Smooth Muscle and Thrombus Thresholds To Unipolar Stimulation of Small Blood Vessels*†

Callahan, Arthur B.; Lutz, Brenton R.; Fulton, George P.; Degelman, John

doi:10.1177/000331976001100107

Cited by 18 publications

(10 citation statements)

References 1 publication

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“…The use of electrical stimulation to induce microvascular thrombi was described quantitatively by Callahan et al in 1960 ( 14 ), though earlier reports had applied electrical stimulation to microvessels in vivo , noting arteriolar vasoconstriction ( 27 ) and venular leukocyte adhesion ( 66 ). This technique involves positioning a microelectrode in close proximity to microvessels and direct application of a unipolar current, typically of at least 0.2 mA ( 13 , 14 , 87 ). Ultrastructurally, microvessels demonstrate extensive endothelial damage and denudation, with platelets adherent to subendothelial matrix components ( 34 ).…”

Section: Electrical Stimulationmentioning

confidence: 99%

Microvascular Thrombosis Models in Venules and Arterioles In Vivo

2005

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Platelets are intimately involved in hemostasis and thrombosis. Under physiological conditions, circulating platelets do not interact with microvascular walls. However, in response to microvascular injury, platelet adhesion and subsequent thrombus formation may be observed in venules and arterioles in vivo. Numerous intravital video microscopy techniques have been described to induce and monitor the formation of microvascular thrombi. The mechanisms of microvascular injury vary widely among different models. Some models induce platelet activation with minimal effects on endothelium, others induce endothelial inflammation or injury, while other models lead to thrombus formation associated with endothelial denudation. The molecular mechanisms mediating platelet-vessel wall adhesive interactions differ among various models. In some instances, differences in responses between venules and arterioles are described that cannot be explained solely by hemodynamic factors. Several models for induction of microvascular thrombosis in vivo are outlined in this review, with a focus on the mechanisms of injury and thrombus formation, as well as on differences in responses between venules and arterioles. Recognizing these characteristics should help investigators select an appropriate model for studying microvascular thrombosis in vivo.

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Section: Electrical Stimulationmentioning

confidence: 99%

Microvascular Thrombosis Models in Venules and Arterioles In Vivo

2005

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“…In hundreds of observations, aggregation never occurred in the former without first occurring in the latter. Callahan et al 20 found that aggregates occurred more readily in venules than in arterioles following electrical injury of vessels in hamster cheek pouch. Kochen and Baez 7 made similar observations after laser injury of vessels in rat mesentary.…”

Section: Differential Speed Of Response In Arterioles and Venulesmentioning

confidence: 99%

“…Kochen and Baez 7 made similar observations after laser injury of vessels in rat mesentary. This result has been explained by the high flow velocity on the arterial side, 20 the idea being that high flow velocity may inhibit platelets from sticking to arteriolar endothelium. However, Begent and Born 21 showed that aggregates actually grow faster as velocity increases, the growth being related to the numbers of aggregates passing a spot in a given period of time.…”

Section: Differential Speed Of Response In Arterioles and Venulesmentioning

confidence: 99%

Platelet aggregation in the cerebral microcirculation: effect of aspirin and other agents.

Rosenblum¹,

El‐Sabban²

1977

Circulation Research

153

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After a certain period of time filtered ultraviolet light produces platelet aggregation in microvessels on the cerebral surface of the mouse, but only when sodium fluorescein is first injected intravascularly to provide a light-absorbing, heat-generating target. The platelet aggregates fluoresce. They occur only in the illuminated field and adhere to arteriolar and venular walls. Vasoconstriction is not detected prior to or up to 30 seconds after aggregation. Electron microscopy reveals damaged endothelium and undamaged red cells, as well as aggregates consisting almost exclusively of platelets in varying stages of aggregation, pseudopod formation, and degranulation. The time between onset of the noxious stimulus and recognition of the first aggregate can be measured as the vessels are observed microscopically. This "time of aggregation" is prolonged by pentobarbital as opposed to urethane anesthesia, and also is related to time elapsed after craniotomy. We also found that aspirin and indomethacin significantly prolong time to first aggregate, but only on the arteriolar side of the circulation. This is so even though the composition of the aggregates is the same on both the arteriolar and venular sides. Heparin has no effect.

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“…Our data revealed that platelet aggregation usually occurs first in the venules rather than in the arterioles. This may be explained by a higher flow velocity in arterioles resulting in delayed adhesion of platelets to arteriolar endothelial cells (Callahan et al, 1960). In this system, the occlusion time is related to the blood flow rate, size of microvessel diameter and dose of fluorescein dye.…”

Section: Discussionmentioning

confidence: 99%

Antithrombotic effect of rutaecarpine, an alkaloid isolated from Evodia rutaecarpa, on platelet plug formation in in vivo experiments

Sheu

Hung

et al. 2000

Br J Haematol

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Summary. In this study, platelet thrombi formation was induced by irradiation of mesenteric venules with filtered light in mice pretreated intravenously with fluorescein sodium. Rutaecarpine (200 mg/g) significantly prolonged the latent period of inducing platelet plug formation in mesenteric venules when it was intravenously injected. Rutaecarpine (200 mg/g) prolonged occlusion time by approximately 1´5-fold (control 127^29 vs. taecarpine 188^23 s). Furthermore, aspirin (250 mg/g) also showed a similar prolongation of the occlusion time in this experiment. On a molar basis, rutaecarpine was approximately twofold more potent than aspirin at prolonging the occlusion time. Furthermore, rutaecarpine was also effective in reducing the mortality of ADP-induced acute pulmonary thromboembolism in mice when administered intravenously at doses of 25 and 50 mg/g. Intravenous injection of rutaecarpine (50 mg/g) significantly prolonged the bleeding time by approximately 1´5-fold compared with normal saline in the severed mesenteric arteries of rats. Continuous infusion of rutaecarpine (5 mg/g/min) also significantly increased the bleeding time 1´5-fold, and the bleeding time returned to baseline within 60 min after cessation of rutaecarpine infusion. These results suggest that rutaecarpine has an effective anti-platelet effect in vivo and that it may be a potential therapeutic agent for arterial thrombosis, but it must be assessed further for toxicity.

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Smooth Muscle and Thrombus Thresholds To Unipolar Stimulation of Small Blood Vessels*†

Cited by 18 publications

References 1 publication

Microvascular Thrombosis Models in Venules and Arterioles In Vivo

Microvascular Thrombosis Models in Venules and Arterioles In Vivo

Platelet aggregation in the cerebral microcirculation: effect of aspirin and other agents.

Antithrombotic effect of rutaecarpine, an alkaloid isolated from Evodia rutaecarpa, on platelet plug formation in in vivo experiments

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