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PubMed1993

Human smooth muscle myosin heavy chain isoforms as molecular markers for vascular development and atherosclerosis.

Smooth muscle myosin heavy chains (MHCs) exist in multiple isoforms. Rabbit smooth muscles contain at least three types of MHC isoforms: SM1 (204 kD), SM2 (200 kD), and SMemb (200 kD). SM1 and SM2 are specific to smooth muscles, but SMemb is a nonmuscle-type MHC abundantly expressed in the embryonic aorta. We recently reported that these three MHC isoforms are differentially expressed in rabbit during normal vascular development and in experimental arteriosclerosis and atherosclerosis. The purpose of this study was to clarify whether expression of human smooth muscle MHC isoforms is regulated in developing arteries and in atherosclerotic lesions. To accomplish this, we have isolated and characterized three cDNA clones from human smooth muscle: SMHC94 (SM1), SMHC93 (SM2), and HSME6 (SMemb). The expression of SM2 mRNA in the fetal aorta was significantly lower as compared with SM1 mRNA, but the ratio of SM2 to SM1 mRNA was increased after birth. SMemb mRNA in the aorta was decreased after birth but appeared to be increased in the aged. To further examine the MHC expression at the histological level, we have developed three antibodies against human SM1, SM2, and SMemb using the isoform-specific sequences of the carboxyl terminal end. Immunohistologically, SM1 was constitutively positive from the fetal stage to adulthood in the apparently normal media of the aorta and coronary arteries, whereas SM2 was negative in fetal arteries of the early gestational stage. In human, unlike rabbit, aorta or coronary arteries, SMemb was detected even in the adult. However, smaller-sized arteries, like the vasa vasorum of the aorta or intramyocardial coronary arterioles, were negative for SMemb. Diffuse intimal thickening in the major coronary arteries was found to be composed of smooth muscles, reacting equally to three antibodies for MHC isoforms, but reactivities with anti-SM2 antibody were reduced with aging. With progression of atherosclerosis, intimal smooth muscles diminished the expression of not only SM2 but also SM1, whereas alpha-smooth muscle actin was well preserved. We conclude from these results that smooth muscle MHC isoforms are important molecular markers for studying human vascular smooth muscle cell differentiation as well as the cellular mechanisms of atherosclerosis.

Aging↗
PubMedDate not supplied

Transient embolic aorto-arteritis. Presentation of a patient.

The clinical and postmortem data from a 14-year-old girl who had transient embolic aorto-arteritis are presented. This disease was first described in 1974 by Peiris and Wickremasinghe in Hindu patients and is characterized by repetitive embolic occlusion of intra- and extracranial vessels of the brain, originating from focal thrombotic lesions in the aorta and its primary branches. The main histopathological lesion is located in the elastic tissue of the media in these arteries with alterations that vary from mild arteritis of the vasa vasorum to degeneration and destruction of the media which predisposes to aneurysm formation. This new entity apparently affects only adolescents and young adults and has no relation to atherosclerosis or other non-specific arteritides previously described. To our knowledge, this is the first such patient reported in America.

Adolescent↗
PubMed1998

Low glucose enhances Na+/glucose transport in bovine brain artery endothelial cells.

BACKGROUND AND PURPOSE: Brain arteries are structurally characterized by the tight junctions of the endothelium and by no vasa vasorum that feed arteries themselves. This raises the question of how brain arteries are provided with glucose. A possible explanation is that glucose uptake into arteries may be mediated by both GLUT1, a facilitative glucose transporter, and a Na+/glucose cotransporter (SGLT)-like glucose transporter. The functional role for the SGLT-like glucose transporter, however, is unknown. In the present study we investigated SGLT-like glucose transporter-operated glucose uptake into brain arterial endothelial cells by recording glucose-evoked Na+ currents and monitoring uptake of [3H]-2-deoxy-D-glucose ([3H]-2-DOG). METHODS: Endothelial cells were cultured from bovine cerebral cortical arteries. Whole-cell patches were made to cells, and glucose-evoked currents were recorded. Cells were incubated with [3H]-2-DOG, and the uptake was determined by a liquid scintillation counter. RESULTS: Glucose and alpha-methyl-D-glucoside (alphaMeDG), a specific compound for the SGLTs, evoked Na+ currents in a whole-cell voltage-clamp configuration, and the currents were enhanced in cells with over 30 minutes' preincubation in glucose-free media. Glucose-induced currents were inhibited by alphaMeDG, by the selective SGLT inhibitor phlorizin, by dinitrophenol (DNP), an inhibitor of energy metabolism, or by deletion of Na+ from extracellular solution, which indicates that glucose uptake into endothelial cells was mediated by a Na+- and energy-dependent glucose transporter. Notably, the currents were desensitized, reduced in a glucose concentration-dependent manner, and markedly inhibited by either a second application of glucose or the addition of glucose to the patch electrode filling solution; they were potentiated, however, by treatment with cytochalasin B, a GLUT1 to GLUT5 inhibitor. Consistent with the results of patch-clamp recordings, uptake of [3H]-2-DOG into endothelial cells was enhanced by glucose-free insult, and the enhancement was mediated by an SGLT-like glucose transporter. CONCLUSIONS: The results presented demonstrate that an SGLT-like glucose transporter takes part in glucose uptake into brain artery endothelial cells and that the uptake is regulated by intracellular glucose concentrations; glucose-free insult and the ensuing low cytosolic glucose enhance activity of the SGLT-like glucose transporter. The SGLT-like glucose transporter in the brain arterial endothelium thus may be important in the maintenance of an adequate glucose concentration in the arterial wall under conditions of stress, such as hypoglycemia.

Animals↗
PubMed2002

Coexistence of hypercholesterolemia and hypertension impairs adventitial vascularization.

We have shown that adventitial vasa vasorum (AVV) formation is enhanced in hypertensive rat aorta to compensate hypoxia in the thickened media and that hypercholesterolemia impairs angiogenesis in rat ischemic hindlimb. Thus, we examined the effects of coexistence of hypercholesterolemia and hypertension on AVV formation. In Wistar rats, hypercholesterolemia was established by high-cholesterol diet from Day -14 (HC rats), and hypertension was induced by a suprarenal aortic constriction at Day 0 (HT rats). At Day 28, we studied AVV density, adventitial area, and medial thickness in the ascending aorta of control (standard diet+sham operation), HC, HT, and HC+HT rats (n=5/group). In HC rats, although the adventitial area was modestly increased, the AVV density and medial thickness were unchanged versus controls. In addition to medial thickening, marked enlargement of the adventitial area accompanied by increased AVV density was observed in HT rats, compared with controls. HC+HT rats showed lower AVV density, despite larger adventitial area, than HT rats, whereas the medial thickness was similar in HT and HC+HT rats. Immunohistostaining revealed hypoxia-inducible factor-1alpha expression in the media only in HC+HT rats but not in the other 3 groups, suggesting persistent medial hypoxia in HC+HT rats. In conclusion, it is suggested that coexistence of hypercholesterolemia and hypertension impairs AVV formation, resulting in insufficient compensation for hypoxia in the thickened media. Our findings provide an insight into the mechanism of the aggravation of arteriosclerosis when both hypercholesterolemia and hypertension are present.

Animals↗
PubMed2002

Natriuretic peptide system gene expression in human coronary arteries.

The natriuretic peptides (NPs) ANF, BNP, and CNP have potent anti-proliferative and anti-migratory effects on vascular smooth muscle cells (SMCs). These properties make NPs relevant to the study of human coronary atherosclerosis because vascular cell proliferation and migration are central to the pathophysiology of atherosclerosis. However, the existence and cytological distribution of NPs and their receptors in human coronary arteries remain undetermined. This has hampered the development of hypotheses regarding the possible role of NPs in human coronary disease. We determined the pattern of expression of NPs and their receptors (NPRs) in human coronary arteries with atherosclerotic lesions classified by standard histopathological criteria as fatty streak/early atherosclerotic lesions, intermediate plaques, or advanced lesions. The investigation was carried out using a combination of immunocytochemistry (ICC), in situ hybridization (ISH), and semi-quantitative polymerase chain reaction (PCR). Both by ICC and ISH, ANF was found in the intimal and medial layers of all lesions. BNP was highly expressed in advanced lesions where it was particularly evident by a strong ISH signal but weak ICC staining. CNP was demonstrable in all types of lesions, giving a strong signal by ISH and ICC. This peptide was particularly demonstrable in the endothelium, as well as in the SMCs of the intima, media, and vasa vasorum of the adventitia and in macrophages. By ISH, NPR-A was not detectable in any of the lesions but both NPR-B and NPR-C were found in the intimal and the inner medial layers. By RT-PCR, mRNA levels of all NPs tended to be increased in macroscopically diseased arteries, but only the values for BNP were significantly so. No significant changes in NPR mRNA levels were detected by PCR. In general, the signal intensity given by the NPs and their receptors by ICC or ISH appeared dependent on the type of lesion, being strongest in intermediate plaques and decreasing with increasing severity of the lesion. This study constitutes the first demonstration of NPs and NPR mRNAs in human coronary arteries and supports the existence of an autocrine/paracrine NP system that is actively modulated during the progression of atherosclerotic coronary disease. This suggests that the coronary NP system is involved in the pathobiology of intimal plaque formation in humans and may be involved in vascular remodeling.

Adult↗
PubMed1999

Differential expression of the cyclic GMP-stimulated phosphodiesterase PDE2A in human venous and capillary endothelial cells.

We developed selective monoclonal antibodies and used them for Western and immunocytochemical analyses to determine the tissue and cellular distribution of the human cyclic GMP-stimulated phosphodiesterase (PDE2). Western analysis revealed PDE2A expression in a variety of tissue types, including cerebellum, neocortex, heart, kidney, lung, pulmonary artery, and skeletal muscle. Immunocytochemical analysis revealed PDE2A expression in a subset of tissue endothelial cells. PDE2A immunostaining was detected in venous and capillary endothelial cells in cardiac and renal tissue but not in arterial endothelial cells. These results were confirmed by in situ hybridization. PDE2A immunostaining was also absent from luminal endothelial cells of large vessels, such as aorta, pulmonary, and renal arteries, but was present in the endothelial cells of the vasa vasorum. PDE2A immunostaining was detected in the endothelial cells of a variety of microvessels, including those in renal and cardiac interstitial spaces, renal glomerulus, skin, brain, and liver. Although PDE2A was not readily detected in arterial endothelial cells by immunocytochemistry of intact tissue, it was detected at low levels in cultured arterial endothelial cells. These results suggest a possible role for PDE2A in modulating the effects of cyclic nucleotides on fluid and inflammatory cell transit through the endothelial cell barrier.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMedDate not supplied

The case for an in situ lesser saphenous vein bypass.

In situ lesser saphenous vein (LSV) graft has been advocated in cases where the greater saphenous vein is not available and the target arteries are confined to the lower leg. This is often the case of diabetic patients, whose occlusive disease pattern typically affects the tibioperoneal vessels, sparing the femoropopliteal segment. The in situ technique offers the potential advantages of decreasing surgical trauma to the vein and its vasa vasorum, better size-matching between vein and artery at the anastomoses, and improving hemodynamics. The authors reviewed the use of in situ LSV graft with attention to its indications and technical requirements. A 73- and a 76-year-old man presented with critical limb ischemia. Both had a history of diabetes, chronic renal failure, and previous use of the greater saphenous veins for coronary or peripheral bypasses. Both had good femoropopliteal inflow and tibioperoneal disease with single runoff through the distal peroneal and common plantar arteries, respectively. Venous mapping showed diminutive veins, with exception of an adequate ipsilateral lesser saphenous vein. The patients were placed in prone position for a posterior approach. The lesser saphenous veins were exposed through a longitudinal incision. Proximal anastomosis was based on the popliteal artery, exposed through the same incision. A successful in situ lesser saphenous vein bypass was performed by using the common plantar and the distal peroneal artery as target vessels. Both bypasses were patent at 24 and 18-months' follow-up, respectively. Selection criteria for in situ LSV bypass are patent femoral arteries; accessible target vessels in prone position through a medial, posterior, or lateral approach; and adequate LSV in diameter and length. In the authors' experience, in situ LSV bypass is a safe and simple option that offers successful distal revascularization.

Aged↗
PubMed1984

Effects of perfusate composition on binding of ruthenium red and gold colloid to glycocalyx of rabbit aortic endothelium.

The effects of perfusate composition on some of the properties of the endothelial glycocalyx were investigated electron microscopically. Rabbit aorta was perfused in situ in preparation for fixation with 1% OsO4 containing 0.1 Ruthenium red (RR) or perfusion with wheat germ agglutinate (WGA)-coated gold particles suspended in 0.9% NaCl, Tyrode's solution, or pooled rabbit serum. Intense RR staining of the intimal glycocalyx was found only in vessels that had been exposed to 150 mmol/L NaCl, pH 7.4, or to albumin (4.0 g/100 ml), gamma-globulin (0.7 g/100 ml), or fibrinogen (0.3 g/100 ml) in Tyrode's solution, pH 7.4, for 5 min prior to fixation. The adherence of WGA-coated gold particles to the intimal and vasa vasorum glycocalyces was found in saline- and Tyrode's-perfused vessels. The density of the WGA-coated gold particles was greatest in the glycocalyx of damaged endothelium. In vessels flushed with serum, no RR stain or WGA-coated gold colloid was seen in the glycocalyx. This study demonstrates that saline perfusion facilitates the passage of RR and WGA-coated gold particles into the endothelial glycocalyx. We conclude that serum proteins and cell-surface glycoprotein chains act cooperatively to impede the access of some molecules to the endothelial surface.

Animals↗
PubMed2002

A comparison of balloon injury models of endovascular lesions in rat arteries.

BACKGROUND: Balloon injury (BI) of the rat carotid artery (CCA) is widely used to study intimal hyperplasia (IH) and decrease in lumen diameter (LD), but CCA's small diameter impedes the evaluation of endovascular therapies. Therefore, we validated BI in the aorta (AA) and iliac artery (CIA) to compare it with CCA. METHODS: Rats underwent BI or a sham procedure (control). Light microscopic evaluation was performed either directly or at 1, 2, 3, 4 and 16 weeks follow-up. The area of IH and the change in LD (LD at 16 weeks minus LD post BI) were compared. RESULTS: In the BI-groups the area of IH increased to 0.14 +/- 0.08 mm2 (CCA), 0.14 +/- 0.03 mm2 (CIA) and 0.12 +/- 0.04 mm2 (AA) at 16 weeks (NS). The LD decreased with 0.49 +/- 0.07 mm (CCA), compared to 0.22 +/- 0.07 mm (CIA) and 0.07 +/- 0.10 mm (AA) at 16 weeks (p < 0.05). The constrictive vascular remodelling (CVR = wall circumference loss combined with a decrease in LD) was -0.17 +/- 0.05 mm in CIA but absent in CCA and AA. No IH, no decrease in LD and no CVR was seen in the control groups. CONCLUSIONS: BI resulted in: (1.) a decrease in LD in CCA due to IH, (2.) a decrease in LD in CIA due to IH and CVR, (3.) no change in LD in AA, (4.) Comparable IH development in all arteries, (5.) CCA has no vasa vasorum compared to CIA and AA, (6.) The CIA model combines good access for 2 F endovascular catheters with a decrease in LD due to IH and CVR after BI.

Animals↗
PubMed2004

The role of monocyte-derived cells and inflammation in baboon ductus arteriosus remodeling.

Inflammatory processes play a crucial role in the pathogenesis of atherosclerosis and other vascular disorders. We hypothesized that ischemia of the ductus arteriosus might initiate an active inflammatory response that could play a role in ductus remodeling and permanent closure. To test this hypothesis, we studied effects of postnatal ductus construction on inflammatory processes and remodeling in late-gestation fetal and newborn baboons, and preterm newborn baboons. After postnatal ductus constriction, the expression of several genes known to be essential for atherosclerotic remodeling [vascular cell adhesion molecule (VCAM)-1, E-selectin, IL-8, macrophage colony stimulating factor-1, CD154, interferon-gamma, IL-6, and tumor necrosis factor-alpha] was increased in the ductus wall. We were unable to detect intercellular adhesion molecule (ICAM)-1, ICAM-2, P-selectin, monocyte chemoattractant protein-1, or IL-1 by either real-time PCR or immunohistochemistry. VCAM-1, which is newly expressed by luminal cells of the closed ductus, is an important ligand for the mononuclear cell adhesion receptor VLA4. After postnatal constriction, VLA4+ monocytes/macrophages (CD68+ and CD14+) and, to a lesser extent, T-lymphocytes adhered to the ductus wall. Neutrophils and platelets were not observed. The extent of postnatal neointimal remodeling (both endothelial cell layering and subendothelial space thickening) was associated with the degree of mononuclear cell adhesion. Similarly, the extent of vasa vasorum ingrowth correlated with the invasion of CD68+ cells, from the adventitia into the muscle media. Based on these data, we conclude that the inflammatory response following postnatal ductus constriction may be as necessary for ductus remodeling as it is for atherosclerotic remodeling.

Animals↗
PubMed1985

Completely thrombosed giant aneurysm of the basilar artery trunk: a case report.

A patient with a completely thrombosed giant aneurysm arising from the trunk of the basilar artery is described. Although it is difficult to differentiate this anomaly from a posterior fossa tumor, negative angiographic findings combined with certain computed tomographic (CT) signs may point to the correct diagnosis. Our case demonstrates that one of these CT signs (viz. ringlike contrast enhancement) can be explained by the presence of vasa vasorum in the aneurysm wall.

Basilar Artery↗
PubMed1999

Tuberculous mycotic aneurysm of the aorta: review of published medical and surgical experience.

To define the epidemiology, pathogenesis, pathology, presentation, and management of tuberculous mycotic aneurysm of the aorta (TBAA) in the therapeutic era, we reviewed all of the cases reported in the English language literature from 1945 to the present. To the 39 cases in the published literature, we add two cases of our own. Although it is exceedingly rare, the prevalence of this lesion has remained relatively constant. In 75% of the cases, TBAA appeared to result from erosion of the aortic wall by a contiguous focus; 25% from direct seeding of the aortic intima or of the adventitia or media (via the vasa vasorum). Most of the aneurysms were saccular (90%) and false (88%). The thoracic and abdominal aortas were affected with equal frequency. The mean (+/- SD) age of the patients was 50+/-16 years. Twenty-two were men, and 19 were women. In 63% of the cases, tuberculosis (TB) was diagnosed at presentation. Disseminated TB was present in 46% of the cases. One or more of three clinical scenarios suggested TBAA: persistent pain, major bleeding, and a palpable or radiographically visible para-aortic mass, especially if it is expanding or pulsatile. In turn, each of these findings suggested a complication of TBAA that may be an indication for surgical intervention. Among the patients who were offered both medical and surgical treatment, 20 of 23 (87%) survived. Among those who were offered only one form of treatment or were offered no treatment at all there were no survivors. Both in situ reconstruction with a prosthetic graft, and extra-anatomic bypass appeared to offer excellent results, provided that an effective regimen of antituberculous drugs was delivered postoperatively. We offer our conclusions: (1) symptomatic TBAA is a rare but uniformly fatal lesion if not diagnosed promptly, (2) in the context of active TB, and especially miliary TB, TBAA should be suspected whenever one or more of the three clinical scenarios are present, and (3) combined medical and surgical therapy appears to offer the best chance of a cure.

Adult↗
PubMed2000

Catheter-delivered in vivo gene transfer into rat myocardium using the fusigenic liposomal mediated method.

We compared the efficacy of four different in vivo hemagglutinating virus of Japan (HVJ)-liposome gene transfer methods, i.e., direct myocardial injection (i.m.), injection into the left ventricular cavity (LV), infusion at the level of the coronary cusps (CI), or injection into the left ventricular cavity with a balloon catheter blocking aortic flow (LV+B) to transfer beta-galactosidase, FlTC-labeled oligodeoxynucleotide (ODN), and/or luciferase genes into the rat heart. I.m. caused highly efficient gene transfer in the limited area around the injection site, which suggests that i.m. may be a suitable method for targeted treatment of focal lesion. In the LV+B group, all rats had myocardial beta-galactosidase staining and fluorescence of FITC-labeled ODN in the nuclei of cardiac myocytes around the coronary arteries and the vasa vasorum, and some transfected myocytes were observed in the middle of the myocardium without any evidence of injury. In contrast, in the CI group, only half of the animals had myocardial expression of beta-galactosidase. In contrast, fluorescence or luciferase activity was present throughout the left ventricle in the LV+B group. However, the percentage of myocytes that exhibited fluorescence was less than 1% of the total ventricular myocyte population and luciferase activity in the LV+B group was 1.6% of that in the i.m. group. No evidence of luciferase expression was observed in brain, lung, liver, kidney, or testis in either the i.m. or LV+B group. These results suggest that HVJ-liposome gene transfer into the myocardium through the coronary arteries using a balloon-catheter technique is safe and has the potential for causing widespread transgene expression with organ-specificity, although the efficiency of gene transfer should be improved.

Animals↗
PubMed1992

Changes in size and shape of smooth muscle cells from the portal vein of spontaneously hypertensive rats: an ultrastructural analysis.

The portal vein was investigated in male spontaneously hypertensive rats (SHR), from Wistar-Kyoto (WKY) and Wistar strains, in animal 16-20 weeks old. In SHR, the inner circular smooth muscle was unchanged, but the outer longitudinal layer showed marked alterations in shape and size, readily observed in three-dimensional micrographs using scanning electron microscopy. The cells in both Wistar and WKY were elongate and tubular with little variation along their lengths and with a relatively smooth sarcolemma. This applied to both the inner and outer layers of smooth muscle. In contrast, the smooth muscle cells from SHR in the outer layer varied considerably in thickness along their lengths, and had very irregular outlines with numerous pits or depressions of varying sizes. In addition, the cells frequently had major forks or branches. The vasa vasorum running through the muscle layer, fibroblasts and nerve bundles were also identified. Sectioned material (transmission electron microscopy) showed a change in shape and hypertrophy of the smooth muscle cells from the portal vein of SHR, and also demonstrated a significant increase in paracellular connective tissue in the outer layer of smooth muscle. Such major morphological alterations in the outer layer of smooth muscle in the portal vein from SHR could have profound effects on functional studies.

Animals↗
PubMed1998

A huge coronary aneurysm resulting from a coronary artery-to-left ventricle fistula.

A huge coronary aneurysm resulting from a coronary artery-to-left ventricle fistula is a rare condition. A 57-year-old male had severe recurrent angina attacks. The cause of angina pectoris was a right coronary artery-to-left ventricle fistula with a huge coronary aneurysm. The histological examination of surgically excised specimens revealed that two vertical smooth muscle layers of media of the aneurysm might be associated with dysplasia. Mucoid degeneration was also shown in the intima and around the vasa-vasorum. Abnormal hemodynamics related to the fistula might have induced these vessel wall changes resulting in the huge coronary aneurysm.

Angina Pectoris↗
PubMed1992

Pulmonary artery disease in Takayasu's arteritis: angiographic findings.

One hundred sixteen arteriographic examinations in 98 patients with Takayasu's arteritis were studied retrospectively to evaluate the extent of aortic and pulmonary disease. Stenosis was the most frequent finding in the aorta and its branches, but occlusion, dilatation, and aneurysms were also seen. Adventitial vascular structures, consistent with dilated vasa vasorum, were observed in five patients (5%) and systemic artery-pulmonary artery communication was seen in six (6%). Twenty-one (70%) of 30 patients who had pulmonary arteriography were shown to have pulmonary artery involvement. Upper lobe pulmonary arterial branches showed abnormalities most frequently; segmental branches, followed by subsegmental branches, were most often involved. The frequency of abnormal findings on pulmonary arteriograms correlated with the number of involved brachiocephalic vessels. Stenotic lesions in the aorta and its branches progressed in five (45%) of 11 patients, and those in the pulmonary artery progressed in one (33%) of three cases. Takayasu's arteritis characteristically involves the systemic and pulmonary arteries, and the extent of arteritis in the major branches of the aortic arch appears to correlate with pulmonary arterial involvement. Both thoracic and abdominal aortographic studies and pulmonary arteriography are necessary to properly diagnose the extent of the disease, and angiography should be repeated for appropriate patient follow-up.

Adolescent↗
PubMedDate not supplied

Atherosclerosis and central adiposity in a pediatric patient with AIDS treated with HAART: autopsy findings.

Several types of cardiovascular lesions may develop in pediatric human immunodeficiency virus-positive (HIV+)/acquired immunodeficiency syndrome (AIDS) patients, namely myocarditis, dilated cardiomyopathy, pericardial effusion, pericarditis, left ventricle hypertrophy, fibrocalcific arteriopathy, and aneurysms. Additional lesions may be discovered by histological examination. These include fibrocalcific lesions in medium-sized arteries and small vessels, mainly of the heart and brain, and vasculitis. In the large arteries the vasa vasorum may present chronic inflammatory infiltrates or leukocytoclastic vasculitis, resulting in aneurysms. We are reporting the case of a 14-year-old girl with mother-to-infant HIV transmission with a long history of several central nervous system infections and AIDS dementia, who received treatment with the HAART protocol (including a protease inhibitor) for 3 years. A year after beginning this treatment, cholesterol serum levels were 2.8 g/L and 3.8 g/L. Autopsy findings showed gross and microscopic features of adult-type atherosclerosis involving the whole thoracic aorta, its main branches, and the coronary arteries. Remarkably, the abdominal aorta and all its branches were almost completely devoid of these lesions. At the same time, although the body presented extreme cachexia, there were obvious subepericardial, periadrenal, and peripancreatic fat deposits. The referred findings may have resulted from the well-known metabolic-dyslipemic syndrome induced by the HAART therapy and have not been specifically mentioned previously in the literature in the particular setting observed in the case of this patient.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Innervation of syngeneic vein grafts in the rat. The regeneration of cholinesterase positive nerves.

The regeneration of cholinesterase positive nerves into segments of the supradiaphragmatic inferior vena cava transplanted from one rat into the abdominal aorta of another rat of the same inbred strain and sex were studied, using a histochemical thiocholine method for the demonstration of cholinesterase. Iso-OMPA and BW-284 C 51 were used as inhibitors for nonspecific cholinesterase (nsChE) and acetylcholinesterase (AChE), respectively. A total of 12 grafts were examined 3, 5, 8, 16, 27 and 32 weeks after transplantation. One single regenerating nsChE reactive nerve was seen near the suture line in a 3-week-old graft. Some solitary regenerating nerves were regularly seen in the grafts at 5 weeks. Eight weeks after grafting some solitary sparsely distributed nerves were found in the outer layers of the graft. In the 16-, 27-, and 32-week-old grafts, nsChE reactive nerves and small nerve bundles were running either solitary or forming nerve plexa in addition to nerves in the vicinity of vasa vasorum. These regenerated nsChE reactive nerves are probably vasomotor in nature. The AChE reaction showed a clear activity in the intimal layer of the grafted veins. No AChE reactive nerves were seen in the 3-, 5-, and 8-week-old grafts. Only occasional AChE positive nerves were observed 16, 28 and 32 weeks after transplantation. These nerves are probably sympathetic cholinergic nerves.

Acetylcholinesterase↗