 8%; restenosis(-): 1.0 +/- 0.1 mm, 44 +/- 3% in Group II]. Multivariate analysis showed that %DS of the main vessel at follow-up was the only powerful predictor of restenosis of the side branch (p = 0.0249, odds ratio = 1.031, confidence interval = 1.004-1.059) in Groups I and II. CONCLUSIONS: Restenosis of the main vessel rather than the initial outcome of the side branch is the major influence on restenosis of the side branch.

Aged↗

Measurement of fractional flow reserve in patients with multi-vessel coronary artery disease and borderline lesions prevents unnecessary revascularisation procedures.

BACKGROUND: Patients with multi-vessel coronary artery disease (CAD) are selected for percutaneous coronary interventions (PCI) or surgical revascularisation. The appropriateness of "ad hoc" PCI of borderline lesions (<70% of lumen diameter) in patients with a multi-vessel CAD has not been proven. However, delayed PCI of another lesion and gaining additional information from non-invasive tests is not a widely accepted strategy. When left anterior descending (LAD) coronary artery is one of the affected vessels, selection for surgical revascularisation is most likely. AIM: To assess long-term outcome in patients with multi-vessel CAD and borderline lesions, including LAD, in whom fractional flow reserve (FFR) in all affected vessels was measured and used for selection for PCI or conservative treatment. METHODS: The study group consisted of 16 patients with stable angina (11 males, mean age 60+/-9 years) with 34 lesions localised in the main epicardial coronary arteries [LAD / left main (LM) / right coronary artery (RCA) / intermediate branch (IB) / circumflex artery (Cx) - 15/1/5/5/8] of which at least two were borderline stenoses. Each lesion underwent FFR measurement. "Ad hoc" PCI was performed when FFR was <0.75, and conservative therapy was instituted when FFR was >0.75. RESULTS: Of 34 lesions, in 8 (23%) the FFR value was <0.75 and these lesions were treated with PCI (LAD/IB/Cx - 3/2/3). In the remaining 26 (77%) lesions, FFR was >0.75 and conservative therapy was instituted. During the mean follow-up of 15+/-6 months (range 6-28 months, median 15 months) in 8 of 9 conservatively treated patients no aggravation of anginal symptoms nor other coronary events were observed. One patient developed acute myocardial infarction due to thrombus occluding a borderline LAD lesion. Of 8 lesions treated with PCI (baseline FFR = 0.63+/-0.10 vs post-PCI FFR = 0.92+/-0.08, p=0.0002), in one case an in-stent restenosis in LAD occurred 9 months after PCI. Of a total of 26 lesions which were conservatively treated (mean FFR 0.91+/-0.05), in 2 (7.7%) the progression of CAD was noted. CONCLUSIONS: In patients with multi-vessel CAD and borderline lesions, FFR measurement identifies those, who can be treated conservatively with a good long-term outcome, and prevents unnecessary PCI.

Aged↗

[Effects of enalapril on plasma Ang II level and the expression of AT1 in blood vessel and kidney of type 2 diabetic rats].

AIM: To study the plasma angiotensin II (Ang II) levels and the expressions of angiotensin II1 receptor (AT1) in blood vessels and kidneys in diabetic and high fat diet rats, and the effects of enalapril on plasma Ang II levels and the expressions of AT1 in blood vessels and kidneys in diabetic rats. METHODS: The plasma Ang II level was assayed with 125I-Ang II radioimmunoassay, and the expression of AT1 in blood vessel and kidney was analyzed with immunohistochemical technique. RESULTS: The plasma Ang II level was significantly higher in type 2 diabetic rats (241 +/- 49) pg x mL(-1) than that in the control (71 +/- 22) pg x mL , high fat diet group (151 +/- 29) pg x mL(-1) (P < 0.01) , and enalapril-treated groups (136 +/- 25) pg x mL(-1) (P < 0.05). The plasma Ang II levels in high fat diet and in enalapril-treated groups were also significantly higher than that in control group ( P < 0.01 ). With immunohistochemical technique, it was found that the expression of AT1 in endothelial cells of blood vessels, vascular smooth muscle cells, and kidneys in diabetic group increased. The expression of AT1 in endothelial cells of blood vessels, vascular smooth muscle cells, and kidney in enalapril-treated group was similar to that in control group. CONCLUSION: The plasma Ang II levels and the expression of AT1 in type 2 diabetic and high fat diet rats increased. Enalapril was shown to decrease the plasma Ang II level and downregulate the expression of AT1 in blood vessels and kidneys in type 2 diabetic rats.

Angiotensin II↗

[Na+-H+ exchanger protein changes in vascular smooth muscle and effect of Na+-H+ exchange inhibitor on vessel stenosis after balloon injuries in rabbits].

OBJECTIVE: To explore the mechanism and effect of sodium/hydrogen exchanger (Na(+)-H(+) exchanger, NHE), amiloride, on vessel stenosis. METHODS: Thirty-two adult male New Zealand white rabbits were randomly divided into groups of amiloride intervention (IG, n = 12), balloon injury (BG, n = 10) and sham-operation (SG, n = 10). A 2.5 mm x 20 mm Foley's tube was used to injury left side iliac artery in the IG and BG groups, whereas a same Foley's tube was inserted into the vessel without any injuries in the SG group. Amiloride (5 mg.kg(-1).d(-1)) was intraperitoneally injected 3 days before balloon injuries and the same dosage normal saline was used in the same way in the BG group for 28 days after operation. The rabbits were killed and the iliac arteries were stained with Hematoxylin-Eosin, alpha-actin and Masson's trichrome to observe the morphologic changes in the vessel cava, neointima, media layer, and vascular smooth muscle cells (VSMCs) migration into the neointima and extracellular matrixes (ECMs). RESULTS: Four weeks after balloon injuries in rabbits, a cave narrow of the iliac artery and neointima were found and the media layer (VSM layer) was proliferated. The quantities of NHE-1 protein from artery smooth muscle in all the groups were 0.21 +/- 0.02, 0.25 +/- 0.04 and 0.11 +/- 0.03 (P < 0.01), respectively. The difference between the BG and SG groups was significant, which indicated that the NHE-1 proteins increased after balloon injury. The quantities of NHE-1 protein from the IG group were lower than those from the BG group. The cave areas were 0.91 mm(2) +/- 0.23 mm(2), 0.68 mm(2) +/- 0.19 mm(2) and 1.08 mm(2) +/- 0.17 mm(2) (P < 0.01), respectively. The intima areas were 0.27 mm(2) +/- 0.15 mm(2), 0.67 mm(2) +/- 0.24 mm(2) and 0.05 mm(2) +/- 0.03 mm(2), respectively (P < 0.01). The ratios of intima to media area were 1.21 +/- 0.24, 1.39 +/- 0.26 and 0.15 +/- 0.08 (P < 0.01), respectively. Amiloride increased vessel cave areas, but decreased intima areas and intima to media ratios in the IG group. In the IG group, alpha-actin positive areas in neointima was higher (16,328.31 microm(2) +/- 6220.27 microm(2)) than those in the SG group (4164.15 microm(2) +/- 1788.37 microm(2)) (P < 0.01). ECMs areas in neointima in the IG group were lower (8910.62 microm(2) +/- 7041.62 microm(2)) than those in the SG group (33,358.76 microm(2) +/- 7290.17 microm(2)) (P < 0.01). CONCLUSIONS: Balloon injuries of iliac artery in rabbits induce VSMCs proliferation, migration, narrowed cave and vessel stenosis. Amiloride, a NHE-1 inhibitor, may relieve this vessel stenosis.

Amiloride↗

[Effect of histamine on intracortical blood vessels of rats].

OBJECTIVE: To investigate histamine-induced changes of the intracortical vessels in the cortical slice of rat brain. METHODS: Immunohistochemistry was employed to detect the expression of H1 and H2 receptors in the intracortical blood vessels of rats. Histamine-induced constriction of the intracortical blood vessels of the brain slices was observed with differential interference contrast microscope. Measurements of the luminal diameter were made on-line during the course of the experiment and confirmed off-line from the stored images. In order to observe whether histamine H1 and H2 receptors affected histamine-induced constriction, the intracortical blood vessels in the brain slices were pre-treated with H1 receptor antagonist diphenhydramine and H2 receptor antagonist cimetidine. RESULTS: Expression of H1 and H2 receptors was detected in the intracortical blood vessels of the rat brain. Histamine (1-100 micromol/L) induced a concentration-dependent constriction from (1.48-/+0.67)% to (32.91-/+7.91)%. The reactions to each histamine concentration were significantly (P<0.01) different from each other, with the exception of the highest histamine concentrations (30 and 100 micromol/L) when maximal constriction due to histamine were observed (P>0.05). With pre-treatment of the slice with 10 micromol/L diphenhydramine, application of histamine did not elicit constriction. Pre-treatment of the slice with 10 micromol/L cimetidine did not completely inhibit but somehow significantly weakened vascular constriction in response to histamine treatment at 10 and 30 micromol/L (P<0.05). CONCLUSION: Histamine can induce constriction of the intracortical blood vessels, which is mediated by H1 receptor.

Animals↗

Absorbed dose calculations to blood and blood vessels for internally deposited radionuclides.

At present, absorbed dose calculations for radionuclides in the human circulatory system used relatively simple models and are restricted in their applications. To determine absorbed doses to the blood and to the surface of the blood vessel wall, EGS4 Monte Carlo calculations were performed. Absorbed doses were calculated for the blood and the blood vessel wall (lumen) for different blood vessels sizes. The radionuclides chosen for this study were those commonly used in nuclear medicine. No penetration of the radionuclide into the blood vessel was assumed nor was cross fire between the vessel assumed. The results are useful in assessing the dose to blood and blood vessel walls for different nuclear medicine procedures.

Adult↗

Microperfusion studies on the permeability of retinal vessels. A new model demonstrating organic anion transport and a reabsorptive fluid flux.

We developed an experimental model to study the permeability of individual retinal vessels in vitro using microperfusion techniques adapted from kidney tubule studies. The retinal vessels were isolated by freehand dissection and mounted on a microperfusion apparatus. When inulin was perfused luminally, it was diluted to 80.2 +/- 2.3% of its initial concentration. However, no radioactive leak into the bath side was observed, suggesting that the dilution was due to fluid flux from bath to lumen. The dilution of fluorescein (81.9 +/- 3.8%) was in the same range as that of inulin, the reference marker. The extremely low lumen-to-bath fluorescein flux, 0.5 +/- 0.9 X 10(-12) mol/min/mm, increased by 68% when probenecid was added to the perfusate and by 210% when probenecid was placed in the bath. The effect was concentration-dependent. When placed in the bath, fluorescein moved rapidly across the retinal vessel walls, accumulating in the lumen to concentrations 40 times higher than in the bath. This movement from bath to lumen, which was much higher (13.6 +/- 0.3 X 10(-12) mol/min/mm) than the lumen-to-bath fluorescein flux for the same fluorescein concentration, decreased by adding probenecid to the bath. The kinetics of this unidirectional movement of fluorescein were consistent with a saturable active transport process. The fluid flux from bath to lumen across the retinal vessels, which was 6.3 +/- 1.0 nl/min/mm for perfusion rates of 6.6 +/- 0.2 nl/min, was temperature-dependent and was coupled to the fluorescein transport. Fluorescein stimulated the fluid flux by 17% when added to the perfusate and by 60% when added to the bath, and this effect could be reversed by probenecid. Our results showed an active transport of fluorescein in the rabbit retinal vessels coupled with net fluid flux from outside the vessels into the lumen.

Animals↗

Media hypertrophy in hypertensive coronary resistance vessels.

Coronary reserve is reduced in human hypertensive hypertrophy and in the model of spontaneously hypertensive rats (SHRs). In isolated coronary resistance vessels, the role of structural and functional changes was evaluated. Furthermore, the effect of long-term antihypertensive therapy was also studied. At the age of 20 weeks, SHR and Wistar-Kyoto (WKY) rats were examined. Distal segments of the left anterior descending coronary artery were dissected and mounted on a myograph developed by Mulvany and Halpern. After recording of radius-wall tension curves, the vessels were set up to a wall tension equal to two-thirds of the systolic blood pressure. In SHRs, the vessel diameters were reduced. After equilibration with Ringer's solution, vessel dilatation was decreased in calcium-free solution (10 +/- 3 vs. 34 +/- 7%, p less than 0.05), but contraction increased after 123 mM of potassium stimulation (78 +/- 19 vs. 33 +/- 9%). There was no difference in calcium sensitivity during methoxamine or potassium activation. In the coronary resistance vessels of SHRs, electron microscopy revealed media hypertrophy (15.6 +/- 2.9 vs. 9.5 +/- 2.1 microns, p less than 0.05) and media hyperplasia (4.5 +/- 3 vs. 3.7 +/- 6 muscle layers, p less than 0.05). Media hypertrophy and a decrease in the vasodilatating capacity of resistance vessels contribute to the reduction of coronary reserve in hypertensive hypertrophy. The minimal coronary vascular resistance, a parameter of the vasodilatating capacity, was significantly increased in SHRs. Antihypertensive therapy with metoprolol and hydralazine or nifedipine resulted in an improvement of coronary reserve.

Animals↗

Interaction between oxygen and the blood vessel wall.

Blood vessels in vivo respond to changes in the supply of oxygen relative to its demand. Whether the vessels which participate in such vasoregulatory responses are directly affected by oxygen remains an open question. Most studies of oxygen sensing by blood vessels have been carried out on strips, rings or segments isolated from relatively large vessels. These preparations are generally sensitive to oxygen from 0 mm Hg to some upper PO2 (10 to 240 mm Hg) whose value depends on experimental conditions. It appears unlikely that reduced energy production secondary to tissue hypoxia is directly responsible for the relaxation usually observed when PO2 is lowered below a critical value. Evidence that an oxygen-linked chemical mediator such as adenosine or prostacyclin is involved in contractile responses to lowered PO2 has been obtained. The site of action of oxygen could be anywhere within the vascular wall, but current evidence suggests a prominent role for the endothelial cells. At present extrapolation of these results to resistance vessels in vivo must be carried out with caution due to potential differences in the behaviour of microvessels relative to large vessels.

Adenosine↗

Measurement of retinal blood vessel width using computerized image analysis.

We report a new method for quantitating retinal blood vessel width from fluorescein angiogram negatives using a computerized image analyser. Interuser and intrauser variability were 3 to 4 times lower than reported with older methods. In addition, model blood vessels were used to test the accuracy of our method under four clinically relevant conditions: variations in vessel width, fluorescein concentration, flash intensity and background fluorescence. Although computed measurements were affected by vessel width, fluorescein concentration and flash intensity, the linearity of the actual versus computed width was maintained during wide variations in all four conditions (r = 0.95, P less than 0.0001). Accuracy was best achieved at a flash intensity of 150 W/sec and a fluorescein concentration of 45 micrograms/ml. The results of this study provide a better understanding of factors affecting the apparent width of retinal blood vessels in fluorescein angiograms. This technique should be useful in rapidly obtaining accurate measurements of blood vessel width from fluorescein angiograms.

Animals↗

Autonomic innervation of preretinal blood vessels of the rabbit.

The preretinal blood vessels, that is, blood vessels lying on the inner surface of the retina, were observed by SEM examination using digestion methods, TEM examination and fluorescence histochemical examination using the Falck-Hillarp method. The nerve endings on the preretinal arterioles were distributed from the optic disc to the periphery. The longest nerve terminals from the optic disc to peripheral arterioles were about 9 mm. There were also a few nerve endings on the preretinal veins. These nerve endings had a series of axonal varicosities with diameters between 0.5 and 1.5 mu, which contained empty synaptic vesicles and cored synaptic vesicles. The number of nerve endings on these arterioles decreased with the shortening of the diameter of the retinal arterioles. Fluorescent nerve fibers with axonal varicosities were distributed on the wall of the preretinal blood vessels in the fluorescence histochemical study. These fluorescent nerve fibers were numerous near the optic disc, but there were only a few fluorescent nerve fibers on the peripheral blood vessels. The nerve endings on the preretinal blood vessels disappeared following superior cervical ganglionectomy. The present study shows that the preretinal blood vessels in rabbit eyes are innervated by the sympathetic nerve originating from the superior cervical ganglion.

Animals↗

Morphological changes in small vessels on endomyocardial biopsy.

Small vessel disease has been described in various cardiac conditions including diabetes mellitus, amyloidosis, and connective tissue disease. Less well understood is the incidence and morphological features of small vessel disease in patients with myocardial disease of unknown etiology. This study examines the incidence, clinical presentation, and pathological changes of small vessel disease in patients with normal epicardial coronary arteries undergoing endomyocardial biopsy. Biopsy specimens in 110 consecutive patients were analyzed by light and electron microscopy. Small vessel abnormalities were present in 16 patients (14.6 percent) of whom five patients had associated hypertension and 11 patients had idiopathic small vessel disease. There were six males and 10 females with a mean age of 53 (26 to 76) years. Clinical presentations were arrhythmias, heart failure, or chest pain. The left ventricular ejection fraction was reduced (less than 50 percent) in 12 of these 16 patients. The morphological features of small vessel disease included marked thickening of the arterial wall owing to subendothelial deposits of heterogeneous electron dense materials consisting of microfibrils, collagen and elastic fibers, cellular debris, and other amorphous substances. Subendothelial deposits comprised a mean 60 percent (40 to 76 percent) of the arterial wall thickness.

Adolescent↗

Resistance vessel growth and remodelling: cause or consequence in cardiovascular disease.

Haemodynamic evidence indicates that in essential hypertension, minimum vascular resistance and vascular pressor response are increased. According to the original concept of Folkow, this is most easily explained in terms of a generalised narrowing of the vasculature and an increase in the ratio of the vessel wall (more specifically, tunica media) thickness to lumen diameter. These predictions have been confirmed, both by histological and in vitro studies of resistance vessels. Moreover, the evidence indicates that these changes are associated mainly with remodelling (rearrangement of the same amount of material) of the vessels rather than growth. However, although the alteration in small artery structure is usually appropriate to the actual blood pressure (BP), the structure is not only a secondary adaptation but is also dependent on other factors, including neurohumoral and genetic factors. Furthermore, although the resistance vessel structure clearly plays an important role in determining BP, it does not appear to be a prime determinant of BP. It thus appears that more emphasis should be placed on Folkow's original idea that resistance vessel structure, like neurohumoral drive, is a mediator of the mechanisms which determine BP. Therefore, although evidence is available that the structure of certain specific parts of the vasculature (namely the renal afferent arterioles) could play a dominant function in the development of hypertension, it is suggested that resistance vessel structure should not in general be considered to have this role.

Animals↗

Relationship of runoff vessels to results following thrombolysis and revascularization for synthetic graft occlusions.

The objective of this study was to evaluate the relation between runoff vessels and the prognosis in patients who have had an occlusion of a previously placed peripheral arterial bypass graft. Over a 4-year period 77 occluded synthetic grafts were treated with urokinase and reconstruction after angiographic study. Follow-up ranged from 1 to 1627 days. The cases were divided into three groups according to the number of patent tibial vessels. Group I consisted of patients who had no vessel runoff. Group II consisted of patients who had single vessel runoff. Group III consisted of patients who had two or three runoff vessels. In Group I, the 1, 2, and 3-year patency rates were 35.8%, 8.9%, and 8.9%; and the limb salvage rates were 50.2%, 40.2%, and 40.2% for 1, 2, and 3 years, respectively. The Group II patency rates were 31.2%, 26.0%, and 13.0% and the limb salvage rates were 72.3%, 62.9%, and 62.9%. The Group III patency rates were 50.0%, 26.1%, and 20.9%; and the limb salvage rates were 93.1%, 79.1%, and 79.1%. There is no statistically significant difference in patency rates among any of the groups. The limb salvage rate was significantly increased in Group III, compared to I (P < 0.01) and Group II (P < 0.05), and in Group II, compared to Group I (P < 0.05). These results indicate that the higher rate of limb salvage in this study statistically correlated with the number of runoff vessels.

Adult↗

Histopathological study of intrahepatic aberrant vessels in cases of noncirrhotic portal hypertension.

Aberrant vessels, which are defined as dilated blood vessels immediately adjacent to the peripheral portal tract, appear under conditions of extrahepatic portal obstruction and nodular regenerative hyperplasia as well as idiopathic portal hypertension. Our study was undertaken to compare their morphological aspects in these three disease cases. Aberrant vessels were found in 84% of cases of idiopathic portal hypertension, 67% of cases of extrahepatic portal obstruction infantile type, 78% of cases of extrahepatic portal obstruction adult type and 83% of cases of nodular regenerative hyperplasia. They were divided into three types: type I--no communication with the portal vein, the lumen of which is normally open; type II--communication with the portal vein; and type III--no communication with the portal vein, which is occluded. The most common types of aberrant vessel were type III in idiopathic portal hypertension (51%), type I in extrahepatic portal obstruction infantile type (46%), type II in extrahepatic portal obstruction adult type (43%) and type III in nodular regenerative hyperplasia (45%). Serial sections revealed transition between types I, II and III, at frequencies between types II and III, types I and II, and types I and III of 35.7%, 33.7% and 30.6%, respectively. Aberrant vessels demonstrated the same immunoreactivity as portal veins for collagen type IV, laminin, factor VIII and ulex europaeus agglutinin-I. They were concluded to arise from the vasa septalis or inlet venules, which would be used as intrahepatic shunts draining portal blood flow blocked by stenosed portal veins. Increased portal pressure would be expected to enhance development of aberrant vessels.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Vessels↗

Two light attenuation models for automatic diameter measurement of the blood vessels.

The Lambert-Beer's law of the absorption of the light by blood in a vessel is used to model the light attenuation by a blood vessel that is transilluminated. Two models are used for an automatic vessel diameter determination for intravital microscopy. Some requirements for the photometric system have to be met in order to reduce errors due to light scattering. In these conditions, a videodensitometric pattern of the cross-section of the vessel can be fitted by the different models in order to obtain the diameter of the vessel. The first model proposed uses a uniformly distributed red blood cell column. A non-linear estimation of the diameter is done with the Levenberg-Marquardt method in 2 sec, using a regular PC386 microcomputer. The second one takes in account the presence of a plasma layer and computes the diameter of the red blood cell column and the diameter of the vessel in one minute. These models can be used for pharmacological studies or for a better understanding of the formation of a transilluminated intravital image. They can also be used for angiographic images.

Algorithms↗

Localization and characterization of endothelin-1 receptor binding in the blood vessels of human pulmonary tumors.

We have demonstrated endothelin-1 (ET-1) binding sites in the blood vessels of human pulmonary tumors by in vitro autoradiography. The blood vessels of the tumors were confirmed by immunostaining with von Willebrand factor. Specific [125I]ET-1 binding was identified in the blood vessels of all sizes in both tumor and stromal tissues. Nonspecific binding was observed in squamous cell carcinomas and in carcinoids. The ET-1 binding in blood vessels was specific, saturable, and time-dependent. The binding reached equilibrium at 120 min. Scatchard analysis of [125I]ET-1 binding to sections of blood vessels of squamous cell carcinoma indicated binding to a single class of binding sites, with a dissociation constant (Kd) of 0.16 nM and a maximal density of binding sites (Bmax) of 126 amol/mm2. The binding was competitively inhibited by ET-1 >> VIC > ET-2 > sarafotoxin (SRb) > ET-3 but not by other unrelated peptides. Our results provide evidence that ET-1 binding is localized in the blood vessels of pulmonary tumors and in stromal tissues surrounding the tumor nest. ET may play a role in the angiogenesis of tumor growth.

Autoradiography↗

Sural nerve biopsy in vasculitic neuropathies: morphometric analysis of the caliber of involved vessels.

We performed histologic and morphometric analyses of the sural nerve in 13 patients with vasculitic neuropathies. The ratio of vessels with vasculitis, the caliber of involved vessels, and pathologic changes of myelinated fibers were evaluated. In patients with polyarteritis nodosa (PN), rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE), marked vasculitis with inflammatory cell infiltration and occlusion were observed in epineurial arteries greater than 100 microns in diameter, and mild vasculitic changes were noted in arterioles 40 to 100 microns in diameter. In vessels less than 40 microns, mild vasculitis with perivascular cuffing was noted in patients with RA and SLE, but not in PN. In a patient with microscopic PN, mild inflammatory cell infiltration was encountered around small vessels at diameters less than 40 microns as well as those greater than 100 microns. In a patient with nonsystemic vasculitic neuropathy, vasculitic changes were identified only in vessels less than 40 microns. In patients with Churg-Strauss syndrome (CSS), there were no distinct findings of vasculitis in any biopsy material. In conclusion, morphometric analyses of the caliber of involved vessels may be useful in the differential diagnosis and classification of underlying vasculitic neuropathies.

Aged↗