Thrombin-induced vasospasm: Cellular signaling mechanisms

Jerius, Hilde; Beall, Arthur C.; Woodrum, David A.; Epstein, Aaron; Brophy, Colleen M.

doi:10.1016/s0039-6060(98)70227-2

Cited by 34 publications

(21 citation statements)

References 18 publications

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“…TF initiates the coagulation cascade within seconds, resulting in thrombin generation and fibrin deposition. Thrombin is able to induce vasospasm 26,27 by activation of protease-activated receptors. 28,29 In fact, inhibition of thrombin with hirudin was shown to limit infarct size in a rabbit coronary ligation model.…”

Section: Discussionmentioning

confidence: 99%

Coronary no-reflow is caused by shedding of active tissue factor from dissected atherosclerotic plaque

Bonderman

Teml

Jakowitsch

et al. 2002

Blood

128

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Defined angiographically, no-reflow (NR) manifests as an acute reduction in coronary flow in the absence of epicardial vessel obstruction. One candidate protein to cause coronary NR is tissue factor (TF), which is abundant in atherosclerotic plaque and a cofactor for activated plasma coagulation factor VII. Scrapings from atherosclerotic carotid arteries contained TF activity (corresponding to 33.03 ؎ 13.00 pg/cm 2 luminal plaque surface). Active TF was sedimented, indicating that TF was associated with membranes. Coronary blood was drawn from 6 patients undergoing coronary interventions with the distal protection device PercuSurge GuardWire (Traatek, Miami, FL). Fine particulate material that was recovered from coronary blood showed TF activity (corresponding to 91.1 ؎ 62.16 pg/mL authentic TF). To examine the role of TF in acute coronary NR, blood was drawn via a catheter from coronary vessels in 13 patients during NR and after restoration of flow. Mean TF antigen levels were elevated during NR (194.3 ؎ 142.8 pg/mL) as compared with levels after flow restoration (73.27 ؎ 31.90 pg/mL; P ‫؍‬ .02). To dissect the effects of particulate material and purified TF on flow, selective intracoronary injection of atherosclerotic material or purified relipidated TF was performed in a porcine model. TF induced NR in the model, thus strengthening the concept that TF is causal, not just a bystander to atherosclerotic plaque material. The data suggest that active TF is released from dissected coronary atherosclerotic plaque and is one of the factors causing the NR phenomenon. Thus, blood-borne TF in the coronary circulation is a major determinant of flow. (Blood. 2002;99:2794-2800)

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Section: Discussionmentioning

confidence: 99%

Coronary no-reflow is caused by shedding of active tissue factor from dissected atherosclerotic plaque

Bonderman

Teml

Jakowitsch

et al. 2002

Blood

128

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“…36 Although vascular endothelial and smooth muscle cells are capable of expressing thrombin receptor, 37 and thrombin causes the immediate contraction of smooth muscle cells via activated thrombin receptor, 38,39 the peak thrombinantithrombin III complex concentration in the CSF of SAH patients was apparently earlier (on days 2 to 5) than the development of human cerebral vasospasm, which indicated that thrombin activation and its vasoconstrictive effect were not a direct cause of cerebral vasospasm. 34,39 In the search for factors downstream to thrombin activation due to SAH, elevated immunoreactivity for PDGF-BB was first demonstrated in the endothelial and smooth muscle cells of the basilar artery after SAH. Regulations of PDGF production in smooth muscle cells by thrombin have been reported.…”

Section: Discussionmentioning

confidence: 99%

Broad-Spectrum and Selective Serine Protease Inhibitors Prevent Expression of Platelet-Derived Growth Factor–BB and Cerebral Vasospasm After Subarachnoid Hemorrhage

Zhang

Nagata

Kikuchi

et al. 2001

Stroke

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Background and Purpose-Plasma serine protease cascade, including the complement system and thrombin, is activated in the subarachnoid space during the acute phase after subarachnoid hemorrhage (SAH). To examine the effect of protease cascade-based inflammation and subsequent vascular repair in the development of cerebral vasospasm, we examined the effect of 2 synthetic serine protease inhibitors-FUT-175, an inhibitor of thrombin and the complement system, and argatroban, a selective inhibitor of thrombin-on the development of cerebral vasospasm in a rabbit SAH model. Methods-One hundred Japanese White male rabbits were used in the study. The SAH was simulated by a single injection of autologous arterial blood into the cisterna magna. To evaluate the development of cerebral vasospasm, the caliber of the basilar artery was measured on x-ray film before and at 2 days after SAH. Nine groups of rabbits (nϭ6 each) were treated with continuous intravenous injection of FUT-175 (2.5, 5, 10, or 20 mg/d), argatroban (1.25, 2.5, or 5 mg/d), or the same amount of saline (vehicle) for 48 hours, starting 40 minutes after SAH. Two days after SAH, the expression of homodimer of platelet-derived growth factor-BB (PDGF-BB) in the basilar artery was examined with immunohistochemical techniques. In 20 normal rabbits, 5 g of recombinant PDGF-BB or vehicle was injected into the cisterna magna, and the basilar arteries were examined on angiograms for 48 hours. Results-Significant differences were observed in the caliber of the basilar arteries between the vehicle group and the groups with the 3 larger doses of FUT-175 (vehicle, 52Ϯ5.0%; 5 mg, 79Ϯ5.7%; 10 mg, 80Ϯ2.5%; 20 mg, 80Ϯ3.7%) and between the vehicle group and the groups with the 2 larger doses of argatroban (vehicle, 52Ϯ6.4%; 2.5 mg, 81Ϯ9.0%; 5 mg, 85Ϯ4.1%) (PϽ0.05). In the histological examination, administration of effective doses of FUT-175 or argatroban suppressed the expression of PDGF-BB in the endothelial and medial smooth muscle cell layers. Exogenous PDGF-BB caused delayed and prolonged vasoconstriction on normal basilar arteries. Conclusions-Activation

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“…Thrombin levels in the CSF of SAH patients in the acute phase correlate with the development of DCI [87], and thrombin causes immediate contraction of arteries [88] by activating the specific thrombin receptor on VSMCs [89]. After SAH, the contractile response of cerebral arteries was markedly enhanced by upregulation of the receptor [90].…”

Section: Thrombin Also Mediates the Development Of Cerebral Vasospasmmentioning

confidence: 99%

The Role of the Host Defense System in the Development of Cerebral Vasospasm: Analogies between Atherosclerosis and Subarachnoid Hemorrhage

Yanamoto¹,

Kataoka

Nakajo

et al. 2012

Eur Neurol

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Similar to atherosclerosis, platelet-derived growth factor (PDGF)-BB, a major growth factor for vascular smooth muscle cells, is produced in arterial walls to repair arteries after subarachnoid hemorrhage (SAH). On review of a series of research articles that focus on defensive host responses to SAH, PDGF-BB is identified as a spasmogen, based on the following findings: (1) foreign substances injected into the subarachnoid space cause persistent constriction of cerebral arteries with a time course and histological features almost identical to those seen after SAH; (2) persistent constriction induced by SAH or a foreign substance is dependent on the complement system; (3) the complement system, which stimulates platelets, macrophages and endothelial cells to secrete PDGF-BB, is activated in both the cerebrospinal fluid (CSF) and plasma immediately after SAH; (4) PDGF-BB levels in the CSF are significantly elevated in patients with delayed cerebral ischemia; (5) the immunodensity of PDGF-BB in the arterial walls correlates well with the severity of cerebral vasospasm; (6) intracisternal injection of PDGF-BB induces persistent constriction of cerebral arteries in a dose-dependent manner; (7) prolonged contact with blood clots promotes the contractile response of cerebral arteries to PDGF-BB, and (8) administration of an antagonist of PDGF-BB function suppresses the development of cerebral vasospasm.

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Thrombin-induced vasospasm: Cellular signaling mechanisms

Cited by 34 publications

References 18 publications

Coronary no-reflow is caused by shedding of active tissue factor from dissected atherosclerotic plaque

Coronary no-reflow is caused by shedding of active tissue factor from dissected atherosclerotic plaque

Broad-Spectrum and Selective Serine Protease Inhibitors Prevent Expression of Platelet-Derived Growth Factor–BB and Cerebral Vasospasm After Subarachnoid Hemorrhage

The Role of the Host Defense System in the Development of Cerebral Vasospasm: Analogies between Atherosclerosis and Subarachnoid Hemorrhage

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