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PubMed2001

Extrinsic ureteropelvic junction obstruction from a crossing renal vessel: demography and imaging.

BACKGROUND: The increase in the use of prenatal ultrasound has revolutionized the detection of hydronephrosis and has had an unanticipated consequence. OBJECTIVE: To describe the new demographics of symptomatic ureteropelvic junction (UPJ) obstruction and the characteristic imaging findings, when the obstruction is extrinsic, from a crossing renal vessel. MATERIALS AND METHODS: From a uroradiology database (1994 through 1999) we identified children with surgically corrected UPJ obstruction from intrinsic and extrinsic causes. RESULTS: One hundred children had symptomatic UPJ obstruction treated by surgery. In 51 (49 %), obstruction was due to a crossing vessel. One hundred and one had UPJ obstruction detected by prenatal sonography. Only 11 (11%) were due to a vessel. Two clinical and imaging findings were strongly suggestive of obstruction from a vessel: (1) in 5 of the 100 children the symptoms (pain, nausea, and vomiting) were intermittent. Only when symptoms were present were there hydronephrosis and obstruction; (2) in 51 of the 100 children a short segment of ureter, just below the UPJ, was filled with contrast or urine (on renal sonography, intravenous urography, or retrograde/antegrade ureterography). CONCLUSIONS: Extrinsic UPJ obstruction caused by a vessel is an uncommon cause of obstruction when all patients are considered. However, in symptomatic older patients whose hydronephrosis was not first identified on prenatal sonography, a vessel was the cause of obstruction in one half.

Child↗

PubMed2005

CT imaging of peripheral pulmonary vessel disease.

The diseases concerning the small pulmonary vessels are difficult to diagnose. Pathologic findings are rarely limited to the small vessels, and a continuum between the involvement of small and large vessels is frequent. Moreover, small vessels can be affected by various disease entities with overlapping radiologic features and a wide spectrum of clinical manifestations. Nevertheless, these various entities can be easily separated into two different groups by imaging techniques, particularly by computed tomography: obstructive and inflammatory diseases. Radiologic findings of obstructive diseases are relatively constant, dominated by the manifestation of pulmonary hypertension. In contrast, radiologic manifestations of inflammatory diseases are often florid and nonspecific. After a recall of the classification of small vessel diseases and the imaging techniques, we show the computed tomography features of the principal diseases involving the small pulmonary vessels by classifying them in these two principal groups.

Arterial Occlusive Diseases↗

PubMed2004

Photodynamic therapy and indocyanine green guided feeder vessel photocoagulation of choroidal neovascularization secondary to choroid rupture after blunt trauma.

PURPOSE: To describe photodynamic therapy (PDT) and additional indocyanine green (ICG) guided feeder vessel photocoagulation as a treatment of choroidal neovascularization (CNV) secondary to choroidal rupture in case of blunt head trauma. DESIGN: Interventional case report. METHODS: A 61-year-old woman developed subfoveal CNV originating from a choroid tear 8 years after blunt head trauma. Four sessions of PDT were applied and an additional two consecutive sessions of selective ICG-guided feeder vessel photocoagulation conducted. RESULTS: Transient reduction of leakage and closure of feeder vessels could not prevent further growth of the CNV. CONCLUSIONS: PDT reduced leakage temporarily and additional ICG-guided feeder vessel photocoagulation closed treated feeder vessel and CNV. New feeder vessel formation and growth of CNV in case of traumatic choroid rupture could not be treated effectively by these two laser treatment modalities to prevent severe deterioration of visual acuity.

Choroid↗

PubMed2002

Decrease of elastic tissue fibres in stem villus blood vessels of the human placenta during IUGR and IUGR with concomitant pre-eclampsia.

In a recent study we described an increase of elastic tissue fibres in blood vessel walls of placental stem villi during pre-eclampsia when compared to uncomplicated pregnancies. Furthermore, the thickness of these blood vessel walls was enhanced in pre-eclampsia. Since it is known that elastic tissue fibres increase in systemic hypertension, it may be assumed that the enhancement of elastic tissue fibres in placental stem villi during pre-eclampsia may be induced by the hypertension. To get further insight into this assumption, we examined the amount of elastic tissue fibres in stem villus blood vessels of placentae of pregnancies complicated by intrauterine growth retardation (isolated IUGR, fourteen cases), a disease without hypertension of the mother and such with pre-eclampsia and concomitant IUGR (IUGR+PE, nine cases). Each study group was compared with uncomplicated pregnancies (twenty-six cases). Unfixed cryostat serial sections were processed for conventional orcein staining and for the demonstration of alpha-actin-immunoreactivity. The intensity of orcein staining of stem villus blood vessel walls was evaluated by a semiquantitative score method. Significant lower intensities of orcein staining were calculated for blood vessel walls of placentae of isolated IUGR (P=0.0007) and IUGR+PE (P=0.0039) when compared to uncomplicated pregnancies each. Additionally, the blood vessel wall thickness of stem villi of isolated IUGR (P=0.0081) and IUGR+PE (P=0.0007) was significantly reduced. In comparison to the above mentioned investigation, our results show that, in contrast to isolated pre-eclampsia, elastic tissue fibres are decreased during pregnancies complicated by IUGR, independently of the occurrence of concomitant pre-eclampsia when compared to uncomplicated pregnancies. From our studies it may be considered that the increase of elastic tissue fibres in placentae of patients with isolated pre-eclampsia may be induced by systemic hypertension. Furthermore, our study underline arguments that IUGR may be an independent disease of the fetus.

Adult↗

PubMed1998

The central vessel of the renal countercurrent bundles of two marine elasmobranchs--dogfish (Scyliorhinus caniculus) and skate (Raja erinacea)--as revealed by light and electron microscopy with computer-assisted reconstruction.

The renal countercurrent bundles of elasmobranch fish were studied by light and electron microscopy. The kidneys of the lesser spotted dogfish, Scyliorhinus caniculus Blainville, and the little skate, Raja erinacea Mitchill, were investigated. Three-dimensional reconstruction with computer assistance revealed the spatial association of the renal tubular segments and their relationships to each other, as well as to the microvasculature. Regular association between structures was assessed by quantification of contact points on histological sections. The bundles contain a hairpin loop of neck segment and the beginning of the proximal tubule, PIa. The limbs of this loop closely adhere to each other, and a second loop (the early distal tubule) coils around the first loop at the tip of the bundle. The collecting tubule runs between the two loops, and merges with the collecting duct inside the end portion of the bundle. A single lymph capillary-like vessel originates from a few blind-ended rami at the tip of the bundle and runs in close contact with the collecting tubule along the entire bundle. This central vessel merges via several side branches with the venous sinusoid capillaries of the peritubular blood circulation. Thereby the central vessel provides a channel for convective flow of NaCl-rich fluid unidirectionally to the venous portal system of the mesial tissue zone of the kidney. By the close spatial arrangement of the collecting tubule and the central vessel countercurrent exchange of urea from the collecting tubule urine to the fluid in the central vessel is feasible. Thus, the spatial organisation of renal tubular segments and the central vessel is considered to represent the morphological correlate to urea retention by the kidney of Elasmobranchii.

Animals↗

PubMed2000

Pre-eclampsia associated alterations of the elastic fibre system in umbilical cord vessels.

Although pre-eclampsia (PE) is often associated with fetal hypoxia, hypertension and/or disturbed function of the fetal circulation, the effect of these altered hemodynamic parameters on the structure and composition of umbilical vessels has not been systematically investigated before. Therefore, this study focuses on PE-associated changes of the elastic fibre system in umbilical cord vessels investigated by light and electron microscopy, immunocytochemistry and biochemistry. In umbilical cord veins, no changes in thickness of the vessel wall or of any sublayer were observed. However, the internal elastic lamina of the veins was split in 80% of the PE-group in contrast to 20% in uncomplicated pregnancies. This effect was significant (alpha <0.01) from 36 weeks of gestation onwards. In umbilical cord arteries, the entire arterial vessel wall was found to be 15% thicker in PE than in uncomplicated pregnancies. The enlargement was caused by an increase of both the tunica intima and tunica media. The thickening of the tunica intima was attributed to a migration of smooth muscle cells towards the endothelium, accompanied by a splitting of the internal elastic lamina. Compared to uncomplicated pregnancies, smooth muscle cells of arteries and veins in PE showed a metabolic activation demonstrated by highly dilated endoplasmic reticulum. A semiquantitative score method as well as a quantitative dot blot assay indicated a PE-associated reduction of elastin expression in the arterial vessel walls. In summary, PE obviously induces a decrease of the elastin content accompanied by a thickening of the vessel wall in umbilical cord arteries. This remodeling of the elastic fibre system, together with an increased migration of smooth muscle cells, might represent part of the functional adaptation system of the umbilical cord arteries on the altered hemodynamic conditions in PE.

Adult↗

PubMed2006

Large vessel - sternum adhesion after cardiac surgery; a risk-factor analysis.

PURPOSE: To study the clinical results of resternotomy in patients with dense and direct adhesion between the large vessels and the sternum, and define the morphologic features of the adhesion. METHODS: Between 2000 and 2003, 67 patients with a history of cardiac surgery underwent median resternotomy. We studied each patient's profile and the measurements taken from preoperative computed tomography scans. We then conducted multivariate logistic regression analysis to determine the predictive morphologic features of adhesion between the large vessels and the sternum in these 67 patients. RESULTS: Twenty (29.9%) of the 67 patients had direct adhesion between the large vessels and the sternum. Sternal re-entry was performed without injury to the large vessels in 18 (90%) but the aorta was injured in 2 (10%) patients, resulting in catastrophic hemodynamic disorder and operative death in one. Multivariate logistic regression analysis revealed that an extracardiac conduit and a high occupying rate of the aorta and pulmonary artery in the mediastinal space were significant morphologic factors. CONCLUSION: The morphologic features of large vessels to sternal dense adhesion as possible risk factors for injury to the large vessels are the presence of an extracardiac conduit and a large ascending aorta or pulmonary artery in relation to the mediastinal space.

Adult↗

PubMed1999

Balloon angioplasty induces heat shock protein 70 in human blood vessels.

Balloon angioplasty produces a mechanically induced injury to the blood vessel wall. Heat shock protein 70 (HSP70) is a molecular chaperone whose expression can be induced by chemical or thermal stress. Thus, we hypothesized that the mechanical injury associated with balloon angioplasty would lead to increases in the expression of HSP70 in vascular smooth muscle. Segments of popliteal and trifurcation vessels from above-the-knee amputations were subject to transluminal balloon angioplasty, excised, and placed in organ cultures. Neighboring vessel that was not subjected to balloon angioplasty served as controls. Some vessels were treated with sodium arsenite (positive control, known to induce HSP70 expression). The vessels were homogenized and the proteins were separated by gel electrophoresis and transferred to Immobilon. Western blots with an antibody specific for the inducible form of HSP70 were analyzed by densitometry. Our results showed that HSP70 expression can be induced by the mechanical injury associated with balloon angioplasty in human atherosclerotic vessels.

Analysis of Variance↗

PubMed2003

Lymphatic vessels in colorectal cancer and their relation with inflammatory infiltrate.

PURPOSE: The aim of this study was to determine why colorectal tumors confined to submucosa rarely metastasize. Under normal conditions, the submucosa contains many large lymphatic vessels with thin walls that would presumably favor the spread of cancer cells through the lymphatic system. METHODS: Specimens of colorectal cancer tissue, the border between tumor and normal tissue, and normal tissue were obtained from patients undergoing radical resection of colorectal cancer. The material was embedded in methacrylate resin for light microscopy and Epon for transmission electron microscopy examination. Light microscopy observations were routinely performed on serial sections. RESULTS: No lymphatic vessels were ever found in the tumor mass. The border area contained peritumoral inflammatory infiltrate of variable thickness. Where submucosal lymphatic vessels came into contact with peritumoral inflammatory infiltrate, they were profoundly altered: their endothelium was fragmented, and their walls were disrupted. These altered lymphatic vessels were almost always accompanied by mast cells, which were observed in the process of degranulating toward the lymphatic endothelium. No such alterations were detected in blood vessels. CONCLUSION: Our results suggest that mast cells, probably influenced by inflammatory infiltrate and/or colorectal cancer cells, destroy lymphatic vessels, which prevents cancer cells from spreading through the lymphatic system.

Aged↗

PubMed1993

Identification of high-risk patients with left main and three-vessel coronary artery disease using stepwise discriminant analysis of clinical, exercise, and tomographic thallium data.

This large-scale study examined the ability of stepwise discriminant analysis of clinical, exercise, and thallium tomographic data to detect high-risk patients with three-vessel or left main disease. There were 834 patients, 229 with three-vessel or left main disease (group 1) and 605 (group 2) with either two-vessel disease (n = 236), one-vessel disease (n = 195), or no coronary artery disease (n = 174). The two groups were different in age, exercise heart rate, ST segment depression during exercise, exercise systolic blood pressure, abnormal thallium scans, reversible perfusion defects, extent of thallium abnormality, number of vascular territories with perfusion abnormalities, left ventricular cavity dilatation, and increased lung thallium uptake. On multivariate stepwise discriminant analysis, only three variables were independent predictors of high risk. These included multivessel thallium abnormality (F = 107, p < 0.001), exercise heart rate (F = 27, p < 0.001), and ST segment depression (F = 8, p < 0.01). Based on these three variables, patients could be stratified into three categories with different prevalences of left main or three-vessel disease; the prevalence was 53% in 239 patients, 24% in 271 patients, and 12% in 324 patients. Thus high-risk patients with left main or three-vessel disease can be identified by exercise thallium tomographic imaging that uses a model based on stepwise discriminant analysis. The thallium data are far more powerful than the clinical or treadmill exercise data.

Aged↗

PubMed1981

Effects of a progesterone-releasing intrauterine contraceptive device on endometrial blood vessels: a morphometric study.

The concentration of microscopically detectable blood vessels was significantly lower in endometrium exposed to progesterone-releasing intrauterine contraceptive devices (IUDs) than in control endometrium (mean vessel density 2.39 and 3.92, respectively). The percentage of vessels with defects was significantly higher in IUD samples (35.0%) than in control samples (13.4%). There was no significant difference in hemostatic response to vessel injury between the IUD and control samples. Although they were more defective than in controls, the blood vessels of progesterone IUD-exposed endometrium were far fewer in number, which may account for significantly less uterine blood loss in the users of these devices. In addition, the progesterone IUDs do not appear to inhibit hemostasis in the endometrium so that blood loss from injured vessels may be minimized.

Endometrium↗

PubMed1995

Contractile proteins in human fetoplacental vessels.

OBJECTIVE: Our purpose was to compare the protein isoform composition of the contractile apparatus at different levels of the fetoplacental vessel musculature at term. STUDY DESIGN: Umbilical, chorionic, and stem villi vessel protein extracts were run on one- and two-dimensional gel electrophoresis; previously characterized human myometrium proteins were used as the smooth muscle proteins of reference. RESULTS: Fetoplacental vessel musculature exhibited a high actin/myosin ratio. The presence, in varying quantities, of myosin heavy chain and actin isoforms of smooth muscle type in the different vessels reflected their degree of differentiation. The presence of nonmuscle protein isoforms, particularly in stem villi vessels, indicated a certain degree of immaturity. CONCLUSIONS: The presence of smooth muscle contractile protein isoforms indicates that fetoplacental vessel musculature is highly differentiated. Regional modulation of fetoplacental blood flow could be, in part, the result of local differences in contractile apparatus protein composition.

Actins↗

PubMed1996

Blood vessel invasion is a major prognostic factor in resected non-small cell lung cancer.

BACKGROUND: We examined the prognostic value of histologic indices in non-small cell lung cancer with particular interest in major blood vessel invasion. METHODS: We studied 593 patients who had curative resection between November 1983 and December 1988. We determined the histology, T and N status, peritumoral lung tissue invasion, tumor stroma, necrosis, mitotic rate, and blood vessel invasion. RESULTS: The median patient survival of the whole series was 3.2 years, with a 5-year survival of 38.9%. In univariate analysis, a high T stage, a high percentage of necrosis, blood vessel invasion, and N stage significantly worsened the survival. In multivariate analysis, only blood vessel invasion and, less significantly, T stage and lymph node metastasis remained independent prognostic factors. CONCLUSIONS: These results highlight the negative prognostic value of blood vessel invasion in non-small cell lung cancer and suggest that blood vessel invasion, T stage, and node metastasis are three unrelated and distinctive characteristics of resected non-small cell lung cancer.

Analysis of Variance↗

PubMed1985

Neurochemical studies on the existence, origin and characteristics of the serotonergic innervation of small pial vessels.

Substantial concentrations of serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA), comparable to those found in brain tissue, were measured in the small pial vessels of the rat, rabbit and cat. Both rat and rabbit pial vessels exhibited a high affinity uptake process with kinetic parameters similar to those identified for the cerebral cortex. Labelled 5-HT, taken up by isolated rabbit pial vessels was released, in a calcium-dependent manner, by potassium-induced depolarization. Various pharmacological manipulations were carried out in the rat. Systemic administration of the 5-HT precursor, 5-hydroxytryptophan and the monoamine oxidase inhibitor, pargyline, significantly increased the concentration of 5-HT in the pial vessels; in contrast, two depleting agents (p-chloroamphetamine and reserpine) and the tryptophan hydroxylase inhibitor, p-chlorophenylalanine, all decreased the perivascular 5-HT levels. A serotonergic antagonist (methysergide) and a 5-HT receptor agonist (MK 212) respectively increased and decreased the concentrations of 5-HIAA in the pial vessels. These pharmacologically induced changes observed in pial vessels were not dissimilar from those noted for cortical tissue. Electrolytic lesions of the nuclei raphes medianus and/or dorsalis markedly decreased the levels of 5-HT and 5-HIAA in these small cerebral arterioles. Electrical stimulation of these nuclei decreased 5-HT although 5-HIAA concentrations tended to increase. A number of conclusions may be drawn from these studies. Thus, there is a serotonergic innervation of the cerebral circulation in several laboratory species which unequivocally originates in the raphé nuclei. Furthermore, these perivascular fibres possess synthetic, storage, release, inactivation and autoregulatory processes for 5-HT which, when further elucidated, may offer some rationale for the treatment of those cerebrovascular diseases in which this neurotransmitter and vasoactive agent is believed to be of pathological importance.

Animals↗

PubMed1986

Effects of calcium entry blockers on Ca2+-induced contraction of depolarized and noradrenaline-exposed rat resistance vessels.

The effects of four calcium entry blockers (CEBs), diltiazem (D), verapamil (V), nifedipine (NF) and nicardipine (NC), were investigated on Ca2+ concentration-effect curves of rat depolarized (K+, 40 mM) or noradrenaline (NA, 3 microM)-exposed mesenteric resistance vessels. Under control conditions, NA-exposed vessels were more sensitive to Ca2+ (pD2: 4.12 +/- 0.11) than depolarized vessels (pD2: 3.16 +/- 0.02, P less than 0.01) whereas the maximal active wall tensions were not significantly different (2.86 +/- 0.11 mN/mm and 2.11 +/- 0.34 mN/mm respectively). In depolarized vessels, D, V, NF and NC induced a concentration-dependent shift to the right and a depression of the maximal effect of the Ca2+ curves, which suggested a non-competitive antagonism. The IC50 (concentration of CEB producing a 50% inhibition of the maximal contractile response from control curve) values were: D: 3 X 10(-7), V: 1.3 X 10(-7), NF: 4.5 X 10(-9), NC: 3 X 10(-9) M. In NA-exposed vessels, the CEBs produced a concentration-dependent shift to the right of the Ca2+ curves before depressing their maximal effect. This suggested that the antagonism was different from that observed in depolarized arteries. In this case, the IC50 values were: D: 4.5 X 10(-7), V: 2 X 10(-7), NF: 9 X 10(-9), NC: 7 X 10(-9) M. Although the gating mechanisms activated in this study were differently affected by CEBs, since there were marked qualitative differences in their antagonistic effects on Ca2+ concentration-effect curves, depolarization and NA promoted the entry of Ca2+ into smooth muscle cells of rat resistance vessels by mechanisms with the same sensitivity to CEBs as expressed by IC50 values.

Animals↗

PubMed1987

Responses of femoral resistance vessels to angiotensin in vitro.

The effect of angiotensin II and angiotensin I on isolated rat resistance vessels (inner diameter ca. 200 micron) was investigated. Angiotensin II caused a contraction (ED50 = 0.58 +/- 0.17 X 10(-8) M) of rat femoral and cerebral arteries and to a lesser extent of mesenteric and renal arteries. However, all vessels showed strong tachyphylaxis on repeated stimulation with angiotensin II. Tachyphylaxis was avoided by inducing submaximal tone in the vessels with either K, noradrenaline or serotonin. The response to angiotensin II was inhibited by saralasin but not by captopril. Angiotensin I also caused contraction of the femoral arteries (ED50 = 2.68 +/- 0.32 X 10(-8) M). These responses were inhibited by captopril and saralasin. Functional removal of the endothelium had little effect on the contractile responses to either angiotensin I or II. These results indicate that there are functional receptors to angiotensin II in the resistance vessels of the rat and that, in the presence of tone (a more physiological condition), the vessels contract to angiotensin II without tachyphylaxis. In addition, angiotensin II may be formed from angiotensin I by the angiotensin converting enzyme which may be situated in the vessel wall as well as in the endothelium.

Angiotensin II↗

PubMed1989

Endothelin-1 induces potent constriction of lymphatic vessels in situ.

The response of lymph vessels, arterioles and venules in the exteriorized rat mesentery to endothelin-1, vasopressin and norepinephrine was examined with the aid of high-resolution television microscopy. On a molar basis, endothelin-1 was more potent than vasopressin to contract the three types of vessels. Norepinephrine, which could constrict blood microvessels, did not act on lymph vessels. Acetylcholine, sodium-nitroprusside and isoproterenol were ineffective to block the constrictive responses of lymph vessels to endothelin-1 and vasopressin. At the same concentrations, however, acetylcholine and sodium-nitroprusside antagonized the responses of arterioles and venules to endothelin-1 and norepinephrine, whereas the responses of blood microvessels to vasopressin remained unaffected. Isoproterenol, at doses capable of blocking the response of the arterioles and venules to norepinephrine, did not interfere with the constriction induced by endothelin-1 and vasopressin on these vessels. It is suggested that endothelin-1 might play a role in the regulation of lymphatic contractility apart from its vasoconstrictor activity on blood vessels.

Animals↗

PubMed1991

Effects of sympathetic nerves on collateral vessels in the limb of atherosclerotic primates.

This study was performed to examine effects of sympathetic nerves on collateral vessels in the limb. We studied normal (N) and atherosclerotic (AS) cynomolgus monkeys that were fed atherogenic diet for 21 months. A common iliac artery was ligated 13 months before hemodynamic measurements. Using histofluorescence microscopy, a plexus of noradrenergic nerves was identified in the adventitia of collateral vessels. We measured blood flow to the limb with microspheres, and the pressure gradient from aorta to the iliac artery beyond the occlusion. The lumbar sympathetic chain was stimulated electrically at 3 Hz (SNS-3) and 15 Hz (SNS-15). In normal monkeys, conductance of collateral vessels (in ml/min per 100 g per 100 mm Hg) was 19 +/- 3.6 (mean +/- SE) during control, 14 +/- 1.6 during SNS-3, and 9.8 +/- 0.9 during SNS-15 (P less than 0.05 vs control). In AS monkeys, collateral conductance was 12 +/- 2.9 during control, 7.5 +/- 1.7 during SNS-3 and 3.9 +/- 1.8 during SNS-15 (P less than 0.05). In summary, collateral vessels in the limb are innervated and sympathetic stimulation produces pronounced constriction of collateral vessels in both normal and atherosclerotic monkeys. Thus, the effectiveness of collateral vessels in maintaining blood flow to the limb may be compromised by increased activity of sympathetic nerves.

Animals↗