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PubMed2000

Recipient origin of neointimal vascular smooth muscle cells in cardiac allografts with transplant arteriosclerosis.

BACKGROUND: Coronary artery disease is today's most important post-heart transplantation problem after the first perioperative year. Histologically, coronary artery disease is characterized by transplant arteriosclerosis. The current view on this vasculopathy is that vascular smooth muscle (VSM) cells from the media of affected arteries proliferate and migrate into the sub-endothelial space (intima) in response to signals from inflammatory cells and damaged graft endothelium. According to this model, the intimal VSM cells in transplant arteriosclerotic lesions should originate from donor tissue. Using recipient-specific polymerase chain reaction (PCR) analysis of microdissected, single, neointimal VSM nuclei, we recently showed that after allogeneic aorta transplantation the neointimal VSM cells are of recipient and not of donor origin. In this study, we analyzed whether VSM-cell replacement with recipient-derived cells also takes place after allogeneic heart transplantation. METHODS: Cardiac allografts, when transplanted from female donors to male immune-modulated recipient rats, eventually developed transplant arteriosclerosis. We microdissected alpha-actin positive neointimal VSM cells from tissue sections and determined the origin (donor or recipient) using recipient-specific (male), single-cell, PCR analysis. RESULTS: In total, we analyzed 35 VSM-cell nuclei from 3 allografts, and PCR analysis revealed that 30/35 (86%) of the samples displayed the male-specific 128 base pair DNA fragment. These results indicate that after allogeneic cardiac transplantation, at least 86% of VSM cells in transplant arteriosclerotic lesions are of recipient origin. CONCLUSIONS: In contrast to current thought, the neointimal VSM cells in cardiac allografts that show transplant arteriosclerosis are of recipient and not of donor origin.

Actins↗
PubMed1991

Dose response of fish oil versus safflower oil on graft arteriosclerosis in rabbit heterotopic cardiac allografts.

With the advent of cyclosporin A, accelerated coronary arteriosclerosis has become the major impediment to the long-term survival of heart transplant recipients. Due to epidemiologic reports suggesting a salutary effect of fish oil, the dose response of fish oil on graft coronary arteriosclerosis in a rabbit heterotopic cardiac allograft model was assessed using safflower oil as a caloric control. Seven groups of New Zealand White rabbits (n = 10/group) received heterotropic heart transplants from Dutch-Belted donors and were immunosuppressed with low-dose cyclosporin A (7.5 mg/kg/day). Group 1 animals were fed a normal diet and served as control. Group 2, 3, and 4 animals received a daily supplement of low- (0.25 mL/kg/day), medium- (0.75 mL/kg/day), and high- (1.5 mL/kg/day) dose fish oil (116 mg n-3 polyunsaturated fatty acid/mL), respectively. Group 5, 6, and 7 animals were supplemented with equivalent dose of safflower oil (i.e., 0.25, 0.75, and 1.5 mL/kg/day). Oil-supplemented rabbits were pretreated for 3 weeks before transplantation and maintained on the same diet for 6 weeks after operation. The extent of graft coronary arteriosclerosis was quantified using computer-assisted, morphometric planimetry. When the animals were killed, cyclosporin A was associated with elevated plasma total cholesterol and triglyceride levels in the control group. While safflower oil prevented the increase in plasma lipids at all dosages, fish oil ameliorated the cyclosporin-induced increase in total cholesterol only with high doses. Compared to control animals, there was a trend for more graft vessel disease with increasing fish oil dose, as assessed by mean luminal occlusion and intimal thickness. A steeper trend was observed for increasing doses of safflower oil; compared to the high-dose safflower oil group, animals supplemented with low-dose safflower oil had less mean luminal occlusion (16.3% +/- 5.9% versus 41.4% +/- 7.6%, p less than 0.017) and intimal thickness (7.9 +/- 1.9 microns versus 34.0 +/- 13.0 microns, analysis of variance: p = 0.054). Low-dose safflower oil also had a slight, but nonsignificant, beneficial effect on graft vessel disease when compared to control rabbits. The same trends were observed in the degree of histologic rejection (0 = none to 3 = severe) in fish oil- and safflower oil-treated animals. Rejection score correlated weakly but significantly (p = 0.0001) with mean luminal occlusion (r = 0.52) and intimal thickness (r = 0.46). Therefore allograft coronary disease in this model appeared to exhibit an unfavorable, direct-dose response to fish oil and safflower oil, independent of effects on plasma lipids.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Experimental graft arteriosclerosis. II. Immunocytochemical analysis of lesion development.

The development of progressive graft arteriosclerosis causes the majority of late deaths occurring in cardiac transplant recipients. The pathogenesis of this process remains unclear. In order to characterize the cellular composition of lesions progressively, we employed a model of graft arteriosclerosis in the rat involving untreated heterotopic cardiac allografts transplanted across minor histocompatibility barriers. Immunocytochemical studies were performed on arterial lesions in allografts removed at 15, 45, 75, and 120 days posttransplantation, using monoclonal antibodies specific for smooth muscle cells (HHF35, CGA7), monocytes/macrophages (ED1), T cells (W313), and endothelial cells (anti-vWf). We found areas of coronary intimal thickening demonstrated marked cellular heterogeneity. The earliest lesions involved the adherence of monocytes and T cells to the coronary endothelial surface. At later time points, we noted marked subendothelial accumulations of macrophages and occasional T cells in areas of intimal thickening. In contrast, smooth muscle cells were the major cell type identified in intimal lesions in 120-day-old allografts. Intimal macrophages are frequently seen in spontaneous human arteriosclerotic lesions; our findings suggest that macrophages, perhaps interacting with T cells, play an important role in the pathogenesis of graft arteriosclerosis.

Animals↗
PubMed1998

Inhibitory effect of Multiglycosidorum tripterygii on coronary arteriosclerosis after heart transplantation.

BACKGROUND: Graft coronary arteriosclerosis (GCA) is the major limiting factor for long-term survival after heart transplantation. In this study, we investigated the effect of Multiglycosidorum tripterygii (MT) on GCA and platelet-derived growth factor A (PDGF-A) mRNA expression of transplanted hearts. METHODS: Two groups of Lewis rats (n=7/group) underwent heterotopic heart transplantation from Wistar-King donors and were treated with either cyclosporine (CsA;10 mg/kg/day) or MT (30 mg/kg/ day). Histological evaluations of rejection and coronary arteriosclerosis, as well as Northern blot analysis on graft PDGF-A mRNA expression were made 60 days after transplantation. RESULTS: Morphometric results indicated no significant difference in rejection between the CsA- and MT-treated groups. However, the extent of GCA in the MT-treated group was significantly less than that seen in the CsA-treated group (P<0.01). The expression of PDGF-A mRNA of cardiac allograft was also significantly suppressed in the MT-treated group when compared with the CsA-treated group (P<0.01). CONCLUSION: MT is superior to CsA in preventing graft coronary arteriosclerosis, and this efficacy is probably associated with the depressed expression of graft PDGF-A mRNA in the MT-treated group.

Animals↗
PubMed1995

Quantitative assessment of coronary arteriosclerosis in hypertensive rats.

Following Skelton's procedure with unilateral adrenonephrectomy, contralateral adrenal enucleation and application of 1% NaCl with the drinking fluid, genetically normotensive rats develop hypertension and a generalized arteriosclerosis, i.e. necrotizing hypertensive angiopathy. In the present study, the effect of high blood pressure was investigated in 13 Skelton hypertensive rats and 13 normotensive control rats. Systolic blood pressure was investigated by tail plethysmography over a period of 7 weeks. During the experiments, 3 of the Skelton rats died with final high blood pressure values, whereas all controls remained alive. Mean systolic blood pressure of the 10 surviving Skelton rats increased from 108 to 223 mm Hg. The control rats remained normotensive. Accordingly, heart weights of the hypertensives were higher than those of the controls (p = 0.0027). At the end of the experiment, arteriosclerosis was quantified by counting the heart arteries and arterioles with deposits of fibrinoid in the vascular wall in 10 histological cross-sections per heart. In the right ventricular wall of 6 of the 10 surviving Skelton rats, arteries and arterioles with deposits of fibrinoid in the vascular wall were detected. No such alteration was observed in the left ventricular wall or in the interventricular septum. About one third of the altered blood vessels showed fibrinoid necrosis. In contrast, the normotensive control rats had neither fibrinoid necrosis nor sclerotic arteries in corresponding sections of the hearts (p = 0.0052). The findings show that Skelton hypertension can be used as an experimental model for quantitative histological investigation of coronary arteriosclerosis in hypertensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Inhibition of transplant coronary arteriosclerosis in rabbits by chronic estradiol treatment is associated with abolition of MHC class II antigen expression.

BACKGROUND: Accelerated coronary arteriosclerosis is a major complication in long-term survivors of cardiac transplantation. Estrogen prevents transplant arteriosclerosis in experimental cardiac and aortic allografts and may act by an immune mechanism. METHODS AND RESULTS: New Zealand White rabbits immunosuppressed with cyclosporine were recipients of cardiac allografts from Dutch Belted rabbits. The recipients received either estradiol or placebo daily until they were killed 6 weeks later. Histological cross sections of the cardiac allograft were used for quantification of major histocompatibility complex (MHC) class II antigen expression, T lymphocytes, and macrophages by immunohistochemistry using monoclonal antibodies. MHC class II antigen expression was not detectable in allograft coronary arteries from any of the estradiol-treated recipients, whereas this antigen expression was present in the allograft coronary arteries from all the placebo-treated recipients. Macrophage and lymphocyte infiltration of the allograft coronary artery myointima was significantly less frequent in the estradiol-treated group. Rejection was moderate but slightly less in the estradiol-treated group. These findings were associated with a 60% decrease in allograft coronary artery myointimal thickening (determined by morphometry) in the estradiol-treated compared with the placebo-treated group. CONCLUSIONS: Estradiol treatment of cardiac allograft recipients abolishes MHC class II antigen expression in the coronary arteries and decreases macrophage infiltration in all three layers of the vessel wall, whereas T-lymphocyte infiltration is decreased only in the myointima. These findings are associated with estradiol inhibition of myointimal proliferation. Thus, estradiol treatment may have a beneficial effect on graft arteriosclerosis through immune mechanisms.

Animals↗
PubMed1998

Role of endogenous endothelin in the development of graft arteriosclerosis in rat cardiac allografts: antiproliferative effects of bosentan, a nonselective endothelin receptor antagonist.

BACKGROUND: The purpose of this study was to determine whether endothelin-1 (ET-1) contributes to the development of graft arteriosclerosis and whether the orally active nonpeptide endothelin receptor antagonist bosentan, which blocks both ETA and ETB receptors, can protect against this pathologic damage. METHODS AND RESULTS: Recipient male Lewis rats were divided into three groups; group 1 received heterotopic heart transplantations from Lewis donors and groups 2 and 3 received transplantations from Brown-Norway donors; group 3 recipients also received bosentan orally at the dose of 20 mg/kg per day for 120 days. All recipients were given cyclosporine and were euthanized at examination 120 days after transplantation. Plasma ET-1 levels were significantly higher in group 2 than in group 1 (6.99+/-0.91 and 4.15+/-.83 pg/mL, respectively). Strong ET-1 immunoreactivity was seen in both the thickened neointima and the media of the coronary arteries in group 2 but not in group 1. The mean ratio of the coronary luminal area to the total vascular area in group 2 (19.0+/-11.7%) was significantly lower than that in group 1 (34.2+/-9.9%) and was significantly increased in group 3 (33.2+/-9.2%). CONCLUSIONS: These results show that local upregulation of ET-1, mainly in the thickened neointima and the media of the coronary arteries, may play an important role in the pathogenesis of graft arteriosclerosis by stimulating ETA receptors, ETB receptors, or both. Orally active bosentan might be a useful agent for the clinical prevention of graft arteriosclerosis.

Actins↗
PubMed2005

Chronic myocardial infarction due to arteriosclerosis of coronary arteries followed by acute thromboembolism of caudal abdominal aorta in a cat.

A 10-year-old cat with the paresis of hind limbs was initially diagnosed as a hypertrophic cardiomyopathy followed by acute thromboembolism of caudal abdominal aorta from the findings of the medical examinations. However, this case was proved to be an chronic myocardial infarction due to arteriosclerosis of coronary arteries by the pathologic diagnosis. In the left ventricular, the hypertrophy and the narrowing were slight, and a coagulative infarction was seen obviously. The intramural coronary arteriosclerosis showed thickening of the wall due to medial hyperplasia by fibrosis, and arterial stenosis. Myocardial infarction and arteriosclerosis are scarcely any reports of these lesions in cats. This case is valuable for an extremely rare case of myocardial infarction in the cat.

Animals↗
PubMed2000

Insulin-like growth factor-binding protein-3 is associated with the presence and extent of coronary arteriosclerosis

Aging is associated with the progression of arteriosclerosis and the decline of several endocrine functions. We therefore investigated the association of coronary arteriosclerosis with hormones, the serum concentrations of which change during aging. Coronary angiograms of 189 men <70 years old were evaluated by 3 semiquantitative score systems to estimate the extent of focal and diffuse vessel wall alterations. Fasting sera were analyzed for levels of glucose, lipids, thyroid-stimulating hormone, insulin, insulin-like growth factor I (IGF-I), IGF-binding protein-3 (IGFBP-3), dehydroepiandrosterone sulfate (DHEAS), testosterone, and sex hormone-binding globulin (SHBG). After adjustment for age, body mass index, and waist-to-hip ratio, 92 patients with >/=1 stenoses >70% differed from 97 patients without such focal lesions by higher serum levels of glucose, total and LDL cholesterol, and apolipoprotein (apo) B, as well as by lower serum levels of IGFBP-3. Multivariate analyses revealed significant and independent correlations of all 3 coronary scores with LDL cholesterol (or apoB) and IGFBP-3; of 2 coronary scores with age, glucose, and insulin; and of 1 score with IGF-I. No significant correlations existed for waist-to-hip ratio (or body mass index) and DHEAS (or testosterone or SHBG). IGFBP-3 explained 9% to 14% and 3.5% to 10% of the variances of focal and diffuse lesions, respectively. In conclusion, IGFBP-3 and, with much less strength and consistency, insulin and IGF-I, but not markers of hypothyroidism, adrenopause, and andropause, have statistically significant and independent associations with coronary arteriosclerosis in men.

Journal Article↗
PubMed2000

Insulin-like growth factor-binding protein-3 is associated with the presence and extent of coronary arteriosclerosis

Aging is associated with the progression of arteriosclerosis and the decline of several endocrine functions. We therefore investigated the association of coronary arteriosclerosis with hormones, the serum concentrations of which change during aging. Coronary angiograms of 189 men <70 years old were evaluated by 3 semiquantitative score systems to estimate the extent of focal and diffuse vessel wall alterations. Fasting sera were analyzed for levels of glucose, lipids, thyroid-stimulating hormone, insulin, insulin-like growth factor I (IGF-I), IGF-binding protein-3 (IGFBP-3), dehydroepiandrosterone sulfate (DHEAS), testosterone, and sex hormone-binding globulin (SHBG). After adjustment for age, body mass index, and waist-to-hip ratio, 92 patients with >/=1 stenoses >70% differed from 97 patients without such focal lesions by higher serum levels of glucose, total and LDL cholesterol, and apolipoprotein (apo) B, as well as by lower serum levels of IGFBP-3. Multivariate analyses revealed significant and independent correlations of all 3 coronary scores with LDL cholesterol (or apoB) and IGFBP-3; of 2 coronary scores with age, glucose, and insulin; and of 1 score with IGF-I. No significant correlations existed for waist-to-hip ratio (or body mass index) and DHEAS (or testosterone or SHBG). IGFBP-3 explained 9% to 14% and 3.5% to 10% of the variances of focal and diffuse lesions, respectively. In conclusion, IGFBP-3 and, with much less strength and consistency, insulin and IGF-I, but not markers of hypothyroidism, adrenopause, and andropause, have statistically significant and independent associations with coronary arteriosclerosis in men.

Journal Article↗
PubMed1991

[Modification of coronary arteriosclerosis in man by calcium antagonists?].

Calcium channel blockers may retard development and progression of coronary arteriosclerosis in man because of protective effects on membranes, (especially the endothelium), relaxation of vessel walls, inhibition of various platelet functions, impairment of proliferation and migration of smooth muscle cells in the vessel wall, and an improvement of vascular cholesterol metabolism. In animal trials development of atheromas in large arteries induced by cholesterol-rich food and other stimuli of atherogenesis could be successfully retarded by a broad variety of calcium channel blockers. Some clinical observations in patients with coronary artery disease pointed at positive effects of calcium antagonists in coronary arteriosclerosis. To date, the results of three prospective placebo-controlled trials with calcium antagonists in coronary arteriosclerosis are available. In all trials progression of atherosclerosis was assessed by serial angiograms: 1) INTACT (nifedipine: 20 mg four times daily; observation period: 3 years, two coronary angiograms); 2) Study of the Montreal Heart Institute (nicardipine: 30 mg three times daily; observation period: 2 years, two coronary angiograms); 3) FIPS (Frankfurt Isoptin Progression Study) (verapamil: 120 mg three times daily; observation period: 3 years, three coronary angiograms). Target variables in these studies were progression or regression of preexisting lesions, development of new lesions and the incidence of vessel occlusions. The INTACT and the Nicardipine studies preferably included patients in early stages of coronary artery disease. The patients of FIPS who were entered into the study immediately after coronary bypass surgery suffered from severe, advanced coronary artery disease. In the latter study progression of coronary artery disease was assessed separately in different vascular regions (bypassed and non-bypassed segments) and in the bypass grafts.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium Channel Blockers↗
PubMed1989

Functions of vascular wall cells related to development of transplantation-associated coronary arteriosclerosis.

The accelerated form of arteriosclerosis that occurs in the coronary circulation of transplanted hearts currently presents a major limitation to the long-term success of this therapy. The pathogenesis of this lesion is unclear. Recent advances in vessel wall biology have disclosed interplay between mediators of the immune response and functions of vascular cells of potential significance in the formation of this accelerated form of arterial disease. We hypothesize that the development of accelerated arteriosclerosis in the arteries of transplanted hearts represents a form of chronic immunologic reaction resembling delayed-type hypersensitivity localized in the graft's arteries, a manifestation of cellular immunity mediated in large part by a regionally acting cytokine network. We emphasize the active responses of intrinsic vessel wall cells, including inappropriate expression of HLA and the likely participation of cytokines derived from vascular cells as well as from infiltrating leukocytes in amplification and propagation of this localized chronic immune reaction. This mechanism, which involves helper T cells interacting with class II HLA, may distinguish transplantation-associated arteriosclerosis from typical acute rejection, which may involve primarily cytolytic T cells interacting with class I HLA. Lesions of the common variety of atherosclerosis manifest certain features of immune activation. Therefore, we further hypothesize that the transplantation-associated form represents an extreme case of processes that also contribute to usual coronary atherosclerosis. For this reason, study of the accelerated disease may aid understanding of atherogenesis in general. Unraveling the basic pathobiology of these clinically important arterial diseases should lay the groundwork for rational design of selective therapeutic strategies to prevent or retard their development.

Animals↗
PubMed1980

[The LDL-HDL ratio in patients with coronary arteriosclerosis (author's transl)].

In 171 patients with coronary arteriosclerosis the severity of the angiographic findings was assessed by the score of Friesinger. The total serum cholesterol concentration showed an only weak positive correlation with the extent of coronary arteriosclerosis. In contrast, a strict correlation could be documented with the LDL-HDL ratio. The LDL-HDL ratio was 1.49 in the control group with angiographically free coronary arteries, 1.95 in patients with an angiographic score of 1-5, 2.39 at a score of 6-10, and 2.75 at a score of 11-15. The corresponding total serum cholesterol values (control group: 219 mg/100 ml) were 229 mg/100 ml, 242 mg/100 ml and 258 mg/100 ml. Especially at still normal serum cholesterol concentrations an already pathological shift in the lipoprotein pattern in correlation with the extent of coronary arteriosclerosis was indicated by the LDL-HDL ratio. Thus a greater predictive power for coronary risk is attributed to the LDL-HDL ratio rather than to the total serum cholesterol concentration.

Cholesterol↗
PubMedDate not supplied

Endothelialitis and accelerated arteriosclerosis in human heart transplant coronaries.

We have analyzed the autopsy material of 11 cardiac allograft recipients, whose grafts became nonfunctional less than 1 year after transplantation. All patients had received routine triple-drug immunosuppression. Two of these patients showed accelerated transplant arteriosclerosis; the graft loss was associated with strong intimal proliferative response affecting the first-order and second-order intramuscular branches of the major coronary vessels. Histologic evidence showed only a slight inflammatory reaction in the vascular adventitia. The media was mostly intact, and the internal elastic lamina showed occasional breaks. A very prominent inflammatory reaction was noted in the subendothelial space in the intima. Immunohistochemistry with monoclonal antibodies revealed that the luminal part of the intima was invaded by anti-leukocyte common antigen and anti-UCHL1 positive T lymphocytes, whereas the abluminal part consisted mostly of anti-smooth muscle alpha-actin-positive smooth muscle cells. We call this subendothelial accumulation of lymphocytes endothelialitis. The suggestion has been made that accelerated arteriosclerosis may be associated with cyclosporine treatment. Correlation with the recipient's cytomegalovirus status in this study suggests that cytomegalovirus infection may contribute to the development of endothelialitis and accelerated arteriosclerosis in heart transplant recipients.

Adult↗
PubMed1953

Peripheral arteriosclerosis; present concepts of management.

Three hundred patients with clinical manifestations of ischemia due to peripheral arteriosclerosis were studied. An accurate demonstration of the extent of the arterial occlusive process by means of aortography was of major importance in determining therapy and prognosis. The results from thromboendarterectomy to restore the arterial lumen in cases of segmental thrombosis or stenosis greatly exceeded those obtained from other methods of therapy for peripheral arteriosclerosis. The indications for and the limitations of lumbar sympathectomy as a palliative procedure are described. Medical treatment, except for the use of specific protective measures, was of little value in altering either the symptoms or prognosis.

Arterial Occlusive Diseases↗
PubMed2005

MMP-2 expression is associated with rapidly proliferative arteriosclerosis in the flexor tenosynovium and pain severity in carpal tunnel syndrome.

Due to the lack of correlation between symptom severity and electrophysiology or nerve function, the 'container hypothesis' has emerged as a new concept in carpal tunnel syndrome (CTS). This proposes that symptoms relate to connective tissue alteration rather than to nerve fibre pathology. This study was conducted to investigate the pathology of the flexor tenosynovium and its relationship with symptomatology. The subjects comprised 40 patients with electrophysiologically proven CTS who underwent open carpal tunnel release (age range: 31-79 years). In all patients, subjective symptom severity was assessed with a Likert scale and symptom duration was recorded preoperatively. Flexor tenosynovium biopsied during surgery was analysed for arterial and connective tissue alteration. Proliferative arteriosclerosis was graded using the modified Banff score. Gelatin zymography and immunohistochemistry were also performed to investigate the role of gelatinase in CTS. Relationships were evaluated using Spearman rank correlation coefficients. Proliferative arteriosclerosis occurred with disease progression in the flexor tenosynovium, in the absence of inflammation. This event did not correlate with patient age but correlated closely with symptom duration. Immunohistochemistry with antibodies against MMP-2 and elastic van Gieson staining revealed that arterioles express high levels of MMP-2 within 3 months of symptom onset and that intimal hyperplasia proceeded rapidly between 4 and 7 months, resulting in severe vascular narrowing. Gelatin zymography showed that MMP-2 activity correlated negatively with symptom duration and positively with pain severity.

Adult↗
PubMed1989

The visualization of femoral vessels in delayed bone scans--a sign of arteriosclerosis? A comparison of 99mTc-MDP and 99mTc-DPD.

The activity of femoral vessels in delayed bone scans was evaluated visually in 237 consecutive patients and quantified in 40 female patients. In visual analysis the patients were randomly divided into three groups and in quantitative analysis into four groups of equal size. Two different MDP preparations and one DPD preparation were used as bone-seeking agents. With aging, the activity in femoral vessels increased with all agents in visual analysis, significantly with MDPs (P less than 0.001) between patients less than or equal to 60 years and greater than 60 years. In female patients with all agents a significant increase in femoral activity was found (P less than 0.001 with MDPs, P less than 0.05 with DPD). In patients greater than 60 years, the femoral uptake was significantly higher with MDP when compared with the DPD uptake (P less than 0.01 with MDP1, P less than 0.05 with MDP2). Between the MDPs no significant differences were found. In quantitative analysis the femoral vessel to soft tissue ratio was significantly higher in patients greater than 70 years when compared with patients less than or equal to 50 years with MDP. No difference was found with DPD. Histological examination of excised arteries of ten patients with intense femoral uptake of MDP showed arteriosclerosis and calcification in all cases. The findings suggest that the femoral visualization in delayed bone scans is probably related to arteriosclerosis and is not a non specific finding. There may be age-related differences in the distribution of MDP and DPD.

Age Factors↗
PubMed1995

Effects of angiopeptin on transplant arteriosclerosis in the rat.

The influence of the somatostatin analogue angiopeptin on transplant arteriosclerosis was investigated using two aortic transplantation rat models. One was characterized by ischemia/reperfusion-induced changes in syngeneic transplants while immunologically induced changes dominated in the other allogeneic model. Angiopeptin, 100 micrograms/kg per day, was administered continuously until the sacrifice of the rats after 8 weeks. No additional immunosuppression was used in either model. An image analysis system was used to quantify the intimal and medial thicknesses of the grafts. In the syngeneic grafts, the intimal thickness was less than 50% of that of control grafts (P < 0.05), but no difference was seen in the allogeneic model. The expression of selected cells, TGF-beta s, and PDGF and PDGF alpha-receptors was detected immunohistochemically and displayed a similar picture in control and angiopeptin-treated grafts in both models. We conclude that angiopeptin has no clear immunosuppressive properties but may counteract ischemia-induced transplant arteriosclerosis.

Animals↗