A Standardized ‘In Vivo’ Model for the Study of Experimental Arterial Thrombosis: Description of a Method

Bourgain, R.H.; Vermariën, H.; Andries, R.; Vereecke, F.; J, Jacqueloot; Rennies, J.; Blockeel, E.; Six, F.

doi:10.1007/978-1-4684-4895-5_62

Cited by 16 publications

(8 citation statements)

References 13 publications

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“…These parameters were not tested in previous studies [4, 7]. A main finding of this work was the beneficial effect of TQ on atherogenesis parameters.…”

Section: Discussionmentioning

confidence: 89%

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Attenuated Combined Action of Cyclosporine A and Hyperlipidemia on Atherogenesis in Rabbits by Thymoquinone

Ragheb

Attia

Elbarbry

et al. 2011

Evidence-Based Complementary and Alternative Medicine

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This descriptive study investigates in a rabbit model of atherosclerosis (i) the extent of atherogenesis induced by cyclosporine A (CsA) or hyperlipidemia alone or in combination and (ii) whether thymoquinone (TQ), a known herbal antioxidant, offers protection against these effects. New Zealand White female rabbits were assigned to five groups of six animals each: Group I, control; Group II, CsA [25 mg kg−1 day−1 orally (PO)]; Group III, 1% cholesterol; Group IV, 1% cholesterol + CsA (25 mg kg−1 day−1 PO); and Group V, 1% cholesterol + CsA (25 mg kg−1 day−1 PO) + TQ (10 mg kg−1 day−1 PO). Lipids and oxidative stress parameters [Malondialdehyde (MDA) and protein carbonyl] and aortic atherosclerosis were compared. CsA alone did not show a significant effect on either serum lipids and did not induce atherosclerosis. High-cholesterol diet induced atherosclerosis (45 ± 11% of the intimal surface of aorta was covered with atherosclerotic plaques). CsA and high-cholesterol diet increased atherosclerosis severity as measured from intimal and media lesions, but did not affect the extent of atherosclerosis. TQ decreased aortic MDA by 83%. It was also associated with reduced aortic atherosclerosis extend by 52% compared with Group IV. We concluded that (i) CsA aggravates hyperlipidemia-induced atherosclerosis and (ii) TQ attenuates the oxidative stress and atherogenesis induced by the combined effect of CsA and hyperlipidemia.

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“…These parameters were not tested in previous studies [4, 7]. A main finding of this work was the beneficial effect of TQ on atherogenesis parameters.…”

Section: Discussionmentioning

confidence: 89%

“…First, rabbits have been used reliably to induce an atheroma model with intact endothelium, which resembles human atherosclerosis [7, 8]. Secondly, oxidative stress has been linked to tissue injury by hyperlipidemia [9, 10].…”

Section: Introductionmentioning

confidence: 99%

Attenuated Combined Action of Cyclosporine A and Hyperlipidemia on Atherogenesis in Rabbits by Thymoquinone

Ragheb

Attia

Elbarbry

et al. 2011

Evidence-Based Complementary and Alternative Medicine

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“…The aim of this study was to evaluate the role of active PAI-1 during the generation and lysis of a thrombus induced in the microcirculation. For this purpose, we have infused a monoclonal antibody, known to induce the substrate form of PAI-1 in rats, at a dose which rapidly inactived PAI-1 and we have studied its effects on the formation and lysis of a platelet-rich thrombus generated in a 200-300 µm arteriole of the rat mesenteric microcirculation after electric stimulation and adenosine diphosphate superfusion (9).…”

Section: Introductionmentioning

confidence: 99%

Inactivation of Plasminogen Activator Inhibitor-1 Accelerates Thrombolysis of a Platelet-rich Thrombus in Rat Mesenteric Arterioles

Rupin

Martin²,

Vallez³

et al. 2001

Thromb Haemost

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SummaryTo investigate the role of active plasminogen activator inhibitor 1 (PAI-1) in the evolution of a microthrombus generated in the arteriolar microcirculation, the monoclonal antibody, 33H1F7, which transforms active PAI-1 to a tissue type plasminogen activator (t-PA) substrate, was evaluated in an arteriolar thrombosis model in the rat mesentery. Arterioles (200-300 μm) were stimulated electrically to create an endothelial lesion; ADP was then perfused for 2 min to induce the formation of a platelet-rich thrombus which lysed spontaneously in 140 ± 24 s. Two successive ADP superfusions produced comparable thrombi which lysed in comparable times. Different doses of 33H1F7 were infused to rats for 30 min and the dose which inactivates rapidly and totally active rat PAI-1 (300 μg/kg/min) was selected to be tested on the thrombosis model. Infusion of 33H1F7 beginning 10 min before the ADP application significantly reduced the lysis time in comparison to the control (123 ± 30 s versus 169 ± 33 s, P < 0.05, paired Student’s t-test) and the cumulative thrombus area during the lysis period was decreased by 56 ± 7%. These results demonstrate that inactivation of PAI-1 is able to accelerate lysis of a platelet-rich clot in a mesenteric arteriole of the rat. Thus active PAI-1 most likely participates to the resistance to thrombolysis in the arteriolar microcirculation and its inactivation may shorten ischemic periods after microvascular obstruction such as e.g. during cerebral stroke.

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“…In particular, interaction of platelets and polymorphonuclear leukocytes (PMNs) with the blood vessel wall at sites of vascular injury is considered to be an early event in the pathogenesis of these diseases. Morphological studies of platelet plugs and thrombi in vascular lesions frequently demonstrate that they are also rich in PMNs (Henry, 1965;Bourgain et al, 1984), suggesting a close interaction between platelets and PMNs, and possibly among these cells along with the vascular endothelial cells. However, the molecular mechanisms that mediate the cell-cell interactions are still unclear.…”

Section: Introductionmentioning

confidence: 99%

Platelet‐leukocyte interaction in adhesion to endothelial cells induced by platelet‐activating factor in vitro

Hirafuji

Satoh

1991

British J Pharmacology

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1 Platelet-activating factor (PAF, 10 nM) did not induce platelet adhesion to endothelial cells cultured in monolayer but it induced their adhesion to protein-coated plastic. However, PAF induced a marked platelet adhesion to endothelial cells when polymorphonuclear leukocytes (PMNs) were present. Lyso-PAF had no effect. 2 Phase-contrast microscopic examination showed that single platelets rather than their aggregates adhered to the endothelial cell surface around aggregating and adhering PMNs. 3 Significant platelet adhesion was induced by PAF at concentrations higher than 0.01 nm with the maximal response at 10nm. Platelet adhesion occurred within minutes after PAF addition, reaching a maximum approximately after 30 min. Platelet adhesion also occurred significantly at a PMN : platelet ratio of 1: 800, and linearly up to 1: 50. 4 The PAF-induced platelet adhesion was suppressed by three structurally unrelated PAF antagonists, WEB 2086, ONO 6240 and BN 52021, in a concentration-dependent manner. 5 PAF also increased PMN adhesion to endothelial cell monolayers, which was further augmented by the presence of platelets. 6 The present study demonstrates that PAF induces platelet adhesion to endothelial cells in vitro when PMNs are present and that there is a close interaction between platelets and PMNs in their adhesion to endothelial cells. The present study further suggests that PMNs could play a central role in platelet adhesion to vascular endothlium in certain pathological conditions.

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A Standardized ‘In Vivo’ Model for the Study of Experimental Arterial Thrombosis: Description of a Method

Cited by 16 publications

References 13 publications

Attenuated Combined Action of Cyclosporine A and Hyperlipidemia on Atherogenesis in Rabbits by Thymoquinone

Attenuated Combined Action of Cyclosporine A and Hyperlipidemia on Atherogenesis in Rabbits by Thymoquinone

Inactivation of Plasminogen Activator Inhibitor-1 Accelerates Thrombolysis of a Platelet-rich Thrombus in Rat Mesenteric Arterioles

Platelet‐leukocyte interaction in adhesion to endothelial cells induced by platelet‐activating factor in vitro

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