Journal of thrombosis and haemostasis : JTH · 2025
Intravenous tenecteplase bridging reperfusion ameliorates cerebral ischemia/reperfusion injury by improving microvascular circulation in rats.
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Ning Yue-Xin, Cai Ji-Ru, Wang Ting-Ting, Wang Yi-Han, Cui Yu, Chen Hui-Sheng
Аннотация
BACKGROUND: Endovascular thrombectomy (EVT) alone was not demonstrated to be noninferior to intravenous alteplase bridging EVT in acute large vessel occlusion stroke. Using the cerebral ischemia/reperfusion (I/R) injury model, intravenous tenecteplase (TNK) was administrated after ischemia, followed by reperfusion at various time points.
OBJECTIVES: To investigate whether intravenous TNK bridging EVT vs EVT alone could improve I/R injury, and this effect may be associated with the time from TNK to reperfusion.
METHODS: Rats received intravenous TNK (1.4 mg/kg) or vehicle (sterile water) 1.0 hours after middle cerebral artery occlusion, followed by reperfusion after 0.5 or 1.0 hours following TNK. Neurological deficit scores, infarct volume, and brain edema were measured 24 hours after middle cerebral artery occlusion. Microthrombi were determined by immunofluorescence staining for CD31+/fibrinogen+ and CD31+/thrombocyte+. Inflammatory cell infiltration in the ischemic brain region was determined by flow cytometry.
RESULTS: Compared with vehicle, TNK significantly reduced neurological deficit scores, brain infarction, neuroinflammation, and blood-brain barrier disruption, and significantly reduced intravascular fibrin and platelet deposition and brain inflammatory cell infiltration in the penumbra of I/R rats. Furthermore, a better beneficial trend was found in TNK bridging reperfusion at 0.5 hours after TNK compared with TNK bridging reperfusion at 1.0 hours after TNK.
CONCLUSION: Our results demonstrate that intravenous TNK bridging reperfusion produced neuroprotective action through dissolving microvascular thrombus and alleviating inflammatory cell infiltration to improve microcirculation, with the result of maintaining blood-brain barrier integrity and inhibiting neuroinflammation, and the neuroprotective benefit may be associated with the time from TNK to reperfusion.
OBJECTIVES: To investigate whether intravenous TNK bridging EVT vs EVT alone could improve I/R injury, and this effect may be associated with the time from TNK to reperfusion.
METHODS: Rats received intravenous TNK (1.4 mg/kg) or vehicle (sterile water) 1.0 hours after middle cerebral artery occlusion, followed by reperfusion after 0.5 or 1.0 hours following TNK. Neurological deficit scores, infarct volume, and brain edema were measured 24 hours after middle cerebral artery occlusion. Microthrombi were determined by immunofluorescence staining for CD31+/fibrinogen+ and CD31+/thrombocyte+. Inflammatory cell infiltration in the ischemic brain region was determined by flow cytometry.
RESULTS: Compared with vehicle, TNK significantly reduced neurological deficit scores, brain infarction, neuroinflammation, and blood-brain barrier disruption, and significantly reduced intravascular fibrin and platelet deposition and brain inflammatory cell infiltration in the penumbra of I/R rats. Furthermore, a better beneficial trend was found in TNK bridging reperfusion at 0.5 hours after TNK compared with TNK bridging reperfusion at 1.0 hours after TNK.
CONCLUSION: Our results demonstrate that intravenous TNK bridging reperfusion produced neuroprotective action through dissolving microvascular thrombus and alleviating inflammatory cell infiltration to improve microcirculation, with the result of maintaining blood-brain barrier integrity and inhibiting neuroinflammation, and the neuroprotective benefit may be associated with the time from TNK to reperfusion.