Cholesterol feeding impairs endothelium-dependent relaxation of rabbit aorta

1985 ◽  
Vol 63 (9) ◽  
pp. 1206-1209 ◽  
Author(s):  
R. L. Jayakody ◽  
M. P. J. Senaratne ◽  
A. B. R. Thomson ◽  
C. T. Kappagoda
Keyword(s):  
New Zealand ◽  
Thoracic Aorta ◽  
Rabbit Aorta ◽  
Cholesterol Diet ◽  
Cholesterol Feeding ◽  
New Zealand White Rabbits ◽  
Conventional Diet ◽  
Endothelium Dependent Relaxation

Experiments were designed to assess the effect of cholesterol feeding on the endothelium-mediated relaxation of the rabbit aorta to acetylcholine. Age-matched male New Zealand white rabbits were fed either a 2% cholesterol diet or standard rabbit chow. The animals were anaesthetized with sodium pentobarbitone and sacrificed after 4 and 8 weeks on these diets. Rings were prepared from the proximal thoracic aorta and examined in tissue baths. These rings were contracted first with norepinephrine (−6 log mol/L) and acetylcholine was added to demonstrate the endothelium-mediated relaxation. The endothelium-dependent relaxation was significantly less in aortas from rabbits fed the 2% cholesterol diet than in aortas from animals fed the conventional diet. This impairment of relaxation was apparent after both 4 and 8 weeks of cholesterol feeding. In both groups of animals no relaxation was seen in rings from which the endothelium was removed. These results show that cholesterol feeding leads to an impairment of endothelium-mediated relaxation of the rabbit aorta to acetylcholine.

Persistent impairment of endothelium-dependent relaxation to acetylcholine and progression of atherosclerosis following 6 weeks of cholesterol feeding in the rabbit

1989 ◽  
Vol 67 (11) ◽  
pp. 1454-1460 ◽  
Author(s):  
Laal Jayakody ◽  
Manohara P. J. Senaratne ◽  
Alan B. R. Thomson ◽  
Nadarajan Sreeharan ◽  
C. Tissa Kappagoda
Keyword(s):  
Rabbit Aorta ◽  
Atherogenic Diet ◽  
Acute Stage ◽  
Standard Laboratory ◽  
Cholesterol Feeding ◽  
Functional Abnormality ◽  
New Zealand White Rabbits ◽  
Standard Laboratory Diet ◽  
Endothelium Dependent Relaxation ◽  
Progression Of Atherosclerosis

The synthesis and (or) release of endothelium-dependent relaxant factor released by acetylcholine is impaired in New Zealand white rabbits fed an atherogenic diet. Experiments were designed to investigate whether the synthesis and (or) release of the endothelium-dependent relaxant factor from rabbit aortas are restored after reversal from an atherogenic diet to a non-atherogenic diet. Atherosclerosis was induced by feeding a diet containing lipids and 2% cholesterol for 6 weeks. Rabbits were sacrificed after 6 weeks on the atherogenic diet and 36 weeks after return to a standard laboratory diet. Synthesis and (or) release of the factor from the thoracic aorta was assayed using a bioassay system. The relaxant responses produced in the assay tissue were impaired both in the acute stage and after 36 weeks on non-atherogenic food. This impaired relaxation is probably due to a persistent functional abnormality in the aortic endothelium resulting in the failure to synthesize and (or) release endothelium-dependent relaxation factor 36 weeks after induction of atherosclerosis.Key words: endothelium dependent relaxation, rabbit aorta, atherosclerosis, regression, cholesterol feeding.

A model for demonstration of reversal of impairment of endothelium-dependent relaxation in the cholesterol-fed rabbit

1990 ◽  
Vol 68 (7) ◽  
pp. 845-850 ◽  
Author(s):  
C. Tissa Kappagoda ◽  
Alan B. R. Thomson ◽  
Manohara P. J. Senaratne
Keyword(s):  
Rabbit Model ◽  
Rabbit Aorta ◽  
Control Group ◽  
Standard Diet ◽  
Cholesterol Feeding ◽  
High Cholesterol ◽  
Experimental Animals ◽  
New Zealand White Rabbits ◽  
Experimental Group ◽  
Endothelium Dependent Relaxation

This investigation was undertaken to determine whether it was possible to restore endothelium-dependent relaxation (EDR) in the cholesterol-fed rabbit model of atherosclerosis following discontinuation of the cholesterol. New Zealand white rabbits, approximately 8 weeks of age, were randomized into (i) control group (9 animals fed a standard rabbit diet) and (ii) experimental group (27 animals: fed the same diet supplemented with 2.5% cholesterol). The experimental animals were restored to the standard diet after 3 weeks. EDR to acetylcholine (−9.0 to −5.0 log mol/L) was examined in the experimental animals at 3, 7, and 15 weeks after commencement of the study (n = 9 at each stage) and the nine control animals examined after 7 weeks. At the end of 7 weeks, EDR to acetylcholine (−6.0 log mol/L) was significantly (p < 0.05) impaired in the experimental group (34.3 ± 3.8%) compared with that in the control group (79.8 ± 3.0%). The loss of EDR was not apparent in the experimental group at 3 weeks (relaxation: 81.7 ± 4.7%). At the end of 15 weeks, the EDR was significantly restored in the experimental group (relaxation: 63.6 ± 5.1%). These findings demonstrate that it is possible to reverse the loss of EDR that occurs with cholesterol feeding in the rabbit by limiting the period of exposure to a high cholesterol diet.Key words: atherosclerosis, endothelium-dependent relaxation, rabbit aorta, regression.

Cholesterol diet and effect of long-term withdrawal on plaque development and composition in the thoracic aorta of New Zealand White rabbits

2010 ◽  
Vol 210 (2) ◽  
pp. 407-413 ◽  
Author(s):  
Karen Riedmüller ◽  
Stephan Metz ◽  
Gabriel A. Bonaterra ◽  
Olaf Kelber ◽  
Dieter Weiser ◽  
...  
Keyword(s):  
New Zealand ◽  
Thoracic Aorta ◽  
Cholesterol Diet ◽  
Plaque Development ◽  
New Zealand White Rabbits

A Cytochemical Study of Glucose-6-Phosphatase (G-6-PASE) in Cells Participating in Atherogenesis of Rabbit Aorta

1975 ◽  
Vol 33 ◽  
pp. 460-461
Author(s):  
Sidney D. Kobernick ◽  
Edna A. Elfont ◽  
Neddra L. Brooks
Keyword(s):  
Lipid Metabolism ◽  
New Zealand ◽  
Aortic Wall ◽  
Rabbit Aorta ◽  
Plaque Formation ◽  
Metabolic Changes ◽  
Atherosclerotic Plaques ◽  
Cytochemical Study ◽  
Cellular Alteration ◽  
New Zealand White Rabbits

This cytochemical study was designed to investigate early metabolic changes in the aortic wall that might lead to or accompany development of atherosclerotic plaques in rabbits. The hypothesis that the primary cellular alteration leading to plaque formation might be due to changes in either carbohydrate or lipid metabolism led to histochemical studies that showed elevation of G-6-Pase in atherosclerotic plaques of rabbit aorta. This observation initiated the present investigation to determine how early in plaque formation and in which cells this change could be observed.Male New Zealand white rabbits of approximately 2000 kg consumed normal diets or diets containing 0.25 or 1.0 gm of cholesterol per day for 10, 50 and 90 days. Aortas were injected jin situ with glutaraldehyde fixative and dissected out. The plaques were identified, isolated, minced and fixed for not more than 10 minutes. Incubation and postfixation proceeded as described by Leskes and co-workers.

Endothelium-dependent relaxation and experimental atherosclerosis in the rabbit aorta

1986 ◽  
Vol 64 (11) ◽  
pp. 1451-1453 ◽  
Author(s):  
N. Sreeharan ◽  
R. L. Jayakody ◽  
M. P. J. Senaratne ◽  
A. B. R. Thomson ◽  
C. T. Kappagoda
Keyword(s):  
Rabbit Aorta ◽  
Experimental Atherosclerosis ◽  
Isometric Tension ◽  
Dependent Manner ◽  
Bicarbonate Buffer ◽  
New Zealand White Rabbits ◽  
Set Up ◽  
And Control ◽  
Dose Dependent ◽  
Endothelium Dependent Relaxation

This study was undertaken to determine whether the production or release of the endothelium-dependent relaxatory factor is impaired in atherosclerotic New Zealand White rabbits. Atherosclerosis was induced by feeding a diet containing 2% cholesterol for 6 weeks. The production or release of endothelium-dependent relaxatory factor was assayed as follows. A 5-cm length of aorta donor was perfused with Krebs–bicarbonate buffer and the perfusate drained over a deendothelialized ring of recipient aorta set up for recording isometric tension. The recipient was precontracted with norepinephrine (0.2 μmol/L) in the perfusate. When acetylcholine was added to the perfusate, the recipient relaxed in a dose-dependent manner. This assay was used to compare the relaxatory responses produced in recipient rings by adding acetylcholine to donors from atherosclerotic and control rabbits. The relaxation produced by atherosclerotic donors were smaller than those generated by control donors (16.5 ± 4.9 vs. 32.7 ± 5.3%; n = 10, p < 0.05). It is suggested that in atherosclerotic rabbits the ability of aortic endothelium to produce or release endothelium-dependent relaxatory factor is impaired.

Cholesterol feeding enhances vasoconstrictor effects of products from rabbit polymorphonuclear leukocytes

1995 ◽  
Vol 269 (1) ◽  
pp. H1-H6
Author(s):  
J. L. Hart ◽  
C. G. Sobey ◽  
O. L. Woodman
Keyword(s):  
Polymorphonuclear Leukocytes ◽  
Plasma Cholesterol ◽  
Rabbit Aorta ◽  
Cholesterol Diet ◽  
Cholesterol Feeding ◽  
Short Term ◽  
Receptor Reserve ◽  
Atherosclerotic Lesions ◽  
Cholesterol Levels ◽  
Before And After

We have studied the vasoactive properties of products released from rabbit polymorphonuclear leukocytes (PMNs) before and after short-term (4 and 8 wk) dietary supplementation with 1% cholesterol. Plasma cholesterol levels were similar after 4 and 8 wk of cholesterol diet, whereas gross atherosclerotic lesions were present at 4 wk but significantly more extensive after 8 wk. PMN products from all rabbits caused endothelium-dependent contraction of isolated, control (nonatherosclerotic) rabbit aorta submaximally contracted with phenylephrine. However, both 4 and 8 wk of cholesterol feeding resulted in equivalent contractions by PMN products, which were significantly greater than contractions by control PMNs. Endothelium-dependent contraction (by PMN products) and relaxation (by acetylcholine) were attenuated by 8 wk of cholesterol feeding. PMN products attenuated acetylcholine-induced relaxation of aorta from cholesterol-fed rabbits and of control aorta treated with phenoxybenzamine to reduce muscarinic receptor reserve. We conclude that elevation of plasma cholesterol results in increased release of a PMN product(s) that causes endothelium-dependent constriction.

Effects of low-dose ketanserin on atherosclerosis in rats and rabbits

2010 ◽  
Vol 88 (11) ◽  
pp. 1054-1060 ◽  
Author(s):  
Yong-Sheng Yu ◽  
He-Hui Xie ◽  
Ling Li ◽  
Shu-Wei Song ◽  
Ping Han ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Vitamin D ◽  
New Zealand ◽  
Treatment Group ◽  
Low Dose ◽  
Control Group ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
New Zealand White Rabbits

The present study was designed to test the hypothesis that a small dose of ketanserin, which enhances baroreflex activity, prevents the early lesions of atherosclerosis. In experiment 1, baroreflex sensitivity (BRS) was measured in 31 spontaneously hypertensive rats (SHRs) in a conscious state using a computerized blood pressure monitoring system. Four weeks later, the rats were administered vitamin D3 and fed a high-cholesterol diet for 8 weeks to induce atherosclerosis. Then their hearts and aortae were removed for pathological examination. A negative correlation was found between BRS and the scores of coronary (r = –0.460, P < 0.01) and aortic atherosclerosis (r = –0.448, P < 0.05) in SHR. In experiment 2, SHRs were divided into 3 groups (n = 10 in each group) and received a dose of ketanserin of 0.3, 1.0, and 3.0 mg/kg (i.g.), respectively. At the smallest dose (0.3 mg/kg), ketanserin did not lower blood pressure but enhanced BRS. In experiment 3, SHRs were administered vitamin D3, fed a high-cholesterol diet, and simultaneously treated with low-dose ketanserin. The atherosclerosis scores of the treatment group were significantly lower than those of the control group (coronary score: 0.90 ± 0.14 vs. 1.76 ± 0.27, P < 0.05; aortic scores: 1.00 ± 0.39 vs. 2.18 ± 0.41, P < 0.05). In experiment 4, male New Zealand White rabbits were fed a high-cholesterol diet and treated with low-dose ketanserin at the same time. The atherosclerosis scores of the treatment group were significantly lower than those of the control group (aortic scores: 0.26 ± 0.20 vs. 0.60 ± 0.31, P < 0.05). In conclusion, the present study demonstrated, for the first time, that low-dose ketanserin prevented the development of atherosclerosis independent of its blood pressure lowering action in SHRs and New Zealand White rabbits at least in part via enhancement of arterial baroreflex function.

scholarly journals Trihoney improves testicular weight change and histopathological alterations in hypercholesterolemic rabbits

2020 ◽  
pp. 75-87
Author(s):  
Zenab B. Hamad Mohamed ◽  
Hamad Abdulsalam Hamad Alfarisi ◽  
Azantee Yazmie Abdul Wahab ◽  
Azliana binti Abd Fuaat ◽  
Che Anuar Che Mohamad ◽  
...  
Keyword(s):  
New Zealand ◽  
Histopathological Examination ◽  
Testicular Tissue ◽  
Degenerative Changes ◽  
Lipid Lowering ◽  
Cholesterol Diet ◽  
Histopathological Changes ◽  
Histopathological Alterations ◽  
Testicular Weight ◽  
New Zealand White Rabbits

Histopathological examination of testicular tissue is the most reliable and sensitive method for detecting effects on spermatogenesis. Hypercholesterolemia reduces testicular weight, induces testicular degenerative changes, impairs spermatogenesis, affects Leydig and Sertoli cells and induces inflammation and fibrosis of testicular tissue. Based on numerous studies, honey has the ability to improve testicular histopathological abnormalities. To date, whether honey has any protective role against the effects of hypercholesterolemia on male reproductive functions is yet to be explored. This study investigated the effects of Trihoney (a mixture of Trigona, Mellifera and Tualang honeys) on changes in testicular weight and histopathological alterations induced by hypercholesterolemia in male New Zealand white rabbits. These changes were compared with the effects of atorvastatin (a lipid lowering agent) based on the same parameters. Forty-eight male New Zealand white rabbits were assigned into 6 groups and received different diets as follows; Control: commercial pellet; CH: commercial pellet and 0.6 g/kg/day Trihoney; HCD: 1% cholesterol diet; DH1: 1% cholesterol diet and 0.3 g/kg/day Trihoney; DH2: 1% cholesterol diet and 0.6 g/kg/day Trihoney; DAt: 1% cholesterol diet and 2 mg/kg/day atorvastatin. After 12 weeks, blood samples were collected for lipid analysis, the rabbits were sacrificed and the testes were harvested to evaluate any weight and histopathological changes. Administration of 1% cholesterol diet either alone or in combination with atorvastatin caused a significant reduction in the testicular weight, testicular tubular degenerative changes and spermatogenesis impairment. Trihoney, particularly, at the dose of 0.6 g/kg/day improved testicular weight, ameliorated the testicular tubular degenerative changes and enhanced spermatogenesis. The findings of this study suggest that Trihoney plays a favourable role in the protection against testicular weight reduction and histopathological changes induced by hypercholesterolemia. On the other hand, atorvastatin per se may have toxic effects on testicular tissue.

Sign in / Sign up

Export Citation Format

Share Document