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PubMed2004

The powerful microbubble: from bench to bedside, from intravascular indicator to therapeutic delivery system, and beyond.

This review discusses the development, current applications, and therapeutic potential of ultrasound contrast agents. Microbubbles containing gases act as true, intravascular indicators, permitting a noninvasive, quantitative analysis of the spatial and temporal heterogeneity of blood flow and volumes within the microvasculature. These shelled microbubbles are near-perfect reflectors of acoustic ultrasound energy and, when injected intravenously into the bloodstream, reflect ultrasound waves within the capillaries without disrupting the local environment. Accordingly, microbubble ultrasound contrast agents are clinically useful in enhancing ultrasound images and improving the accuracy of diagnoses. More recently, ultrasound contrast agents have been used to directly visualize the vasa vasorum and neovascularization of atherosclerotic carotid artery plaques, thus suggesting a new paradigm for diagnosis and treatment of atherosclerosis. Future applications of these microscopic agents include the deliver of site-specific therapy to targeted organs in the body. Medical therapies may use these microbubbles as carriers for newer therapeutic options.

Animals↗
PubMed2003

Shear modulus of porcine coronary artery: contributions of media and adventitia.

The epicardial coronary arteries experience significant torsion in the axial direction due to changes in the shape of the heart during the cardiac cycle. The objective of this study was to determine the torsional mechanical properties of the coronary arteries under various circumferential and longitudinal loadings. The coronary artery was treated as a two-layer composite vessel consisting of intima-medial and adventitial layers, and the shear modulus of each layer was determined. Eight porcine hearts were obtained at a local abattoir, and their right coronary and left anterior descending arteries were isolated and tested in vitro with a triaxial torsion machine (inflation, longitudinal stretch, and circumferential twist). After the intact vessel was tested, the adventitia was dissected away, leaving an intact media that was then tested under identical triaxial loading conditions. We proposed a biomechanical analysis to compute the shear modulus of the adventitia from the measured shear moduli of the intact vessel and the media. To validate our predictions, we used four additional hearts in which the shear modulus of the adventitia was measured after dissection of media. Our results show that the shear modulus does not depend on the shear stress or strain but varies linearly with circumferential and longitudinal stresses and in a nonlinear way with the corresponding strains. Furthermore, we found that the shear modulus of the adventitia is larger than that of the intact vessel, which is larger than the vessel media. These results may have important implications for baroreceptor sensitivity, circulation of the vasa vasorum, and coronary dissection.

Animals↗
PubMed1982

Arterial wall oxygen consumption rate varies spatially.

The ratio of the O2 consumption rate (Q) to the O2 transmissibility (diffusivity-solubility product, Dk) was estimated by curve-fitting O2 tension profiles measured in vascular strips in vitro and in blood vessels in vivo. For rabbit aortic tissue in vitro, Q/Dk was 2.51 +/- 0.28 (SE) X 10(5) Torr/cm2 (n = 9). For various dog vessels in vivo, Q/Dk ranged from 0.15 to 47 X 10(5) Torr/cm2. In most cases, Q/Dk was higher near the endothelium than in the outer wall. This difference appears to be caused by a higher Q. Computer simulations using a two-layer O2 transport model with estimated Q/Dk indicate that the O2 supply from the vasa vasorum is essential to prevent medial wall hypoxia.

Animals↗
PubMed1997

Lung capillary changes in hepatic cirrhosis in rats.

The hypoxemia of the hepatopulmonary syndrome may result from dilated intrapulmonary vascular segments. Knowledge of the size, density, and branching frequency of the lung capillaries might confirm this hypothesis and suggest that the pathogenesis may involve vascular dilatation or angiogenesis. To investigate these changes, the common bile duct of rats was tied off to cause biliary cirrhosis. Later (4 wk), the pulmonary vasculature of these animals was cast, and the casts were studied with scanning electron microscopy. In the ligated animals, evidence for enhancement of the bronchial to pulmonary circulation was found: cast vasa vasorum of the pulmonary arteries and cast bronchial veins emptying into pulmonary veins. Ligated animals had more adherent intracapillary cells per alveolus than the sham-operated animals. The diameters of all capillary beds were larger in the ligated animals. The alveolar capillary density was increased, but the branching frequency was not. A few areas suggesting angiogenesis were found. Induction of biliary cirrhosis enhances the pulmonary-systemic circulation, increases intracapillary adherent cells, capillary diameter, and density, and may be associated with angiogenesis.

Animals↗
PubMed1991

Influence of bronchial arterial PO2 on pulmonary vascular resistance.

In six anesthetized and mechanically ventilated adult sheep, the bronchial artery was perfused with blood from an oxygenator-pump circuit. When the lungs were ventilated with 100% O2 and the bronchial O2 tension (PbrO2) was approximately 600 Torr, the mean of the pulmonary vascular resistances (PVR) measured at the beginning (3.32 +/- 0.29 units) and end (3.17 +/- 0.13 units) of the experiment was 3.24 +/- 0.20 units. When the PbrO2 was changed to 58 +/- 1 Torr, the PVR (2.99 +/- 0.14 units) did not change significantly. However, when the lungs were ventilated with air as PbrO2 was decreased to 91 +/- 4, 77 +/- 3, 56 +/- 2, and 42 +/- 1 Torr, the PVR increased to 3.67 +/- 0.18, 4.03 +/- 0.16, 4.79 +/- 0.19, and 4.71 +/- 0.35 units, respectively. However, when the PbrO2 was decreased further to 26 +/- 1 and 13 +/- 1 Torr, the PVR decreased to 3.77 +/- 0.28 and 3.91 +/- 0.30 units, respectively. In contrast, the bronchial vascular resistance decreased monotonically as PbrO2 decreased. The bronchial circulation supplies vasa vasorum to the walls of all but the smallest pulmonary arteries, and it is therefore suggested that the PO2 of the bronchial circulation is responsible for the bimodal response of the pulmonary vasculature, with stimulation of hypoxic pulmonary vasoconstriction at moderate hypoxemia and of hypoxic pulmonary vasodilation at profound hypoxemia. The physiological and pathophysiological significance of the influence of systemic PO2 on pulmonary vascular tone is discussed.

Animals↗
PubMed2000

Takayasu arteritis and cutaneous necrotizing vasculitis.

Takayasu arteritis (TA) is an inflammatory arteriopathy involving predominantly the aorta and its main branches. The disease evolves in two phases: a first, nonspecific inflammatory stage and a late 'pulseless' stage, in which complications related to arterial stenosis and aneurysm formation predominate. In both phases, skin manifestations, such as inflammatory nodules, erythema-nodosum- and pyoderma-gangrenosum-like ulcers, have been described. We report 2 patients with TA, who had cutaneous necrotizing vasculitis as presenting manifestation of the disease. A review of the literature revealed 8 similar cases. TA does not only involve large arteries, but also small blood vessels. The observation that in TA the inflammatory process of the large arteries affects regions of the walls supplied by the vasa vasorum, the anatomy of which bears resemblance to the cutaneous vessel system, suggests that primary involvement of small vessels contributes to the development of the clinicopathological features of TA. Knowledge of the skin manifestations associated with TA remains important for its diagnosis and prompt instauration of life-saving treatment.

Adult↗
PubMed1979

The physiopathogenetic basis for the angiographic diagnosis of bacterial infections of the brain and its coverings in children. I. Leptomeningitis.

This is a descriptive analysis of the angiographic characteristics of leptomeningeal infections in 36 children and a correlation of these angiographic observations with anatomopathologic changes. Vascular, meningeal and parenchymal changes are described and discussed. In the normal situation, tracer protein particles injected into the subarachnoid space perfuse easily through the extracellular spaces but stop at the outer continuous arachnoidal layer. The parenchymal layer, pia-arachnoid, on the other hand, consists of a uni or pluricellular layer which is regularly crossed by tracer particles. Though the internal carotid, vertebral and basilar arteries have some anatomical characteristics: thinner tunica media and adventitia, the absence of vasa vasorum and the presence of a fluid cushion (CSF) in which they are bathed. The most striking angiographic observation in leptomeningitis is the transmural extravasation of the contrast meding 'halo' formation. Long after the cerebral circulation time, one may identify contrast media 'pooling' within the cisterns and sulci.

Acute Disease↗
PubMed1982

Specific endothelial granules in venous patch neoendothelium in the rat.

Weibel-Palade bodies were observed in the neoendothelium and capillaries of vasa vasorum of autologous 'venous patches' grafted in the common carotid artery of the rat. These corpuscles varied in number and distribution but were most frequently found in the luminal area of endothelial cytoplasm. In venous patch neoendothelium, the shape, size and substructure of Weibel-Palade bodies were similar to those in other types of vascular endothelium. These specific endothelial granules were more numerous during the week following neoendothelium formation. It is proposed that these corpuscles may play a role in the proliferation of endothelial cells in venous patches.

Animals↗
PubMed1989

The pathophysiology of acute myocardial infarction.

Recent work has now clearly established that coronary arterial thrombosis is the direct cause of acute myocardial infarction. This thrombotic event occurs when a pre-existing atherosclerotic plaque ruptures or fissures, thereby exposing underlying thrombogenic material to the circulation. Platelets are thus activated and the clotting cascade is initiated. It is as yet unclear why a previously stable atherosclerotic plaque should fissure or rupture. However, suggested mechanisms include release of vasoactive substances from activated platelets, coronary arterial vasomotion, mechanical stress fatigue of the atherosclerotic plaque, and rupture of vasa vasorum within the atherosclerotic plaque. The resultant cessation of myocardial blood flow produces specific biochemical and physiological alterations secondary to myocardial ischemia. Intracellular acidosis, loss of high-energy phosphates, reduced sensitivity of contractile proteins to calcium, and accumulation of inorganic phosphate and lipid, all occur within the ischemic myocyte. Diastolic compliance is markedly reduced by ischemia followed by cessation of systolic contractile activity. Most of these alterations are reversible if ischemia is relieved promptly. Prolonged ischemia leads to delayed biochemical and physiological recovery and/or cell necrosis.

Collateral Circulation↗
PubMedDate not supplied

Long-term behavior of an arterial autograft: a new role for intimal hyperplasia?

The long-term behavior of an arterial autograft was studied with special attention to the evolution of intimal hyperplasia. An arterial autograft measuring approximately 5 mm in length was implanted in the right common iliac artery of female Sprague-Dawley rats. Animals were sacrificed at 90, 120, 150, 180, 240, 360, 400, 540 and 730 days after implantation. Grafts were evaluated by optical microscopy, electron microscopy, and morphometry. Myointimal cells were marked using an antiactin monoclonal antibody and studied by transmission electron microscopy. In the long term, the myointima of the arterial wall appeared as a consolidated layer formed by smooth muscle cells of contractile phenotype, abundant extracellular material consisting of clumps of elastin and collagen fibers. Cell maturity and degree of differentiation were demonstrated by the incorporation of antiactin antibody. The medial layer of the grafted segment suffered a marked long-term loss of cells and became an acellular layer sustained by the elastic layers. The adventitial layer was markedly cellular and had abundant vasa vasorum. Morphometry showed that the myointimal layer in the operated territory was not uniform and consisted of tongues of varying thickness. The total thickness of the arterial wall did not differ significantly (p > 0.05) between the graft and the proximal and distal areas. The results suggest that the intimal hyperplasia originating during the repair process could assume some functions of the degenerated medial layer, maintaining long-term vascular homeostasis.

Animals↗
PubMed1976

Distribution and variation of fibrinolytic activity in the walls of human arteries and veins.

A systematic study on the location and intensity of the fibrinolytic activity in more than 500 samples of human arteries and veins from 50 routine necropsies and 35 blood vessel biopsies was performed. Data were obtained for an overall comparison of the fibrinolytic activity along and across the walls of human blood vessels by the use of a standardized fibrin slide technique. Arteries generally showed little or no fibrinolytic activity in the intima and media but strong activity in the adventitia. Veins showed a comparable strong fibrinolytic activity in the external layer of loose connective tissue. Fibrinolytic activity in the venous intima, media and adventitia was generally weaker but varied greatly according to position in the body. Veins situated in the lower parts of the body had less fibrinolytic activity than the veins at the upper levels. Fibrinolytic activity was found to be related to the endothelium of the vasa vasorum and/or of the main lumen of the vascular wall. Increased fibrinolytic activity was observed in arteries and veins in cases of sudden death, vasogenic shock, cerebral hemorrhage and cirrhosis. Decreased fibrinolytic activity was encountered in blood vessels in cases of endotoxin shock, hyaline membrane disease and a case of Waterhouse-Friderichsen syndrome.

Arteries↗
PubMed2006

IL-20 is expressed in atherosclerosis plaques and promotes atherosclerosis in apolipoprotein E-deficient mice.

OBJECTIVE: Atherosclerosis is a chronic inflammatory disease with immune cell infiltration. Various cytokines and chemokines have been characterized as pro- or antiatherogenic factors. Interleukin-20 (IL-20) belongs to the IL-10 family and is a proinflammatory cytokine involved in the pathogenesis of psoriasis. However, the association between IL-20 and atherosclerosis is undetermined. Therefore, we sought to investigate whether IL-20 is associated with atherosclerosis. METHODS AND RESULTS: We examined the expression of IL-20 and its receptor complex IL-20R1/IL-20R2 in atherosclerotic lesions of humans and mice using immunohistochemical staining. IL-20 was expressed in macrophage-rich areas. Both IL-20 and IL-20R1/IL-20R2 were expressed by endothelial cells lining the intimal microvessels, vasa vasorum, but rarely in nonatherosclerotic arteries. We used reverse-transcription polymerase chain reaction to analyze gene expression. IL-20 transcripts increased in hypoxic monocytes and monocytes treated with oxidized low-density lipoprotein. The expression of IL-20R1 and IL-20R2 was also upregulated by human umbilical vein endothelial cells in response to hypoxic treatment. Incubating IL-20 with human umbilical vein endothelial cells upregulated CXCL9 and CXCL11 transcripts. Furthermore, in vivo administration of IL-20 expression vector using intramuscular electroporation promoted atherosclerosis in apolipoprotein E-deficient mice. CONCLUSIONS: Our data suggest that IL-20 is a proatherogenic cytokine that contributes to the progression of atherosclerosis.

Animals↗
PubMedDate not supplied

Different efflux pathways for high and low density lipoproteins from porcine aortic intima.

To study the efflux of high (HDL) and low (LDL) density lipoproteins from the arterial wall in vivo, a surgical model in pigs was used. An isolated segment of the lesion-free thoracic aorta was pulse labeled from the lumen of the artery with 3H-cholesteryl ester labeled HDL and 14C-cholesteryl ester labeled LDL. Subsequently, the labeled aortic segment was exposed to cold chase in vivo. The transfer of HDL cholesteryl ester from plasma into intima expressed as intimal clearance was three to seven times greater than that of LDL cholesteryl ester. At least 50%, but possibly as much as 95%, of the HDL cholesteryl ester that entered the arterial intima during a period of 4 hours penetrated the arterial wall beyond the internal elastic lamina. In contrast, less than 15% of the LDL cholesteryl ester that entered the arterial intima in the same period penetrated beyond the luminal layer. After 24 hours of cold chase in vivo, more than 80% of both labeled HDL esterified cholesterol and labeled LDL esterified cholesterol had disappeared from the arterial wall. Transmural profiles after 9 hours of cold chase showed that labeled HDL was present throughout the entire arterial wall, whereas labeled LDL in quantitative amounts was present only in the luminal layer. The results suggest that the most important efflux route for HDL esterified cholesterol is through the vasa vasorum and lymphatics in the outer media and adventitia, whereas LDL esterified cholesterol predominantly leaves intima via the lumen of the artery.

Animals↗
PubMed1994

Expression of LDL receptor-related protein/alpha 2-macroglobulin receptor in human normal and atherosclerotic arteries.

Low-density lipoprotein receptor-related protein/alpha 2-macroglobulin receptor (LRP/alpha 2-MR) is a multifunctional cell-surface receptor that is responsible for the clearance of lipoprotein remnants, proteases, or cytokines/growth factors in complex with alpha 2-macroglobulin as well as of plasminogen activators complexed with inhibitors. We investigated the expression of LRP/alpha 2-MR in healthy and atherosclerotic human arteries by in situ hybridization using an LRP/alpha 2-MR mRNA-specific riboprobe and immunocytochemistry using specific monoclonal antibodies. The cell types expressing LRP/alpha 2-MR were identified by immunolabeling of antigens specific for endothelial cells, smooth muscle cells, and macrophages. In normal arteries, LRP/alpha 2-MR mRNA and protein were found in smooth muscle cells of the media and vasa vasorum and in adventitial fibroblasts. Endothelial cells were negative for LRP/alpha 2-MR protein but positive for its mRNA. Atherosclerotic arteries exhibited a strong labeling for LRP/alpha 2-MR mRNA and protein that was observed in intimal smooth muscle cells exhibiting normal or foam cell characteristics and in lipid-laden cells positive for macrophage markers. A particularly high expression was detected in macrophages located in the cap of the lipid-rich necrotic core. These results suggest that cellular components of the atherosclerotic plaque express LRP/alpha 2-MR. This receptor may play an important local scavenger role for lipoprotein remnants, for growth factors/cytokines, and for extracellular protease-inhibitor complexes.

Arteries↗
PubMed1995

Plasminogen activator expression in human atherosclerotic lesions.

The plasminogen activator (PA) system may participate in the pathogenesis of atherosclerosis by modulating the turnover of intimal fibrin and extracellular matrix deposits and by contributing to intimal cell migration. We present an analysis of tissue-type PA (tPA) and urokinase-type PA (uPA) expression at three levels: mRNA by in situ hybridization, antigen by immunohistochemistry, and enzymatic activity by histoenzymology and zymography. For PA colocalization with cellular or matrix components, we used double immunofluorescence labeling in conjunction with confocal microscopy. In normal arteries, tPA antigen and mRNA were detected in endothelial cells and smooth muscle cells (SMCs). In atherosclerotic arteries, tPA antigen and mRNA were increased in intimal SMCs and in macrophage-derived foam cells of fibro-fatty lesions. Part of the tPA was detected in the extracellular space and colocalized with fibrin deposits. uPA antigen and mRNA were detected in association with the intimal macrophages and SMCs. A particularly high uPA expression was noted on macrophages localized on the rims of the necrotic core. Moreover, using a novel histoenzymological assay as well as classic zymography, we revealed uPA-dependent lytic activity in the advanced lesions, whereas in normal arteries, only tPA-dependent activity was detected, mainly over the vasa vasorum. Also, strong tPA and uPA staining was detected in neomicrovessels of the plaques, suggesting that PAs may play a role in plaque angiogenesis. Our results suggest a local dynamic process of PA-dependent proteolysis in lesion areas that is associated with macrophages and SMCs. A better comprehension of these proteolytic mechanisms in advanced atherosclerotic plaques may provide the basis for therapeutic approaches for plaque stabilization.

Aorta↗
PubMed1999

Cyclooxygenase-2 is widely expressed in atherosclerotic lesions affecting native and transplanted human coronary arteries and colocalizes with inducible nitric oxide synthase and nitrotyrosine particularly in macrophages.

Inflammation appears to have a major role in the development of atherosclerotic lesions affecting native and transplanted coronary arteries. The subsequent risk of plaque rupture and acute ischemic events correlates with the degree of inflammation and may be modified by aspirin, an anti-inflammatory cyclooxygenase inhibitor. Cyclooxygenase-2 (Cox-2) and inducible nitric oxide synthase (iNOS) are involved in the inflammatory response via the rapid and exaggerated production of prostanoids and nitric oxide, both of which may have proatherosclerotic effects. These effects may be mediated by the formation of peroxynitrite in the case of nitric oxide and involve "cross talk" between the two enzyme systems. This study aimed to investigate native and transplant atherosclerosis for the presence and distribution of Cox-2 and iNOS. Immunocytochemical studies were performed on atherosclerotic lesions from patients with native (n=12) and transplant (n=5) coronary disease by using antibodies to Cox-2, iNOS, and nitrotyrosine (an indicator of peroxynitrite production). Control tissue was obtained from unused donor hearts and at the time of autopsy. Cox-2 and iNOS colocalized predominantly in macrophages/foam cells in both types of atherosclerosis. Cox-2 expression was also detected in medial smooth muscle cells and endothelial cells, including those of the vasa vasorum. Nitrotyrosine was found in the same distribution as that of iNOS and was colocalized with Cox-2 in macrophages. Cox-2 and iNOS are coexpressed in native and transplant atherosclerosis, possibly allowing for interaction between the enzymes and suggesting an alternative mechanism for the benefits of aspirin via inhibition of Cox-2 activity.

Animals↗
PubMed1996

Increased accumulation of tissue ACE in human atherosclerotic coronary artery disease.

BACKGROUND: Angiotensin may play a pathophysiological role in experimental and human cardiovascular disease. Clinical studies have shown that ACE inhibitors reduce mortality, recurrent myocardial infarction, and ischemic events in patients with left ventricular dysfunction. Animal studies suggest that tissue ACE, particularly within blood vessels, may be an important target. METHODS AND RESULTS: To study tissue ACE in human coronary artery disease and to identify potential mechanisms of ACE inhibitor action, we examined ACE expression immunohistochemically in nonatherosclerotic and diseased human coronary arteries. In nonatherosclerotic arteries, ACE immunoreactivity was found in luminal and adventitial vasa vasorum endothelium. In early- and intermediate-stage atherosclerotic lesions, ACE was detected prominently in regions of fat-laden macrophages and in association with T lymphocytes. In advanced lesions, ACE immunoreactivity was also localized to the endothelium of the microvasculature throughout the plaques. Immunoreactive angiotensin II was also detected in these areas. ACE expression in macrophages was further examined by in vitro experiments with a monocytoid cell line. ACE activity was induced threefold after differentiation of the cells into macrophages and was further increased after stimulation with acetylated LDL. CONCLUSIONS: These observations demonstrate that significant sources of tissue ACE in human atherosclerotic plaques are regions of inflammatory cells, especially areas of clustered macrophages as well as microvessel endothelial cells. These results suggest that ACE accumulation within the plaque may contribute to an increased production of local angiotensin that may participate in the pathobiology of coronary artery disease. Plaque ACE probably is an important target of drug action.

Adolescent↗
PubMed1998

Reduced endothelial nitric oxide synthase expression and production in human atherosclerosis.

BACKGROUND: NO regulates vascular tone and structure, platelets, and monocytes. NO is synthesized by endothelial NO synthase (eNOS). Endothelial dysfunction occurs in atherosclerosis. METHODS AND RESULTS: With a porphyrinic microsensor, NO release was measured in atherosclerotic human carotid arteries and normal mammary arteries obtained during surgery. eNOS protein expression was analyzed by immunohistochemistry. In normal arteries, the initial rate of NO release after stimulation with calcium ionophore A23187 (10 micromol/L) was 0.42+/-0.05 (micromol/L)/s (n=10). In contrast, the initial rate of NO release was markedly reduced in atherosclerotic segments, to 0.08+/-0.04 (micromol/L)/s (n=10, P<0.0001). NO peak concentration in normal arteries was 0.9+/-0.09 micromol/L (n=10) and in atherosclerotic segments, 0.1+/-0.03 micromol/L (n=10, P<0.0001). Reduced NO release in atherosclerotic segments was accompanied by marked reduction of immunoreactive eNOS in luminal endothelial cells, although specific endothelial cell markers (CD31) were present (n=13). Endothelial cells of vasa vasorum of atherosclerotic segments, however, remained positive for eNOS, as was the endothelium of normal arteries. CONCLUSIONS: In clinically relevant human atherosclerosis, eNOS protein expression and NO release are markedly reduced. This may be involved in the progression of atherosclerosis.

Aged↗