Thromboxane–prostaglandin receptor antagonist, terutroban, prevents neurovascular events after subarachnoid haemorrhage: a nanoSPECT study in rats View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-02-11

AUTHORS

David Lagier, David Tonon, Philippe Garrigue, Benjamin Guillet, Laura Giacomino, Jean-Charles Martin, Marie-Christine Alessi, Nicolas Bruder, Lionel J. Velly

ABSTRACT

BackgroundSeveral lipid metabolites in cerebrospinal fluid are correlated with poor outcomes in aneurysmal subarachnoid haemorrhage. Most of these metabolites bind to ubiquitous thromboxane–prostaglandin (TP) receptors, causing vasoconstriction and inflammation. Here, we evaluated terutroban (TBN), a specific TP receptor antagonist, for the prevention of post-haemorrhage blood-brain barrier disruption, neuronal apoptosis and delayed cerebral hypoperfusion.MethodsThe rat double subarachnoid haemorrhage model was produced by twice injecting (days 1 and 2) autologous blood into the cisterna magna. Seventy-eight male Sprague-Dawley rats were assigned to experimental groups. Rats exposed to subarachnoid haemorrhage were allocated to no treatment (SAH group) or TBN treatment by gastric gavage during the first 5 days after haemorrhage (SAH+TBN group). Control rats received artificial cerebrospinal fluid injections (CSF group). Sham-operated rats with or without TBN administration were also studied. Body weight and Garcia neurological scores were assessed on day 2 and day 5. We used nanoscale single-photon emission computed tomography (nanoSPECT) to measure brain uptake of three radiolabelled agents: 99mTechnetium-diethylenetriaminepentacetate (99mTc-DTPA), which indicated blood-brain barrier permeability on day 3, 99mTechnetium-annexin V-128 (99mTc-Anx-V128), which indicated apoptosis on day 4, and 99mTechnetium-hexamethylpropyleneamineoxime (99mTc-HMPAO), which indicated cerebral perfusion on day 5. Basilar artery narrowing was verified histologically, and cerebral TP receptor agonists were quantified.Results99mTc-DTPA uptake unveiled blood-brain barrier disruption in the SAH group. TBN mitigated this disruption in the brainstem area. 99mTc-Anx-V128 uptake was increased in the SAH group and TBN diminished this effect in the cerebellum. 99mTc-HMPAO uptake revealed a global decreased perfusion on day 5 in the SAH group that was significantly counteracted by TBN. TBN also mitigated basilar artery vasoconstriction, neurological deficits (on day 2), body weight loss (on day 5) and cerebral production of vasoconstrictors such as Thromboxane B2 and Prostaglandin F2α.ConclusionsBased on in vivo nanoscale imaging, we demonstrated that TBN protected against blood-brain barrier disruption, exerted an anti-apoptotic effect and improved cerebral perfusion. Thus, TP receptor antagonists showed promising results in treating post-haemorrhage neurovascular events. More... »

PAGES

42

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/s13054-019-2338-4

DOI

http://dx.doi.org/10.1186/s13054-019-2338-4

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1112064633

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30744667


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24 schema:description BackgroundSeveral lipid metabolites in cerebrospinal fluid are correlated with poor outcomes in aneurysmal subarachnoid haemorrhage. Most of these metabolites bind to ubiquitous thromboxane–prostaglandin (TP) receptors, causing vasoconstriction and inflammation. Here, we evaluated terutroban (TBN), a specific TP receptor antagonist, for the prevention of post-haemorrhage blood-brain barrier disruption, neuronal apoptosis and delayed cerebral hypoperfusion.MethodsThe rat double subarachnoid haemorrhage model was produced by twice injecting (days 1 and 2) autologous blood into the cisterna magna. Seventy-eight male Sprague-Dawley rats were assigned to experimental groups. Rats exposed to subarachnoid haemorrhage were allocated to no treatment (SAH group) or TBN treatment by gastric gavage during the first 5 days after haemorrhage (SAH+TBN group). Control rats received artificial cerebrospinal fluid injections (CSF group). Sham-operated rats with or without TBN administration were also studied. Body weight and Garcia neurological scores were assessed on day 2 and day 5. We used nanoscale single-photon emission computed tomography (nanoSPECT) to measure brain uptake of three radiolabelled agents: 99mTechnetium-diethylenetriaminepentacetate (99mTc-DTPA), which indicated blood-brain barrier permeability on day 3, 99mTechnetium-annexin V-128 (99mTc-Anx-V128), which indicated apoptosis on day 4, and 99mTechnetium-hexamethylpropyleneamineoxime (99mTc-HMPAO), which indicated cerebral perfusion on day 5. Basilar artery narrowing was verified histologically, and cerebral TP receptor agonists were quantified.Results99mTc-DTPA uptake unveiled blood-brain barrier disruption in the SAH group. TBN mitigated this disruption in the brainstem area. 99mTc-Anx-V128 uptake was increased in the SAH group and TBN diminished this effect in the cerebellum. 99mTc-HMPAO uptake revealed a global decreased perfusion on day 5 in the SAH group that was significantly counteracted by TBN. TBN also mitigated basilar artery vasoconstriction, neurological deficits (on day 2), body weight loss (on day 5) and cerebral production of vasoconstrictors such as Thromboxane B2 and Prostaglandin F2α.ConclusionsBased on in vivo nanoscale imaging, we demonstrated that TBN protected against blood-brain barrier disruption, exerted an anti-apoptotic effect and improved cerebral perfusion. Thus, TP receptor antagonists showed promising results in treating post-haemorrhage neurovascular events.
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30 schema:keywords B2
31 DTPA uptake
32 F2α
33 Garcia neurological scores
34 SAH group
35 Sprague-Dawley rats
36 TBN treatment
37 TP receptor agonist
38 TP receptor antagonist
39 administration
40 agents
41 agonists
42 aneurysmal subarachnoid hemorrhage
43 antagonist
44 anti-apoptotic effects
45 apoptosis
46 area
47 artery narrowing
48 autologous blood
49 barrier disruption
50 barrier permeability
51 binds
52 blood
53 blood-brain barrier disruption
54 blood-brain barrier permeability
55 body weight
56 body weight loss
57 brain uptake
58 brainstem areas
59 cerebellum
60 cerebral hypoperfusion
61 cerebral perfusion
62 cerebral production
63 cerebrospinal fluid
64 cerebrospinal fluid injection
65 cisterna magna
66 control rats
67 day 2
68 day 3
69 day 4
70 day 5
71 days
72 decreased perfusion
73 deficits
74 disruption
75 effect
76 emission
77 events
78 experimental group
79 fluid
80 fluid injection
81 gastric gavage
82 gavage
83 group
84 hemorrhage
85 hemorrhage model
86 hypoperfusion
87 inflammation
88 injection
89 lipid metabolites
90 loss
91 magna
92 male Sprague-Dawley rats
93 metabolites
94 metabolites bind
95 model
96 nanoscale
97 narrowing
98 neurological deficits
99 neurological score
100 neuronal apoptosis
101 neurovascular events
102 outcomes
103 perfusion
104 permeability
105 poor outcome
106 prevention
107 production
108 promising results
109 prostaglandin F2α
110 radiolabelled agents
111 rats
112 receptor agonist
113 receptor antagonist
114 receptors
115 results
116 scores
117 sham
118 single photon emission
119 specific TP receptor antagonist
120 study
121 subarachnoid hemorrhage
122 subarachnoid hemorrhage model
123 terutroban
124 thromboxane B2
125 tomography
126 treatment
127 uptake
128 vasoconstriction
129 vasoconstrictor
130 weight
131 weight loss
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