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At least 721 records · Page 40Linked to original sources
PubMed2000

Large artery vasculopathy in HIV-positive patients: another vasculitic enigma.

Human immunodeficiency virus (HIV) infection has impacted on all the systems of the body, and the cardiovascular system is no exception, with small to medium-sized vessel vasculitis being most frequently described. We present 16 HIV-positive patients with large vessel disease consisting of either aneurysms (often multiple) or occlusive disease. Nine men and 7 women ranging in age from 18 to 38 years presented with rupture of aneurysm, transient ischemic attacks, hypertension, ischemia to the lower extremity, or a mass at the site of the aneurysm. Eight patients had 1 aneurysm, 2 had 2 lesions, and the remaining 6 cases had from 3 to 7 aneurysms. Arteries affected included the common carotid, abdominal aorta, common iliac, femoral, and popliteal. Three patients had intercurrent infections, but none had any obvious infective vascular lesion. Only 1 patient had a positive TPHA test for syphilis. Microbiologic culture of both blood and thrombus contents was positive for Staphylococcus aureus in 1 case; no other organisms were cultured. The key histological features were within the adventitia: leukocytoclastic vasculitis of the vasa vasora and periadventitial vessels, proliferation of slit-like vascular channels, chronic inflammation, and fibrosis. There was associated medial fibrosis with loss and fragmentation of muscle and elastic tissue. Intimal changes consisted of duplication and fragmentation of the internal elastic lamina with calcification. Atheroma and marked intimal thickening were not evident We believe that the occurrence of this large vessel vasculopathy (mainly aneurysmal) often with multiple lesions in young HIV-positive patients, is characteristic of possible infective or immune complex origin, with leukocytoclastic vasculitis of vasa vasora and periadventitial vessels being pivotal in many cases.

Adolescent↗
PubMed2000

Giant cell arteritis and Takayasu aortitis: morphologic, pathogenetic and etiologic factors.

Overlapping features among aortitides are relatively common although the underlining etiologies may differ. Thus, the clinical classification of aortitides is rather difficult and often misleading. Furthermore, morphologic characterizations of these vascular disorders are frequently overlapping and therefore additional clinical and radiologic information is usually required. The greater challenge is aortitides is whether the initiation is due to an exogenous stimulus or due to an autoantigen.

Aorta↗
PubMedDate not supplied

The corrupted feedback hypothesis.

This paper argues that varicose veins are caused by a feedback malfunction. The feedback in question regulates the tone of the vein by dilating it as needed, using noradrenaline (NA), tapped from the circulating pool, for the purpose. The drug, though conventionally classified as a venoconstrictor, dilates the vein when it diffuses from the vasa venarum of the vein into the vein's media; the drug having reached the vasa by reflux from the vein lumen. A varicosity is created when a factor increases the volume of reflux, and, therefore, the quantity of NA, perfusing a unit of the vasa network, selectively. The resultant, exaggerated, localised, dilator effect that the NA has on a section of the vein, constitutes the varicosity radix. In brief, a varicosity, when first created, is seen as being an exaggerated, but appropriate, dilator response of a section of a normal vein to an inappropriate, corrupted, feedback signal. The acute varicosity is believed to transform into the permanent type seen in varicose veins if the factor responsible for it persists long enough.

Endothelium, Vascular↗
PubMed1991

An analysis of the effect of tooth intrusion on the microvascular bed and fenestrae in the apical periodontal ligament of the rat molar.

An analysis of the rat apical periodontal ligament (PDL) microvascular bed and fenestrae was conducted to evaluate the effect of a continuous 1.0 N intrusive tooth load for 30 minutes. The microvascular bed consisted of postcapillary-sized venules, venous and arterial capillaries, and terminal arterioles. Intrusion produced significant increases (p less than 0.01) in vascular volume for postcapillary-sized venules and venous capillaries in three of the four animals. Arterial capillaries, overall, showed a statistically significant increase (p less than 0.01). The endothelial surface area (micron2 x 10(6)) per cubic millimeter of PDL responded variably in postcapillary-sized venules and venous capillaries but showed a strong trend to increase in arterial capillaries. After tooth intrusion a significant reduction (p less than 0.01) occurred in the number of fenestrae per square micrometer of endothelium in postcapillary-sized venules and venous capillaries. Fenestrae in the control PDL had a mean diameter of 51.5 nm +/- 0.6 (SE), whereas those on the intrusion side were smaller (p less than 0.05), measuring 49.9 nm +/- 0.4 (SE).

Animals↗
PubMed1986

The natural history of endothelial structure and function in arterialized vein grafts.

When the saphenous vein is used in the in situ position for arterial bypass surgery, it is associated with more optimal preservation of the endothelial lining and with improved graft patency compared with reversed vein grafts. However, it is not clear whether preservation of endothelial integrity persists after arterialization. The goal of this study was to establish whether preservation of the endothelium before arterialization is a critical factor in the development of late functional and morphologic abnormalities of autogenous vein grafts. Paired reversed and in situ vein grafts were created in 75 mongrel dogs. Veins to be used in the reversed position were excised and stored in either heparinized whole blood at 37 degrees C or saline solution at 4 degrees C. Veins were studied before and after arterialization. The veins were arterialized by anastomosis to the carotid artery and excised at intervals of 1 day to 12 weeks for studies of the luminal production of prostacyclin and thromboxane A2 in addition to luminal morphology. Before arterialization, normothermic whole blood preserved biochemical function of the endothelium significantly better than hypothermic saline solution, but not as well as the in situ vein procedure. Soon after arterialization, all three vein grafts showed significant functional and morphologic abnormalities consistent with injury of the vein graft. Morphologic healing of the endothelial monolayer progressed slowly back to normal; however, the biochemical capacity of the vein graft never matched that of the prearterialized vein, nor that of normal host arteries. Regardless of surgical technique, all vein grafts exhibited a period of abnormal structure and function, which exposed them to the risk of thrombogenesis. This period of potential leukocyte or platelet interaction with the vein wall could lead to release phenomena as well as proliferative changes in the vessel wall.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Expression of receptors for advanced glycation end-products in occlusive vascular and renal disease.

Formation and deposition of advanced glycation end-products (AGEs) has been linked to late diabetic complications. Interactions of AGEs are at least partly mediated by binding of AGEs to their cellular surface receptor RAGE. This review summarizes the immunohistological data obtained for RAGE distribution in vessel segments of diabetic and non-diabetic patients with peripheral occlusive vascular disease and in kidneys of patients with diabetic nephropathy, and inflammatory and non-inflammatory renal disease. It is demonstrated that increased RAGE expression is not restricted to diabetes mellitus but contributes to a range of vascular and renal disorders.

Diabetic Angiopathies↗
PubMedDate not supplied

Experimental hepatic artery embolization with Gelfoam powder. Microfil perfusion study of the rabbit liver.

After hepatic artery embolization with Gelfoam powder in five rabbits, two colors of Microfil (silicone rubber solution) were perfused into the aorta and the portal vein to study hepatic microcirculation under a dissection microscope. In three of the animals, many intrahepatic arterial branches and portions of the hepatic sinusoids were perfused with the arterial Microfil (orange color), whereas in the other two animals no orange Microfil was found in the liver. In the three animals, occlusions of the hepatic artery were random in distribution and often segmental, and arteries as small as 50 microns in diameter were involved. In the latter group, levels of arterial occlusion could not be evaluated. Microcollaterals developed through the capsular artery, peribiliary arterial plexus, and vasa vasora of the portal vein.

Animals↗
PubMed1998

Accompanying arteries of the cutaneous veins and cutaneous nerves in the extremities: anatomical study and a concept of the venoadipofascial and/or neuroadipofascial pedicled fasciocutaneous flap.

The arterial anatomy of the accompanying arteries of the cutaneous veins and cutaneous nerves in the extremities was investigated in 10 fresh cadavers that had been injected with a lead oxide-gelatin mixture throughout the entire body. It is well known that cutaneous nerves have neurocutaneous perforators, but it was found that cutaneous veins also have their own accompanying arteries as well. The accompanying arteries of the cutaneous veins had branches not only to the vein wall, but also to the skin, i.e., venocutaneous perforators. Based on these findings, the concept of the adipofascial pedicled fasciocutaneous flap using the accompanying arteries of the cutaneous veins, cutaneous nerves, or both was proposed.

Adipose Tissue↗
PubMed1996

Plasminogen activators in abdominal aortic aneurysmal disease.

Abdominal aortic aneurysms (AAA) are characterized by the destruction of the extracellular matrix (ECM) of the aortic wall, particularly its elastin elements. The fibrinolytic system is known to mediate proteolysis within the ECM. Plasmin, which is generated by plasminogen activators (PA), is capable of destroying the ECM directly and indirectly via the activation of latent matrix metalloproteases (MMP). In addition, plasmin also synergistically enhances the ability of macrophages to destroy ECM. In AAA tissue, elevated levels of both urokinase-type and tissue-type plasminogen activators (u-PA and t-PA) have been documented. u-PA and t-PA have been localized to macrophages within the inflammatory infiltrate which is characteristic of AAA. mRNA expression of both type PAs is elevated as well in comparison to both normal and atherosclerotic occlusive aorta. Supporting the role of PAs in AAA pathogenesis is the fact that plasmin is elevated in AAA tissue, as are MMP. As with PA, MMP expression has been localized to macrophages. These data all suggest that the aortic wall is being degraded in AAA by a synergistic combination of macrophages, PA, and MMP.

Aortic Aneurysm, Abdominal↗