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PubMed1989

Effects of fish oil on arteriosclerosis in the Japanese quail.

The effects of fish oil on the development of arteriosclerosis were assessed using a special susceptible strain (SEA) of Japanese quail (Coturnix coturnix japonica). Sixty four quail were randomly divided into two groups and placed on isocaloric and approximately isocholesterolic (2% by weight) diets. Group A (control) was supplemented with 10% beef tallow oil, while group B received 10% Menhaden fish oil. The birds were sacrificed at 10 weeks (early) and 15-16 weeks (late). Based on semiquantitative histological grading of the arteriosclerotic lesions in the proximal aorta and brachiocephalic arteries, a score from 1 (no lesion) to 5 (severe, diffuse lesions) was assigned. A total of 57 quail were evaluated (seven died prior to scheduled sacrifice). At the early period, the mean arteriosclerosis scores for group A (n = 8) and group B (n = 8) were 3.3 (SD 1.0) and 1.9(1.0) respectively (p less than 0.017); 63% of the quail in group A and 13% of those in group B had a score greater than or equal to 3 (p less than 0.25, NS). At the late period, the scores for group A (n = 20) and group B (n = 21) were 3.8(0.6) and 2.6(0.9), respectively (p less than 0.001); 95% of the birds in group A and 43% of those in group B had a score greater than or equal to 3 (p less than 0.005). Histopathological examination of the arteriosclerotic lesions revealed disruption of the innermost elastic lamina, increased proteoglycan deposition in the medial interlamellar spaces, and the distinct involvement of macrophage like cells. Compared to human disease, arteriosclerosis in the quail is marked by distinct similarities, as well as differences. The SEA strain of Japanese quail appears to be a practical model for the study of arteriosclerosis; fish oil reduces the severity of disease in these birds when fed a high cholesterol diet.

Animals↗

PubMed1996

Lack of effect of recombinant human superoxide dismutase on cold ischemia-induced arteriosclerosis in syngeneic rat aortic transplants.

Prolonged cold ischemia time and the generation of free oxygen radicals during reperfusion are risk factors for allograft arteriosclerosis. Growth factors are the main pro-proliferative mediators of smooth muscle cells in classical and in allograft arteriosclerosis. Superoxide dismutase is an enzyme that catalyzes the dismutation of superoxide anions into hydrogen peroxide. This study was designed to investigate which smooth muscle cell growth factor contribute to the formation of arteriosclerosis in syngenic vascular grafts with prolonged ischemia time, and whether perioperative intravenous administration of recombinant human superoxide dismutase (rh-SOD) prevents arteriosclerosis in these grafts. DA aortas were transplanted into DA recipients. One group of transplants was made with a short ex vivo ischemia time (15 min), while the other group transplant grafts was stored for 24 hr in cold saline. In addition to morphometric quantitation of the histological alterations, RNA isolated from grafts with short cold ischemia time in a semiquantitative polymerase chain reaction specific for various known smooth muscle cell growth factors. Syngeneic grafts with prolonged cold ischemia time showed severe intimal thickening and prominent medical necrosis, which were not seen in control groups. Approximately 3-fold levels of insulin-like growth factor-1 were found in ischemic syngeneic grafts compared with non-ischemic syngenic grafts, whereas epidermal growth factor levels were slightly lower. No changes in other growth factor mRNAs were found. Perioperative treatment with rh-SOD did not have significant effect on the extent of intimal thickening nor on the intensity of medial necrosis in grafts with prolonged ischemia time, and administration of rh-SOD did not change the expression level of insulin-like growth factor-1 in the grafts, either.

Animals↗

PubMed2002

Indirect allorecognition can play an important role in the development of transplant arteriosclerosis.

BACKGROUND: Indirect allorecognition has been implicated in the initiation of chronic allograft dysfunction. Our aim was to develop an animal model that allowed the contribution of the direct and indirect pathway of allorecognition in the evolution of transplant arteriosclerosis, the main feature of chronic allograft rejection, to be evaluated. METHODS: Aortic allografts mismatched for a single MHC class I antigen were transplanted into athymic NUDE or RAG (-/-) mice. Immunodeficient mice were reconstituted with either CD4(+) (indirect) or CD8(+) (direct + indirect) T cells in the presence or absence of depleting antibodies specific for the opposite T-cell subset. Aortic grafts were analyzed by performing morphometry, immunohistochemistry, and quantitative reverse transcriptase-polymerase chain reaction for the detection of cytokine mRNA production. Donor-specific alloantibody production was measured by fluorescence-activated cell sorter analysis. RESULTS: Reconstitution of athymic nude mice with 4 x 10(7) purified CD4(+) T cells resulted in vascular rejection of MHC class I mismatched aortic grafts. Intimal proliferation was 24+/-8% and did not decrease when nude-derived endogenous CD8(+) T cells were depleted from the nude recipients (intimal proliferation, 21+/-7%). Transplant arteriosclerosis initiated by CD4+ T cells was associated with the presence of intragraft mRNA for interferon-gamma, tumor necrosis factor-alpha, inducible nitric oxide synthase, and interleukin 12. Reconstitution of RAG-1(-/-) mice with 4 x 10(7) purified CD4(+) T cells resulted in a similar degree of transplant arteriosclerosis (intimal proliferation, 20+/-9%) in MHC class I mismatched aortic grafts in the absence of alloantibody production. CONCLUSION: Indirect recognition of donor MHC class I molecules by CD4(+) T cells can play an important role in the process of transplant arteriosclerosis. CD8(+) T-cell effector function and alloantibody production in this model are dependent on CD4(+) T-cell help after indirect allorecognition.

Adoptive Transfer↗

PubMed2002

Kinetics of transplant arteriosclerosis in MHC-Class I mismatched and fully allogeneic mouse aortic allografts.

INTRODUCTION: Transplant arteriosclerosis is still the major complication for long-term allograft survival in clinical transplantation. The aim of our study was to investigate the impact of MHC disparity on the kinetics of the development of transplant arteriosclerosis. METHODS: MHC-class I mismatched CBK (H2k+Kb) or fully allogeneic C57BL/10 (H2b) aortic allografts were transplanted into CBA.CA (H2k) recipients; syngeneic grafts were used as controls. Aortic grafts were analyzed on days 7, 14, and 30 after transplantation by performing morphometry, immunohistochemistry and quantitative reverse-transcriptase polymerase chain reaction (RT-PCR) for the detection of intragraft cytokine mRNA production. Donor specific alloantibody production was measured by FACS analysis. RESULTS: Intimal proliferation developed more rapidly in fully allogeneic grafts (direct and indirect allorecognition by CD4+ T cells) compared to MHC-class I mismatched grafts (indirect allorecognition only by CD4+ T cells) (day 7: 6+/-7 vs. 2+/-3%; day 14: 17+/-8 vs. 5+/-1%; day 30: 65+/-5 vs. 38+/-7% (C57BL/10 vs. CBK). However, by day 60, the level of intimal proliferation in the MHC-class I mismatched grafts was equivalent to that observed with fully allogeneic grafts on day 30. There was also a marked delay in the kinetics of graft infiltration by CD4+, CD8+, CD11b+, and CD40+ leukocytes and alloantibody production when CD4+ T cells were only activated via indirect presentation (MHC-class I mismatched grafts). Expression of interferon-gamma, interleukin-2, and interleukin-4 correlated with the kinetics of leukocyte infiltration, whereas interleukin-10, interleukin-12p40, iNOS, and TGF-beta1 showed a distinct pattern of expression. CONCLUSIONS: These data demonstrate that the degree of MHC incompatibility between donor and recipient markedly influences the kinetics of the development of transplant arteriosclerosis. The onset of disease was delayed when grafts were mismatched for only MHC-class I antigens, but ultimately reached the same levels as seen in fully allogeneic grafts. The pattern of leukocyte infiltration and the kinetics of cytokine production suggest that in the MHC-class I mismatched grafts CD4+ T cells responding via the indirect pathway might play an important role in the development of transplant arteriosclerosis.

Animals↗

PubMed1982

Arteriosclerosis, infarcts, and dementia.

A study was made of 343 elderly mental-hospital patients whose mental disorder had begun late in life. Of the 31 brains examined at autopsy, 14 showed cerebral infarcts without senile brain disease and ten showed senile brain disease without infarcts. The amounts of arteriosclerosis in the two groups were compared. The microscopic evidence was not treated statistically, but the macroscopic evidence was subjected to Fisher's exact test and chi square for comparison of the amounts of arteriosclerosis noted at the base of the brain and the number of plaques on the named arteries within the brain. The results showed an overwhelming preponderance of arteriosclerosis in the infarct patients compared with the senile brain disease patients. It is concluded that in elderly patients with mental disorders, brain infarcts occur in close and causal relationship with cerebral arteriosclerosis. The bearing of this observation upon the concept of multi-infarct dementia is discussed.

Aged↗

PubMedDate not supplied

Chronic rejection in rat aortic allografts. An experimental model for transplant arteriosclerosis.

Chronic rejection has several histological appearances, depending on the type of organ graft. Common to all of them is transplant arteriosclerosis associated with an ongoing inflammatory response in the transplanted graft. To the contrary of classical atherosclerosis, in which the manifestations are mostly focal, proximal, and asymmetric, transplant arteriosclerosis is generalized, and the intimal thickening is concentric. In this article, we describe an experimental animal model whereby transplant arteriosclerosis may be investigated in the inbred rat. Aortic allografts were transplanted from DA (RTIa) to major histocompatibility complex-incompatible WF (RTIv) rats or, for control, to rats of the DA strain. Transplantation was followed by an acute inflammation episode in the aortic adventitia of the allograft, largely lacking in the syngeneic graft, with a prominence of lymphoid activation markers (Cd25) in the cells of the inflammatory infiltrate. The inflammation episode peaked at 2 months after transplantation, became attenuated, and was followed by a proliferative response of myocytes in the allograft media. An increase in the migration of myocytes to the subendothelial space (presumably through small breaks generated in the internal elastic lamina) was observed thereafter, and myocyte proliferation continued in the intima with some intermingled macrophages. Finally, necrosis and disappearance of myocytes and their replacement by fibrous tissue were observed in the media. These alterations are virtually identical with the vascular lesion of chronically rejecting parenchymal organ transplants in human subjects. We suggest that aortic allografts exchanged between histoincompatible rat strains may be used as an experimental model for transplant arteriosclerosis.

Animals↗

PubMed1994

Hyperlipidemia accelerates allograft arteriosclerosis (chronic rejection) in the rat.

The relevance of hyperlipidemia in allograft arteriosclerosis (chronic rejection) is controversial. Isolated hypercholesterolemia induced with cholesterol-cholic acid-diet (CC-diet) or hypertriglyceridemia induced with glycerol-diet (G-diet) had no or only a protective effect on aortic allograft arteriosclerosis in the rat. Combined hyperlipidemia with both diets (CC+G-diet) enhanced allograft arteriosclerosis by doubling intimal thickness and cellularity (P < .05) but had no effect on host arteries. Compared with normolipidemic controls, the CC+G-diet increased the total serum cholesterol concentration 4.8-fold (P < .05). Levels of VLDL2 and IDL increased 4.8- and 18.1-fold (P < .05), and their composition changed from triglyceride-rich to cholesterol-rich lipoproteins in an atherogenic direction. The CC+G-diet had no effect on the structure of inflammation in the vascular wall. Instead, significant lipid deposits were observed, and the expression of epidermal growth factor and insulin-like growth factor-1 was significantly elevated in the vascular wall. Thus, elevations in VLDL and IDL lipoprotein levels and their cholesterol content associate with the generation of allograft arteriosclerosis in rats. Deposition of lipids in the vascular wall seems to induce local synthesis of certain growth factors, which ultimately leads to the induction of smooth muscle cell replication.

Animals↗

PubMed1994

Cyclosporin suppresses transplant arteriosclerosis in the aorta-allografted, cholesterol-clamped rabbit. Suppression preceded by decrease in arterial lipoprotein permeability.

The immunosuppressant cyclosporin has been suggested to aggravate as well as retard the development of transplant arteriosclerosis, the major long-term problem for patients with heart transplants. We examined the effect of human therapeutic levels of blood cyclosporin on the development of experimental transplant arteriosclerosis. The thoracic aorta from one rabbit was transplanted as an end-to-side bypass on the abdominal aorta of another rabbit, and plasma cholesterol was clamped at 5 to 7 mmol/L. Cyclosporin markedly suppressed the severity of transplant arteriosclerosis, judged both biochemically and histologically: cholesterol content in aortic transplants was reduced by 70% and 80% after 10 days and 20 days of cholesterol feeding, respectively (both comparisons, P < .01), and after 20 days of cholesterol feeding myointimal proliferation was totally inhibited in grafts from cyclosporin-treated animals, judged from maximal intimal thickness and intimal area on cross sections of grafts (both comparisons, P < .05). In another group of non-cholesterol-fed, aorta-transplanted rabbits, cyclosporin reduced by 90% (P < .01) an otherwise markedly increased permeability to low-density lipoprotein in transplanted aortas. These results suggest that cyclosporin causes a substantial decrease in the severity of transplant arteriosclerosis and that this effect is mediated at least partly via a large decrease in aortic lipoprotein permeability.

Animals↗

PubMed1998

Exacerbated transplant arteriosclerosis in inducible nitric oxide-deficient mice.

BACKGROUND: Inducible NO synthase (NOS2, or iNOS) is upregulated in grafts with transplant arteriosclerosis. However, the functional role of NOS2 in the pathogenesis of transplant arteriosclerosis remains unclear. NOS2 may regulate lesion development by modulating the early alloimmune response and/or late myointimal thickening. METHODS AND RESULTS: To determine whether NOS2-mediated pathways protect against or promote transplant arteriosclerosis, we used NOS2-deficient mice as recipients in our vascularized chronic cardiac rejection model. The severity of vascular thickening in 55-day grafts placed into NOS2 -/- recipients (n=13) was compared with that in wild-type recipients (n=15). Computer-assisted analysis of all elastin-stained vessels (n=283) showed significantly increased luminal occlusion (77.11+/-9.4% versus 40.8+/-13.6%, P<.0001) and intima/media ratios in allografts from NOS2 -/- recipients (1.9+/-1.3 versus 0.4+/-0.3, P=.0002). To elucidate potential mechanisms, we studied NOS2 effects on T-cell differentiation (Th1/Th2) and neointimal smooth muscle cell accumulation. Normalized mRNA levels for Th1- (signal transducer and activator of transcription [STAT] 4, interleukin [IL]-2, interferon-gamma) and Th2- (STAT 6, IL-4, and IL-5) associated factors were comparable in both groups. In contrast, quantitative analysis of the alpha-actin-positive area showed a significant increase in the contribution of smooth muscle cells within the neointima in allografts from NOS2 -/- recipients (28.2+/-2.0%) compared with wild-type controls (13.2+/-2.3%; P<.0001). CONCLUSIONS: NOS2 plays a protective role in the development of transplant arteriosclerosis, suppressing neointimal smooth muscle cell accumulation.

Animals↗

PubMed2005

Pioglitazone improves aortic wall elasticity in a rat model of elastocalcinotic arteriosclerosis.

Specific treatment of age-related aortic wall arteriosclerosis and stiffening is lacking. Because ligands for peroxisome proliferator-activated receptor gamma have beneficial effects on the arterial wall in atherosclerosis, via an antiinflammatory mechanism, we investigated whether long-term pioglitazone (Pio) treatment protects against another form of vascular wall disease, arteriosclerosis. We evaluated, in a rat model of elastocalcinotic arteriosclerosis (hypervitaminosis D and nicotine [VDN]), whether Pio (3 mg . kg(-1) per day for 1.5 month PO) attenuated arteriosclerosis and its consequences: aortic wall rigidity, increased aortic pulse pressure, and left ventricular hypertrophy. In VDN rats, medial calcification was associated with monocyte/macrophage infiltration and induction of tumor necrosis factor alpha and interleukin 1beta. Pio increased nuclear peroxisome proliferator-activated receptor gamma immunostaining in the aortic wall, decreased tumor necrosis factor alpha (P <0.05 versus VDN Pio-), tended to decrease interleukin 1beta mRNA expression (P =0.08 versus VDN Pio-), blunted aortic wall calcification (271+/-69, P <0.05 versus VDN Pio- 562+/-87 micromol . g(-1) dry weight) and prevented fragmentation of elastic fibers (segments per 10,000 microm2: 8.4+/-0.3; P <0.05 versus VDN Pio- 10.5+/-0.6). Pio reduced aortic wall stiffness (elastic modulus/wall stress: 4.8+/-0.6; P <0.05 versus VDN Pio- 10.0+/-1.6), aortic pulse pressure (30+/-2 mm Hg; P <0.05 versus VDN Pio- 39+/-4) and left ventricular hypertrophy (1.58+/-0.05 g . kg(-1); P <0.05 versus VDN Pio- 1.76+/-0.06). In conclusion, long-term Pio treatment attenuates aortic wall elastocalcinosis and, thus, lowers aortic wall stiffness, aortic pulse pressure, and left ventricular hypertrophy.

Animals↗

PubMed1982

Arteriosclerosis in normal and von Willebrand pigs: long-term prospective study and aortic transplantation study.

In a long-term prospective study, five normal control pigs and five pigs with homozygous von Willebrand's disease received a nonfatty diet from age 3 months to 4 years; then the aortas were analyzed. The fibrous arteriosclerotic plaques in the distal abdominal aortic region involved an average of 28% of the surface area in control pigs and only 7% of the surface area in pigs with von Willebrand's disease (P less than 0.01). In a subsequent study of 3-month-old pigs, the distal abdominal aortic segments from nine normal pigs were cross-transplanted with segments from nine other normal pigs (control study), and aortic segments from four normal pigs were transplanted into four host pigs with von Willebrand's disease (exchange study). All pigs received a 2% cholesterol diet for up to 6 months; then the transplanted aortic segments were analyzed. The donor normal aortic segments in the host normal pigs developed arteriosclerosis that involved an average of 20% of the surface; the endothelial fluorescent pattern of von Willebrand factor was identified. In contrast, the donor normal aortic segments in the host pigs with von Willebrand's disease had arteriosclerosis that involved an average of only 4% of the surface (P less than 0.01); the endothelial cell von Willebrand factor was not identified. The long-term prospective study indicates that pigs with von Willebrand's disease are resistant to the development of spontaneous arteriosclerosis. The aortic transplantation data are compatible with the hypothesis that the absence of von Willebrand factor in pigs with von Willebrand's disease may cause impairment of platelet-arterial wall interaction and resistance to arteriosclerosis.

Animals↗

PubMed1975

Prognostic and therapeutic considerations in pure hypertension vs hypertension and superimposed arteriosclerosis.

In summary, a prognostic and therapeutic evaluation of 227 patients first seen from 1967 to the end of 1969 with a follow-up of 4-7 years was made. The results are indeed depressing. In spite of close follow-up and systematic treatment with modern antihypertensive agents, the mortality of patients having hypertension with superimposed arteriosclerosis was 27% (15 to 56) for males as contrasted to 3% (2 of 75) for females. Since the last casual blood pressure in both living and deceased patients of the mixed group were similar, the level of blood pressure following treatment could not be incriminated for the deceased patients. An exaggerated systolic and pulse pressure cold pressor response emerged as an important indicator of presence of arteriosclerosis alone. When hypertension and arteriosclerosis coexisted there was also exaggeration in diastolic cold pressor response. A further exaggeration in systolic and diastolic cold pressor response was seen in the decreased as compared to living male patients, a finding which appears to have grave prognostic significance for coronary heart disease and stroke. Thus a marked exaggeration in both systolic and diastolic cold pressor response in males might prove to be the single most important predictor of premature death from atherosclerotic vascular disease. A further analysis of the deceased male patients having hypertension and superimposed arteriosclerosis, indicates that treatment of hypertension may prevent oeath from stroke but not form coronary heart disease. Two-thirds of the deaths occur suddenly and only one-third of the deceased patients reached the hospital befor dying. In view of these distressing findings a plea for early detection and treatment of hypertension, prior to the development of superimposed arteriosclerotic changes, particularly in males, is made.

Arteriosclerosis↗

PubMed2003

[Relation of hypertension and glucose tolerance impairment in elderly people to the development of arteriosclerosis--investigation using pulse wave velocity].

Hypertension and diabetes are risk factors for arteriosclerosis and have a synergistic effect on the progression of arteriosclerosis. The aim of this study was to determine the correlation between complications of hypertension and diabetes and arteriosclerosis as assessed by pulse wave velocity (PWV) in elderly subjects. The subjects of this study were 186 people aged 60 years or older (mean age: 68.8 +/- 5.8 years) who were scheduled to undergo health examinations. PWV, systolic blood pressure (SBP), diastolic blood pressure (DBP), body mass index (BMI), fasting blood sugar (FBS), total cholesterol (TC), triglyceride (TG) and HDL cholesterol (HDL) were measured in each subject. The patients were divided according to the American Diabetes Association (ADA) diagnostic criteria for diabetes based on fasting blood sugar level into the following three groups: a normal (NGT) group (FBS < 110 mg/dl), an impaired fasting glucose (IFG) group (110 < or = FBS < 126 mg/dl) and a diabetes mellitus (DM) group (FBS > or = 126 mg/dl or receiving treatment for diabetes). Based on the JNC-VI and WHO/ISH diagnostic criteria, subjects who had a SBP of 140 mmHg or higher or a DBP of 90 mmHg or higher or who had been taking hypotensive drugs were assigned to the hypertension (HT) group, and the other subjects were assigned to the normotension (NT) group. PWV showed significant positive correlations with SBP and FBS (r = 0.499 and r = 0.300, respectively). The effects of hypertension on PWV were significantly higher in subjects with HT than in subjects with NT in all of the glucose tolerance groups (all p < 0.01). Moreover, in the subjects with HT, PWV started to increase from the IFG stage, and PWV was significantly higher in the DM groups than in the NGT group (p < 0.01). In multiple regression analysis using PWV as an objective variable, SBP and FBS were selected as significant explanatory variables. The results of this study indicate the need for stricter management of elderly people with slight glucose tolerance impairment and hypertension in order to prevent the occurrence of arteriosclerosis.

Aged↗

PubMed2001

Critical role for IL-4 in the development of transplant arteriosclerosis in the absence of CD40-CD154 costimulation.

Blockade of the CD40-CD154 pathway can inhibit CD4(+) T cell activation but is unable to prevent immune responses mediated by CD8(+) T cells. However, even in the absence of CD8(+) T cells, inhibition of the CD40-CD154 pathway is insufficient to prevent the development of transplant arteriosclerosis. This study investigated the mechanisms of transplant arteriosclerosis in the absence of the CD40 pathway. C57BL/6 CD40(-/-) (H2(b)) recipients were transplanted with MHC-mismatched BALB/c (H2(d)) aortas. Transplant arteriosclerosis was evident in both CD40(-/-) and CD40(+/-) mice (intimal proliferation was 59 +/- 5% for CD40(-/-) mice vs 58 +/- 4% for CD40(+/-) mice) in the presence or absence of CD8(+) T cells (intimal proliferation was 46 +/- 7% for CD40(-/-) anti-CD8-treated mice vs 50 +/- 10% for CD40(+/-) anti-CD8-treated mice), confirming that CD8(+) T cells are not essential effector cells for the development of this disease. In CD40(-/-) recipients depleted of CD8(+) T cells, the number of eosinophils infiltrating the graft was markedly increased (109 +/- 24 eosinophils/grid for CD40(-/-) anti-CD8-treated mice vs 28 +/- 7 for CD40(+/-) anti-CD8-treated mice). The increased presence of eosinophils correlated with augmented intragraft production of IL-4. To test the hypothesis that IL-4 was responsible for the intimal proliferation, CD8 T cell-depleted CD40(-/-) recipients were treated with anti-IL-4 mAb. This resulted in significantly reduced eosinophil infiltration into the graft (12 +/- 5 eosinophils/grid for CD40(-/-) anti-CD8(+), anti-IL-4-treated mice vs 109 +/- 24 for CD40(-/-) anti-CD8-treated mice), intragraft eotaxin, CCR3 mRNA production, and the level of intimal proliferation (18 +/- 5% for CD40(-/-) anti-CD8(+)-, anti-IL-4-treated mice vs 46 +/- 7% for CD40(-/-) anti-CD8-treated mice). In conclusion, elevated intragraft IL-4 production results in an eosinophil infiltrate and is an important mechanism for CD8(+) T cell-independent transplant arteriosclerosis in the absence of CD40-CD154 costimulation.

Animals↗

PubMed2000

A preliminary investigation of Tanakan in the treatment of hypertensive arteriosclerosis and stroke in rats.

OBJECTIVE: To observe the changes in hypertensive cerebral arteriosclerosis and the incidence of stroke in rats following treatment with Tanakan, a preparation of Ginkgo Biloba (GB). METHODS: Using two-kidney, two clip renovascular hypertensive rats (RHRs) as animal models--we investigated changes in these hypertensive arteriosclerosis-associated factors: A I, A II, ALD, ET, SOD and cGMP. Blood levels were observed after oral administration of GB, at both early and late stages of hypertension. RESULTS: The degree of arteriosclerosis was more severe in both RHRs control and the later treated group than in the early treated group, with blood levels of A I, A II, ALD and ET in the former two groups significantly elevated. The degree of arteriosclerosis in the early treated group decreased and the blood levels of A I, A II, ALD and ET in this group decreased nearly to normal levels. The blood levels of SOD and cGMP were also elevated in the early treated group. CONCLUSIONS: These results reveal that it is important to treat hypertension as soon as possible, in order to reduce the occurrence of stroke.

Animals↗

PubMed2003

[Effect of aspirin combined with perindopril on prostacyclin, thromboxone A2, and norepinephrine in the blood of arteriosclerosis rabbit models and the cardiac function].

OBJECTIVE: To explore the interactive effect of low-dosage aspirin (ASA) combined with perindopril (PER), on prostacyclin (PGI2), thromboxone A2 (TXA2), and norepinephrine (NE) in the blood of arteriosclerosis rabbit models and the cardiac function. METHODS: Sixty adult New Zealand rabbits were randomly distributed into 5 groups with 12 rabbits in each group. One group was fed with standard fodder; the others were fed with high lipoid-diet (1% cholesterol content). Before and after 8 weeks' administration consecutively, LVEDP, LVSP, HR, +/- dp/dtmax, plasma PGI2 and TXA2, serum NE, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-ch), high-density lipoprotein cholesterol (HDL-ch) and triglycerides (TG) were evaluated. RESULTS: TG, TC, LDL-ch and pathological results confirmed arteriosclerosis rabbit models successfully. ASA combined with PER led to a significant increase in PGI2/TXA2 (P < 0.01) together with a significant decrease in the NE levels (P < 0.01) in the rabbits' blood, and then improved the cardiac output, i.e. increased LVSP (P < 0.01), and decreased the heart rate (P < 0.01) and LVEDP (P < 0.01) to a greater extent in the arteriosclerosis rabbit models. CONCLUSION: The ratio of PGI2 to TXA2 increased, and the NE levels decreased significantly; meanwhile, the heart rate decreased and the cardiac function improved during the administration of aspirin combined with perindopril in arteriosclerosis rabbit models. The results suggest that there is a synergism-action between low-dosage aspirin and ACE inhibitors due to increased PGI2/TXA2 and decreased NE levels.

Animals↗

PubMed1992

[Study of quantitative diagnosis of cerebral arteriosclerosis].

On the basis of clinical diagnostic criterion of cerebral arteriosclerosis, we selected, 72 patients with cerebral arteriosclerosis, 72 patients with suspected cerebral arteriosclerosis and 70 healthy individuals and screened 42 variables obtained from clinical and accessory examination with a stepwise discriminant analysis and a stepwise regression analysis. Finally we performed a logistic discriminant analysis of 15 selected variables in order to establish diagnostic discriminant formulas, Ya and Yc. It was found that a diagnostic coincidence rate for rediscriminant analysis of 212 individuals with the formulas was 100%. Very high sensitivity (96.7%), specificity (100%), positive predicted value (100%), negative predicted value (83.3%) and accuracy (97.1%) were noted in a prospective double-blind test on 34 subjects. The authors suggest that the discriminant formulas Ya and Yc established for diagnosis of cerebral arteriosclerosis be widely applicated.

Aged↗

PubMed1990

Cardiac transplantation in the rat. II. Alteration of the severity of donor graft arteriosclerosis by modulation of the host immune response.

Cardiac transplantation between inbred rat strains that differ for weak histocompatibility antigens is associated with the development of arteriosclerosis in the arteries of the donor graft myocardium. The lesions are seen in donor/recipient pairs that differ for both MHC and non-MHC histocompatibility antigens that apparently stimulate a low-level, chronic rejection of the donor heart graft. The arteriosclerosis associated with this chronic rejection consists of a diffuse, concentric proliferation of the intima and pathologically resembles the lesions observed in the coronary arteries of long-term human cardiac graft recipients. We have recently examined the influence of positive and negative manipulation of the host immune response on the development of the graft arteriosclerosis. Our results demonstrate that delayed harvest of the cardiac grafts or immunization with donor skin grafts or splenic lymphocytes increases the sensitivity of the recipient to the donor heart grafts--and, under conditions that allow for the long-term survival of the graft--increases the severity of the arteriosclerotic lesions. Alternatively, suppression of the host immune responses with cyclosporine or FK506, substantially reduces the arteriosclerotic changes. These results suggest that control of accelerated graft arteriosclerosis in long-term human cardiac recipient may require more careful and effective immunosuppression of the allograft reaction.

Animals↗