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PubMed1998

Elevated neointimal endothelin-1 in transplantation-associated arteriosclerosis of renal allograft recipients.

BACKGROUND: Chronic renal allograft rejection is characterized histologically by transplantation-associated arteriosclerosis and glomerulosclerosis (Tx-AA and Tx-AGS). Recent studies in animal models implicate the mitogenic and pressor actions of endothelin-1 (ET-1) in Tx-AA. In humans, however, a link between elevated ET-1 secretion and Tx-AA or Tx-AGS remains unclear. In this study we analyzed expression of ET-1 in the vasculature of renal transplant patients with chronic or acute rejection and in normal controls. METHODS: Renal vascular and glomerular ET-1 was assessed by immunohistochemistry in 12 patients with clinically and histologically defined chronic rejection, in 11 patients with acute rejection, and in 5 normal kidneys. ET-1 staining was also correlated with various clinical parameters and with a morphometric index of neointima formation. ET-1 secretion was measured by ELISA in cultured human vascular cell types treated with T cell- and macrophage-associated cytokines. RESULTS: We found that renal allografts with chronic rejection and Tx-AA expressed 6.1-fold more ET-1 in the vasculature relative to allografts with acute rejection or to normal kidneys (P < 0.01). In Tx-AA, ET-1 was detected predominantly in the neointima, which contained mostly endothelial cells and smooth muscle cells. A strong positive correlation (r = 0.82, P < 0.01) was observed between vascular ET-1 peptide expression and hypertension in patients with chronic rejection. We also showed that macrophage-associated cytokines, but not T cell-associated cytokines, stimulated ET-1 secretion in human endothelial cells, vascular smooth muscle and mesangial cells. CONCLUSIONS: These results demonstrate that elevated ET-1 in the neointima is associated with Tx-AA and chronic rejection. In addition, these results point to an important role for endothelial dysfunction in chronic renal allograft rejection.

Adolescent↗
PubMed1994

[Arteriosclerosis of the orbital arteries].

BACKGROUND: The anatomy of the orbital arteries is well known, and their physiology is under intensive investigation. Their age-related or other pathologic alterations, however, are still largely unknown. METHOD: We obtained at autopsy 16 orbits from 8 persons aged > 70 years, and 4 orbits from 2 persons between 40 and 50 years. Specimens were taken from 20 locations along the orbital arteries, from the internal carotid to the globe, and studied by light microscopy. RESULTS: We observed the following arteriosclerotic changes, in order of decreasing frequency: intimal hyperplasia, medial atrophy, atherosclerotic fibrous plaques, and calcifications of the internal elastic lamina. The frequency and severity generally decreased with smaller arterial caliber. CONCLUSION: Arteriosclerosis was ubiquitous in persons > 70 years of age. Degenerative changes in aged human orbital arteries may play an important role in ophthalmic vascular diseases.

Adult↗
PubMed1994

[Carotid artery wall changes in young type-1 diabetics. The ultrasonic diagnosis of early arteriosclerosis].

In a prospective study high-resolution ultrasonography was used to document any early carotid-artery wall changes (intima-media thickening; plaques), in 165 type I diabetics up to the age of 40 years (66 males, 99 females; mean age 27.5 +/- 6 years; duration of diabetes > 1 year). In two control groups (group 1: 40 with type I diabetes of up to one year's duration; group 2: 20 healthy subjects) the mean intima-media thickness was 0.50 +/- 0.05 and 0.51 +/- 0.06 mm, respectively (maximal value 0.6 mm). In the patients with a longer duration of diabetes it was significantly higher at 0.56 +/- 0.11 mm (P < 0.001). Of the 165 patients with a diabetes duration of more than 1 year, 134 had normal intima-media wall thickness (< 0.6 mm, mean 0.52 +/- 0.07 [group A]), in 15 (group B) it was 0.75 +/- 0.06 mm, and in 16 (group C) there were plaques with a wall thickness of 0.67 +/- 0.15 mm. The incidence of nephropathy and hypertension or hypercholesterolaemia (only in group C) was significantly higher in groups B and C than A (P < 0.01). It is thus clear that these consequential or associated diseases go together, in young type I diabetics, with an increased risk of early arteriosclerosis.

Adult↗
PubMed1981

[Increased cardiovascular arteriosclerosis risk in patients with analgesic nephropathy (author's transl)].

The retrospective investigation of 54 patients with analgesic nephropathy showed the relatively early occurrence of coronary sclerosis and an increased frequency of arteriosclerotic renal artery stenosis. Angina pectoris was found in 14 patients with a mean age of 48 1/2 years. Summation of risk factors is the probable cause of the tendency for arteriosclerosis: hypercholesterolaemia and hypertriglyceridaemia was found in 29 patients, arterial hypertension in 42 patients, which was so severe in half of the patients that combined treatment with two or more drugs was necessary. The causes of lipid metabolism disturbances as well as the pathogenesis of arterial hypertension are not known. Arteriosclerotic renal artery stenoses observed in 8 patients are not likely to be the cause of hypertension.

Adult↗
PubMed1975

Problems of aging: diagnosing and treating leg pain due to arteriosclerosis obliterans.

Management of patients with arteriosclerosis obliterans begins with organization of the history, results of physical examination, and blood flow measurements into a patient profile. This approach permits the practicing physician to monitor the progression of the obstructive process over time. With close observation, a controlled exercise program, and properly timed surgical intervention, if necessary, patients with arterioslcerosis obliterans can enjoy a full and productive life.

Aging↗
PubMed2004

Platelet activation markers, microparticles and soluble adhesion molecules are elevated in patients with arteriosclerosis obliterans: therapeutic effects by cilostazol and potentiation by dipyridamole.

We evaluated the plasma concentrations of platelet activation markers, microparticles and soluble adhesion molecules in patients with arteriosclerosis obliterans (ASO) and compared the beneficial effects of cilostazol alone and combination therapy of cilostazol and dipyridamole in these patients. There was a significant elevation of CD62P, CD63, PAC-1, annexin V, platelet-derived microparticles (PDMPs), sP-selectin, sE-selectin, sICAM-1 and sVCAM-1 in the ASO patients compared with the controls. Platelet aggregation was decreased by 2 weeks of cilostazol monotherapy in the ASO patients. Adding dipyridamole to the cilostazol therapy for 2 weeks further reduced platelet aggregation. While treatment with cilostazol alone reduced levels of CD62P, CD63, PAC-1, annexin V, PDMP, and sP-selectin, the combination therapy reduced these parameters further. While sE-selectin and cell adhesion molecules did not change significantly after 2 weeks of combination therapy, they exhibited a remarkable decrease after 16 weeks of combination treatment. These findings suggest that platelets are activated in ASO patients, and cilostazol is effective to reduce platelet activation. Furthermore, dipyridamole may potentiate the beneficial effect of cilostazol in ASO patients. Combination use of both drugs may help to prevent the onset of cardiovascular complications in patients with ASO by activated platelets and PDMP.

Aged↗
PubMed1987

Exercise attenuates diet-induced arteriosclerosis in the adult rat.

The present investigation was conducted to assess the effects of exercise on diet-induced arteriosclerosis in retired breeder rats. Thirty-two 8- to 9-mo-old male Sprague-Dawley rats were allocated to one of four treatment groups: hypercholesterolemic diet-exercise (HE), hypercholesterolemic diet-sedentary (HS), normocholesterolemic diet-exercise (NE) and normocholesterolemic diet-sedentary (NS). The hypercholesterolemic diet contained 10% lard and 0.4% cholesterol. Exercise consisted of running on a motor-driven treadmill at an 8% grade 1 h per day at 0.5 mph, 6 d weekly for 5 mo. A histological assessment of the aortas demonstrated that although grossly visible atherosclerotic plaques were absent, there were significant microscopic differences among groups in the thoracic aorta, iliac bifurcation and aortic arch. Aortic histopathological changes were greatest in cross sections from rats in the HS group. The accumulation of collagen and sulfated mucosubstances was greater in the HS versus HE group. Our results demonstrate a beneficial effect of exercise on diet-induced histopathological changes in the aortas of male retired breeder rats.

Animals↗
PubMed1976

Factors in the differential rate of arteriosclerosis (AS) between long surviving renal transplant recipients and dialysis patients.

In this study, the incidence of clinical and autopsy arteriosclerosis (AS) was studied in over 300 renal transplant patients (RTP) followed in our clinic up to 13 years post-transplant. Of 45 RTP followed a mean of 10.45 years, the incidence of clinical AS was 6% or 0.58% per year at risk. The incidence of death from AS was 2.2% over 10 years or 0.22% per year at risk. There was no apparent tendency for increase of the risk incidence with increasing time post-transplantation up to 13 years. This incidence of clinical and death-related AS in long term RTP contrasts sharply with a quite high incidence of both clinical and death-related AS in long-term dialysis patients as reported by Scribner's group and both the European and U.S. Dialysis Registry. Of our RTP surviving a decade or more, 77% have normal serum triglycerides and 92% are normotensive, again contrasting sharply with a 70-80% incidence of hyperlipidemia and a 60-80% incidence of hypertension in long-term dialysis patients. These studies suggest that the high rate of accelerated AS in dialysis patients is largely reversed by successful renal transplantation, probably due to a lowering of both blood pressure and hyperlipidemia in the long-term RT patients. Practically, these results suggest that the superior survival of transplant patients over dialysis patients already evident at 10 year mark will widen further during the second post-transplantation decade.

Adolescent↗
PubMed1989

Cardiac transplantation in the rat. I. The effect of histocompatibility differences on graft arteriosclerosis.

The development of arteriosclerosis is the most serious and common complication in long-term survivors of cardiac transplantation. We have used a variety of inbred rat strains with selected histocompatibility differences to examine the influence of prolonged, mild rejection reactions on the development of pathological changes in long-term cardiac allografts. Heterotopic cardiac allografts were exchanged between rat strains that differed for MHC class I (RT1.A and/or RT1.E) antigens or groups of minor, non-MHC antigens in MHC-compatible congenic combinations. Our results demonstrate that in strain combinations in which the allograft reaction is mild and prolonged, the donor hearts exhibit pathological changes that include a diffuse, interstitial myocardial fibrosis, perivascular fibrosis, and intimal proliferation in arteries of the graft myocardium. The lesions were less prominent in animals with more active rejection and infrequent in strains that differ for class I histocompatibility antigens or syngeneic controls. These results suggest that the comparable pathological changes seen in long-term human cardiac survivors may reflect low-level, persistent allograft reactions rather than factors associated with graft anoxia or effects of immunotherapy to prevent graft rejection.

Animals↗
PubMed1995

Endothelial loss and regeneration in a model of transplant arteriosclerosis.

Early endothelial injury may play a role in the development of transplant arteriosclerosis. The present study documents early endothelial changes using a rat aortic graft model. Abdominal aortic allografts from PVG rats were orthotopically transplanted to DA rats. Controls were DA to DA transplants. Endothelial cell (EC) injury, regeneration, and leukocyte infiltration in the intima were evaluated using scanning electron microscopy and histological and immunocytochemical techniques. Nontransplanted aortic segments showed partial loss of ECs after 1 or 2 hr of preservation. Control isografts demonstrated extensive EC denudation and neutrophil adherence to residual ECs at 1 day post-transplantation. After 3 days, isografts showed continued regeneration of ECs in the central area and ingrowth of endothelium from both clamped sites in the recipient aorta. Reendothelialization was complete by day 14. Allografts showed similar findings to isografts up to day 3. In contrast to isografts, however, there was a secondary EC loss beginning at day 7. Monocytes/macrophages and T cells were noted to be adherent to residual ECs in 7- and 14-day allografts. At 20 days, ECs were absent from the luminal surface in the center of allografts. Endothelium did extend from clamped sites toward the midgraft region as in isografts. By 60 days allografts were completely reendothelialized. These results demonstrate that in both isografts and allografts there is initial EC loss due to mechanical trauma and ischemia/reperfusion injury, followed by partial reendothelialization. This latter process continues unabated in isografts, whereas in allografts the secondary EC loss occurs due to an allogenic response. This is followed by complete reendothelialization that occurs during the concurrent development of significant intimal hyperplasia.

Animals↗
PubMed1996

Reversibility of allograft arteriosclerosis after retransplantation to donor strain.

The rat aortic transplant model was modified to investigate whether the vascular wall changes on chronic rejection are reversible. DA (RT1a) aortas were first transplanted to WF (RT1a) recipients. The first transplantation was accompanied, as described earlier, by an increase in intimal cellularity and thickness and typical arteriosclerotic changes of chronic rejection in the allograft intima. A second transplantation was made to DA, WF or to (DAxWF)F1 recipients 10 days-2 months after the first transplantation. In all retransplantations performed at any one of the indicated timepoints, the thickness and number of nuclei of the intima continued to increase. These observations demonstrate that, after an initial trigger, allograft arteriosclerosis proceeds and is irreversible despite elimination of histoincompatibility.

Animals↗
PubMed1997

Acceleration of arteriosclerosis of the rat aorta allograft by insulin growth factor-I.

We demonstrate here, for the first time, the mitogenic effect of insulin-like growth factor-I (IGF-I) on the development of transplant arteriosclerosis in a rat orthotopic aorta allotransplantation model (Brown Norway to Lewis). 125I-IGF-I uptake by the abdominal aorta of male Brown Norway rats occurred within 30 min. Consequently, we exposed the donor abdominal aorta to 0, 200, or 500 ng/ml IGF-I at 37 degrees C for 30 min ex vivo (n=7 per group), before transplantation. Fourteen days after transplantation, intimal thickening of the allografts in each of the three groups was 0.18+/-0.02 (IGF-I at 0 ng/ml), 0.23+/-0.03 (IGF-I at 200 ng/ml), and 0.30+/-0.03 (IGF-I at 500 ng/ml), respectively (mean+/-SEM, P<0.005 for 500 ng/ml vs. 0 ng/ml). [3H]thymidine incorporation (cpm/microg protein) in the transplanted grafts at 7 days after transplantation (n=4 per group) was 40.6+/-7.6, 78.5+/-12.3, and 66.9+/-10.1, respectively (P<0.01 for 200 ng/ml vs. 0 ng/ml). [3H]thymidine incorporation in the native thoracic aorta of the recipient was 23.4+/-4.4. We conclude that acceleration of allograft myointimal proliferation and intimal thickening was induced directly by IGF-I.

Animals↗
PubMed2000

Prevention of cardiac allograft arteriosclerosis using antisense proliferating-cell nuclear antigen oligonucleotide.

Cardiac allograft arteriosclerosis limits long-term survival of recipients and is characterized by intimal thickening comprised of proliferative smooth muscle cells. Proliferating-cell nuclear antigen (PCNA) plays a pivotal role in the cell cycle regulatory genes involved in smooth muscle cell proliferation. To test the hypothesis that antisense PCNA oligodeoxynucleotide (ODN) can prevent allograft arterial intimal hyperplasia, we performed single intraluminal delivery of the antisense or sense PCNA ODN or no transfer into murine cardiac allografts. DBA/2 murine hearts were transfected and transplanted into B10.D2 mice; the allografts were harvested 4 weeks later. Severe intimal thickening with enhanced expression of PCNA was observed in untransfected and sense PCNA ODN-treated allografts, whereas antisense PCNA ODN prevented neointimal formation.

Animals↗
PubMed2001

Accelerated graft arteriosclerosis in cardiac transplants: complement activation promotes progression of lesions from medium to large arteries.

BACKGROUND: A critical role for the terminal components of complement (C5b-C9) has been demonstrated previously in acute allograft rejection with the use of C6-deficient PVG congenic rat strains. The C6 deficiency prevents the formation of membrane attack complex (MAC) by C5b-C9. Hearts transplanted from PVG.1A (RT1a) rats are rejected acutely (7-9 days) by fully MHC-incompatible C6-sufficient PVG.1L (RT11) recipients, but they survive significantly longer in untreated C6-deficient PVG.1L recipients (19 to >60 days). METHODS: To investigate the contribution of MAC to chronic rejection and accelerated graft arteriosclerosis (AGA) in long-term cardiac allografts, hearts were transplanted heterotopically from PVG.1A donors to C6-sufficient and C6-deficient PVG.1L hosts that were treated with cyclosporine 15 mg/kg/day for 14 days after cardiac grafting. Alloantibody responses in hosts were measured by flow cytometry at 4, 8, 12, and 16 weeks after transplantation. Vigorously contracting grafts were removed at 60 days (n=5) and at 90-128 days (n=12) after surgery for morphological evaluation. Computerized planimetry measurements were made in complete cross-sections of grafts on all assessable arteries larger than 16 microns in diameter. RESULTS: The survival of most (six of seven) cardiac allografts in C6-deficient recipients was prolonged by cyclosporine treatment to greater than 90 days. In contrast, 14 of 25 hearts that were transplanted to C6-sufficient recipients were rejected between 21 and 84 days with severe vascular injury. AGA, defined as smooth muscle cells forming a neointima inside the internal elastic lamina and luminal compromise, affected a greater percentage of arteries in C6-sufficient than in C6-deficient recipients. AGA developed earlier and more frequently in arteries of medium (<100 micron) diameter than those of large diameter in both C6-sufficient and C6-deficient recipients. Serial sections demonstrated the lesions in medium arteries to be located adjacent to the smooth muscle sphincters at the junction of arteriolar branches. CONCLUSIONS: These results demonstrate that MAC promotes the pathogenesis of AGA in long-term cardiac allografts.

Animals↗
PubMed2006

Aggressive conservative therapy for refractory ulcer with diabetes and/or arteriosclerosis.

A foot ulcer due to diabetes and/or arteriosclerosis obliterans (ASO) frequently results in an intractable condition that resists treatment. To cope with this condition, we have developed a combination therapy that includes conventional conservative therapy plus surgical therapy. This aggressive conservative therapy using aggressive debridement, trafermin (Fiblast Spray, Kaken, Japan) treatment and vacuum-assisted closure (VAC) therapy was adopted to treat seven patients suffering from diabetes and ASO-related refractory foot ulcer accompanied by bone exposure. With the exception of one patient who died during the treatment, the remaining six patients obtained limb salvage. The mean time to cure was 8.3 months. This approach should be considered before amputation. Some patients may refuse amputation or cannot tolerate highly invasive surgical treatment including tissue transplantation. In such cases, this aggressive conservative therapy can be employed as a highly useful and reproducible technique requiring simple techniques.

Aged↗
PubMed2005

Cytomegalovirus-enhanced development of transplant arteriosclerosis in the rat; effect of timing of infection and recipient responsiveness.

Cytomegalovirus (CMV) is put forward as a risk factor for transplant arteriosclerosis (TA). In this article, we studied CMV-enhanced development of TA in rats in different donor/recipient combinations in relation to the timing of infection. Recipient rats transplanted with an aortic allograft (BN to Lew) were infected with rat CMV (RCMV) at different time-points relative to transplantation. The virus-induced effects on TA development were also determined in other strain combinations (PVG to AO and DA to WF). Finally, transmission of RCMV from aortic grafts and its effect on TA was studied. RCMV infection enhanced TA development only in Lew recipients and only after infection early post-transplantation (days 1-5). Virus transmission to the recipient only occurred from 5 and 10 days infected aortic donor-grafts, however without affecting TA development. These data indicate that the acute alloresponse and acute CMV infection need to occur simultaneously to enhance TA. This effect, however, appears to be strain combination dependent and therefore cannot be generalized.

Animals↗
PubMed1986

The relationship between arteriosclerosis and the wave line of aorta.

The wave line is a structure that is frequently observed in aorta. Grossly this structure (wave line), measuring 0.3-0.5 cm in width and 5-10 cm in length, runs longitudinally or spirally along the long axis of the aorta. The distribution and the relation with arteriosclerotic plaque of wave line were studied. The wave line had three predilection sites: A) the wave line running down from closure of Botallo duct to ostium of 6-8th intercostal artery, B) the wave line between ostium of both renal arteries, C) the wave line running down from lumbar artery to iliac arteries. The wave line observed in the aortae of neonates gradually increased with age. Its frequency is about 80-100% in the second and the third decades. The association of arteriosclerosis with the wave line was frequently observed, especially on "C" region. Fifty-five percent of arteriosclerotic plaques in the fourth decade corresponded with the wave line.

Adolescent↗
PubMed1976

Cyclandelate in the treatment of cerebral arteriosclerosis.

Twenty-one patients with cerebral arteriosclerosis were treated for twelve months with placebo or cyclandelate (Cyclospasmol), 400 mg four times daily, in a double-blind study with medication cross-over after six months. The group included 8 men and 13 women, with a mean age of 69 years. Each patient showed at least 5 of 9 signs or symptoms adopted as "inclusion criteria" for the study. Concomitant psychotropic or other drug therapy was standardized or matched during the trial, and periodic assessments were made of the patients' behavioral, physical, neurologic and psychiatric status. No serious side effects were observed. There was no significant difference between the cyclandelate and placebo phases in measurements of physical state. Changes on the gross behavior scales were insufficient for analysis. Tests of memory, control of manual dexterity and comprehension of everyday situations showed statistically significant improvement during the cyclandelate phase. In contrast to placebo, no measurable intellectual decline occurred during cyclandelate therapy.

Aged↗