Can biliary-cyst communication be predicted by Gd-EOB-DTPA-enhanced MR cholangiography before treatment for hepatic hydatid disease?

AIM: To evaluate the role of gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid (Gd-EOB-DTPA)-enhanced magnetic resonance cholangiography (MRC) in the evaluation of biliary-cyst communication (BCC) before treatment for hepatic hydatid disease (HHD). MATERIAL AND METHODS: Thirty-one patients with clinical and laboratory follow-up for HHD with suspected diagnosis of BCC underwent three-dimensional (3D) T2-weighted MRC and T1-weighted contrast-enhanced MRC, dynamic 3D gradient echo (GRE) sequences, using Gd-EOB-DTPA to identify the presence or absence of BCC. A total of 45 hepatic hydatid cysts in the 31 patients were evaluated for cyst diameter, BCC, and the time to contrast-enhancement of the hydatid cyst after Gd-EOB-DTPA injection. The surgical and interventional radiological procedures and imaging findings were compared. The sensitivity, specificity, and accuracy of both techniques in identification of BCC were calculated. RESULTS: The accuracy of contrast-enhanced MRC for identifying BCC was superior with a sensitivity of 87.4% and accuracy of 90.5% (p < 0.05). A diameter of ≥10 cm was associated with significantly increased risk of BCC on contrast-enhanced MRC images (p < 0.05). CONCLUSION: The use of Gd-EOB-DTPA-enhanced MRC yields information that complements T2-weighted MRC findings and improves identification of BCC. The use of T2-weighted MRC, in addition to contrast-enhanced MRC, is recommended to increase preoperative accuracy of identifying BCC.

Polyorchidism and adenomatous hyperplasia of the rete testis: a case report with sonographic and magnetic resonance imaging findings and review of literature.

Supernumerary testis or polyorchidism is a rare congenital anomaly with about 200 reported cases in the literature. It may be associated with cryptorchidism, testicular torsion and neoplasms. Ultrasonography and magnetic resonance imaging are effective noninvasive methods of accurately detecting polyorchidism. In most cases, ultrasonography is diagnostic and magnetic resonance imaging plays confirmatory role by providing additional information if complicated with neoplasia. We report a case of 16-year-old man with right supernumerary testis associated with adenomatous hyperplasia of the rete testis, its sonographic and magnetic resonance imaging findings and management.

Hyperglycaemia promotes cerebral barrier dysfunction through activation of protein kinase C-ß.

AIM: To examine whether protein kinase C (PKC) and associated downstream mechanisms are involved in hyperglycaemia (HG)-evoked blood-brain barrier (BBB) damage. METHODS: The activities of total PKC (Peptag assay), NADPH oxidase (lucigenin assay) and matrix metalloproteinase-2 (MMP-2; gelatin zymography) were measured in human brain microvascular endothelial cells (HBMEC) exposed to normoglycaemia (5.5 mM) or HG (25 mM) using the specific assays indicated in parentheses. The integrity and function of the in vitro models of human BBB were assessed by measurements of transendothelial electrical resistance and paracellular flux of permeability markers, respectively. Occludin protein expression was studied by immunoblotting. RESULTS: HG significantly compromised the BBB integrity and enhanced total PKC activity to which increases in PKC-ß and PKC-ßII isoforms contributed the most. Elevations in NADPH oxidase and MMP-2 activities and decreases in occludin levels contributed to barrier dysfunction. Selective inhibition of PKC-ß isoform prevented the changes observed in occludin expression and the aforementioned enzyme activities and thus effectively preserved barrier integrity. Similarly, apocynin, a specific NADPH oxidase inhibitor, also effectively neutralized the effects of HG on barrier integrity, MMP-2 activity, occludin expression and PKC-ß activity. CONCLUSION: HG promotes cerebral-barrier dysfunction through activation of PKC-ß and consequent stimulations of oxidative stress and tight junction dissolution.

The utility of multidetector computed tomography for evaluation of congenital heart disease.

BACKGROUND: Congenital heart diseases (CHD) are the leading cause of birth defect-related deaths. Multi detector computed tomography (MDCT) plays an important role for imaging CHD in addition to echocardiography and provides a comprehensive evaluation of complex heart malformations for the referring cardiologist. The aim of the study was to evaluate the utility of MDCT in the assessment of CHD. MATERIALS AND METHODS: A 102 patients with CHD were investigated after initial assessment by echocardiography. The information obtained by MDCT and findings of echocardiography were reviewed together by paediatric cardiologists and cardiac radiologists. Perioperative anatomic descriptions, wherever available(n = 34) formed the gold standard for the comparison. RESULTS: The clinical consensus diagnosis defined 154 cardiovascular lesions in the patients. The results were classified in groups. We present the appearance of various congenital cardiac lesions seen in clinical practice. CONCLUSIONS: MDCT provides important information about anatomic details of CHD for the referring cardiologist. The evaluation of different anatomic structures such as heart, great vessels, lungs and abdomen is possible in one acquisition with this technique.

Partial anomalous pulmonary venous return associated with vascular anomalies of the aorta: multidetector computed tomography findings.

Partial anomalous pulmonary venous return (PAPVR) is a congenital anomaly that involves drainage of one to three pulmonary veins directly into the right heart or systemic venous system, creating a partial left-to-right shunt. This drainage is associated with cardiac abnormalities such as mitral stenosis and pulmonary stenosis, patent ductus arteriosus, and atrial septal defects. We report a case of PAPVR associated with vascular anomalies of the aorta by multidetector computed tomography in an adult female patient.

Subvalvular membrane on the left ventricular outflow tract: multidetector computerised tomography imaging.

In this report, we describe a patient with a subvalvular membrane on the left ventricular outflow tract. Discrete subvalvular membrane is a cause of left ventricular outflow tract narrowing. Multidetector computerised tomography can demonstrate the anatomical three-dimensional view of this region and guide for surgery.

Antioxidants attenuate hyperglycaemia-mediated brain endothelial cell dysfunction and blood-brain barrier hyperpermeability.

AIMS: Hyperglycaemia (HG), in stroke patients, is associated with worse neurological outcome by compromising endothelial cell function and the blood-brain barrier (BBB) integrity. We have studied the contribution of HG-mediated generation of oxidative stress to these pathologies and examined whether antioxidants as well as normalization of glucose levels following hyperglycaemic insult reverse these phenomena. METHODS: Human brain microvascular endothelial cell (HBMEC) and human astrocyte co-cultures were used to simulate the human BBB. The integrity of the BBB was measured by transendothelial electrical resistance using STX electrodes and an EVOM resistance meter, while enzyme activities were measured by specific spectrophotometric assays. RESULTS: After 5 days of hyperglycaemic insult, there was a significant increase in BBB permeability that was reversed by glucose normalization. Co-treatment of cells with HG and a number of antioxidants including vitamin C, free radical scavengers and antioxidant enzymes including catalase and superoxide dismutase mimetics attenuated the detrimental effects of HG. Inhibition of p38 mitogen-activated protein kinase (p38MAPK) and protein kinase C but not phosphoinositide 3 kinase (PI3 kinase) also reversed HG-induced BBB hyperpermeability. In HBMEC, HG enhanced pro-oxidant (NAD(P)H oxidase) enzyme activity and expression that were normalized by reverting to normoglycaemia. CONCLUSIONS: HG impairs brain microvascular endothelial function through involvements of oxidative stress and several signal transduction pathways.

Smoking impairs endothelial function in human saphenous vein in an ex vivo model.

The aim of this ex vivo experimental study was to assess the effect of smoking, diabetes mellitus, and hypertension on endothelial function in human saphenous vein, a commonly used conduit for coronary and peripheral arterial bypass surgery. A segment of long saphenous vein harvested during infrainguinal bypass surgery was mounted in an organ bath for isometric tension studies. Vein rings were precontracted to submaximal contraction with phenylephrine, followed by endothelium-dependent relaxation with acetylcholine. Long saphenous vein segments were collected from 26 patients, including five females, with a mean age of 66.4 years (range 48-92). Current smokers had impaired endothelium-dependent relaxation compared to ex- and nonsmokers (10.2%, n=13, vs. 32.9%, n=13; p<0.010). However, ex-smokers and nonsmokers did not have a significant difference in relaxant responses to acetylcholine (29.1%, n=8, vs. 24.6%, n=5; p=nonsignificant [ns]). Similarly, diabetic and nondiabetic patients did not show a significant difference in endothelium-dependent relaxation (23.1%, n=10, vs. 15.6%, n=16; p=ns). The relaxant responses in hypertensive and normotensive patients were not different (20.4%, n=12, vs. 22.5%, n=14; p=ns). Smoking has a deleterious effect on the endothelial function of saphenous vein, and smoking cessation may improve the long-term durability of saphenous vein used as a bypass graft in patients undergoing arterial reconstruction.

Comparison of the superb microvascular imaging technique and the color Doppler techniques for evaluating children's testicular blood flow.

OBJECTIVE: We have compared conventional Color Doppler (CD) and Power Doppler (PD) techniques, which are used for evaluating the testicular blood flow in small children, and the Superb Microvascular Imaging (SMI), which is a new technique. We have also investigated their contributions to testicular evaluations. PATIENTS AND METHODS: We evaluated blood flow in testicles using a grading system with CD, PD and SMI techniques. We determined the average duration of the three techniques. RESULTS: There was a statistically significant difference between the SMI and CD techniques for all patients (p < 0.001, p = 0.001). When we compared the PD and SMI, either as much or more vascular information was obtained (p = 0.106). There was a statistically significant difference between the application durations of the tests (p < 0.05). CONCLUSIONS: Superb Microvascular Imaging yields more detailed vascular information in blood flow in testicles in small children, than either CD or PD. Furthermore, this technique decreases the duration of the examination at a significant level. Superb Microvascular Imaging may represent an alternative method that can be used safely for evaluating blood flow in the testicles of small children. Additional studies may increase the reliability of SMI.

Selective dysregulation of nitric oxide synthase type 3 in cardiac myocytes but not coronary microvascular endothelial cells of spontaneously hypertensive rat.

OBJECTIVE: Recent studies indicate that endothelial type nitric oxide synthase (NOS3) modulates cardiac systolic and diastolic function and the inotropic responsiveness to beta-adrenergic agonists, and may affect myocardial oxygen consumption. Although NOS3 is a constitutive protein, its levels of expression can be modified by various physiological and pathophysiological stimuli. We investigated whether the cell-specific expression of NOS3 mRNA and protein are altered in cardiac hypertrophy. METHODS: Left ventricular cardiac myocytes and coronary microvascular endothelial cells were freshly isolated from 12 week old male spontaneously hypertensive rat (SHR) and matched normotensive Wistar rat hearts. NOS3 protein levels were assessed by Western analysis, and mRNA levels by RT-PCR and Southern blotting. RESULTS: Left ventricular/body weight ratios were significantly increased in SHR compared to Wistar controls, indicating significant hypertrophy. The levels of NOS3 protein were markedly decreased in SHR compared to Wistar cardiac myocytes (by approximately 85%). By contrast, the expression of NOS3 mRNA normalized for GAPDH was increased approximately 3 fold in SHR cardiac myocytes relative to Wistar controls. In freshly isolated microvascular endothelial cells, however, levels of NOS3 protein and NOS3 mRNA were similar between the two groups. CONCLUSIONS: The expression of NOS3 is selectively altered in cardiac myocytes but not coronary microvascular endothelial cells of young SHR hearts, with a marked decrease in NOS3 protein but an increase in NOS3 mRNA. This dysregulation of NOS3 could contribute to contractile dysfunction in left ventricular hypertrophy.

Expression of functional neutrophil-type NADPH oxidase in cultured rat coronary microvascular endothelial cells.

OBJECTIVES: The production of reactive oxygen species (e.g., superoxide) by endothelial cells is relevant to tissue injury during ischemia-reperfusion, and may also play a role in intracellular signaling pathways. However, the molecular identities of the enzymes responsible for endothelial superoxide production are poorly defined, although xanthine oxidase, NADH/NADPH oxidoreductases and nitric oxide synthase are among proteins suggested to contribute. Recent studies suggest that an NADH/NADPH oxidase similar to that found in neutrophils is an important source of superoxide in vascular smooth muscle. METHODS: We investigated whether a phagocyte-type NADH/NADPH oxidase complex is present in rat cultured coronary microvascular endothelial cells. The expression of NADPH oxidase components was studied by RT-PCR and Western blot analyses, while functional activity was assessed by measurement of superoxide production by lucigenin-enhanced chemiluminescence. RESULTS: The major component of the phagocyte-type NADH/NADPH oxidase complex, a cytochrome b558 heterodimer, was shown to be present both at mRNA and protein levels, using oligonucleotide primers designed from published neutrophil and vascular smooth muscle sequences and anti-neutrophil antibodies respectively. Functional activity of the enzyme was also confirmed by NADPH-evoked superoxide production in cell homogenates, which was inhibited either by the superoxide chelator Tiron or by diphenyleneiodonium, an inhibitor of the oxidase. CONCLUSIONS: A functional phagocyte-type NADPH oxidase is expressed in coronary microvascular endothelial cells, where it may contribute to the physiological and/or pathophysiological effects of reactive oxygen species. These data, together with reports of the presence of a similar oxidase in other non-phagocytic cell types, suggest that this enzyme complex is widely expressed in many tissues where it may subserve signaling and other functions.

Aprotinin impairs endothelium-dependent relaxation in rat aorta and inhibits nitric oxide release from rat coronary endothelial cells.

OBJECTIVE: Aprotinin, a non-specific serine protease inhibitor, reduces postoperative bleeding after coronary artery surgery. The mechanism of action for this 'blood-sparing' effect of aprotinin is only partially clarified. We therefore aimed to investigate the effect of aprotinin on the release of nitric oxide (NO), a vasodilator and antiaggregant factor, from rat coronary microvascular endothelial cells and on the NO-mediated endothelium-dependent relaxation of rat thoracic aorta. METHODS: Endothelium-intact and endothelium-denuded thoracic aortic rings from Wistar rats (250-300 g) were suspended in organ chambers. Contractile and relaxant responses in the absence and presence of aprotinin (125, 250 and 500 KIU/ml) were recorded via a mechanotransducer. Coronary microvascular endothelial cells (CMEC) were isolated on a Langendorff system by collagenase perfusion of the hearts from the same rats. Calcium ionophore- (1 microM) induced release of NO from confluent cells was determined spectrophotometrically by measuring its stable metabolites, nitrite and nitrate, via Griess reaction. RESULTS: Aprotinin selectively enhanced phenylephrine-induced contractions in endothelium-intact rat thoracic aortic rings, but not in the endothelium-denuded rings. The use of a nitric oxide synthesis inhibitor Nomega-nitro-L-arginine methyl ester (100 microM) on endothelium-intact rings produced a similar increase in phenylephrine-induced contractions. KCl-induced contractions remained unaltered. Aprotinin inhibited acetylcholine-, calcium ionophore- and L-arginine-induced endothelium-dependent relaxations, but not sodium nitroprusside-induced endothelium-independent relaxation. Aprotinin had no significant effect on basal nitrite-nitrate release from CMEC, while it inhibited calcium ionophore-induced total nitrite accumulation in the supernatants. CONCLUSION: Aprotinin selectively impairs endothelium-dependent relaxation as well as basal NO availability in rat thoracic aortic rings and inhibits NO release from rat CMEC. This effect of the drug may contribute to its 'blood-sparing' action and may also account for the increase in perioperative restenosis risk observed in clinical practice during aprotinin therapy.

Phenotypic changes in rat and guinea pig coronary microvascular endothelium after culture: loss of nitric oxide synthase activity.

OBJECTIVES: Coronary microvascular endothelial cells (CMVEs) can modulate the contractile performance of the adjacent myocardium by the release of agents such as nitric oxide (NO). Most previous studies using CMVEs have been done in situ, in the intact organ. We set out to study possible differences in NO synthase (NOS) regulation between freshly isolated and cultured rat and guinea pig CMVEs. METHODS: CMVEs were isolated from Wistar rats and Dunkin Hartley guinea pigs and then grown in culture for varying times. Fura-2 fluorescence was used to measure agonist-induced changes in CMVE intracellular calcium levels. Agonist-induced changes in CMVE cGMP levels were measured by commercial radioimmunoassay kit. Western blot analysis was used to measure endothelial, constitutive NOS (ecNOS) and soluble guanylate cyclase (sGC) protein levels. Reverse transcription, polymerase chain reactions and Southern blotting were used to measure ecNOS mRNA transcripts. RESULTS: In both fresh (1 h post-isolation) and cultured (14 days with one passage) CMVEs of the rat and guinea pig, bradykinin (BK) and the calcium ionophore A23187 (both 1 microM) elicited significant (P < 0.01) increases in the fura-2 340/380 fluorescence ratio. In cultured CMVEs, basal cGMP levels were unaffected by exposure to BK or A23187. Exposure to sodium nitroprusside (SNP) or atrial natriuretic peptide (ANP) (both 1 microM) induced significant (P < 0.01) increases in cGMP in guinea pig cells, whereas in rat cells only ANP produced a significant (P < 0.01) response. By contrast, freshly isolated CMVEs of both species had higher basal cGMP levels than cultured cells, and on exposure to BK and A23187, responded with significant (P < 0.01) increases in cGMP. Moreover, exposure of both fresh rat and guinea pig CMVEs to SNP or ANP also resulted in significant (P < 0.01) increases in cGMP. Western blot analysis demonstrated that ecNOS and sGC protein were lost from the rat CMVEs following culture. Furthermore, there was also a significant loss of ecNOS mRNA from the rat cells following culture. CONCLUSIONS: These data demonstrate that freshly isolated rat and guinea pig CMVEs possess ecNOS activity, and that this activity is downregulated following culture. At least for the rat, this effect would seem to lie at both the transcriptional and translational level. Furthermore, rat CMVEs have reduced activity of sGC following culture.

Oxidative stress and its role in the pathogenesis of ischaemic stroke.

Stroke is one of the leading causes of mortality and morbidity, with astronomical financial repercussions on health systems worldwide. Ischaemic stroke accounts for approximately 80-85% of all cases and is characterised by the disruption of cerebral blood flow and lack of oxygen to the affected area. Oxidative stress culminates due to an imbalance between pro-oxidants and antioxidants and consequent excessive production of reactive oxygen species. Reactive oxygen species are biphasic, playing a role in normal physiological processes and are also implicated in a number of disease processes, whereby they mediate damage to cell structures, including lipids, membranes, proteins, and DNA. The cerebral vasculature is a major target of oxidative stress playing a critical role in the pathogenesis of ischaemic brain injury following a cerebrovascular attack. Superoxide, the primary reactive oxygen species, and its derivatives have been shown to cause vasodilatation via the opening of potassium channels and altered vascular reactivity, breakdown of the blood-brain barrier and focal destructive lesions in animal models of ischaemic stroke. However, reactive oxygen species are involved in normal physiological processes including cell signalling, induction of mitogenesis, and immune defence. Primarily, this review will focus on the cellular and vascular aspects of reactive oxygen and nitrogen species generation and their role in the pathogenesis of ischaemia-reperfusion phenomena. Secondly, the proposed mechanisms of oxidative stress-related neuronal death will be reflected upon and in summation specific targeted neuroprotective therapies targetting oxidative stress and their role in the pathogenesis of stroke will be discussed.

Carotid intima-media thickness: is it correlated with stroke side?

OBJECTIVE: The objective of the present study was to investigate the possible correlation between the common carotid artery (CCA) intima-media thickness (IMT) and the infarct side. METHOD: The CCA IMTs in patients with atherosclerotic non-lacunar stroke were measured. RESULTS: The mean age of the patients was 64.3 +/- 10.7 years (range 40-83 years) and 42 of 100 patients were male. The infarcts were at the left side in 53 patients and at the right side in 47 patients. The mean CCA IMT was 1.02 +/- 0.18 mm at the infarct side and 0.87 +/- 0.17 mm at the contralateral side. The difference between them was statistically significant (P < 0.01). Although the mean age of the patients with a left-sided infarct was greater than that of the patients with a right-sided infarct, the difference was not statistically significant. CONCLUSION: Our results suggest that CCA IMT may be used in prediction of possible infarct side, and in the prediction of potential risk of stroke by evaluating the IMT of both CCAs separately.