Outcome in Acute Stroke with Different Intra-Arterial Infusion Rate of Urokinase on Thrombolysis

Gan, Xiaosong; Luo, Yumin; Li, Feng; Ji, Xunming; Chen, J.; Ding, Yuchuan

doi:10.1177/159101991001600311

Cited by 10 publications

(5 citation statements)

References 17 publications

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“…Treatment with conventional-dose intravenous rt-PA and its combination with intraarterial urokinase were safe and feasible in patients. This strategy achieved high rates of complete arterial recanalization and good functional outcomes [32]. The administration of urokinase within 24 h after onset of stroke significantly improved the clinical outcomes as compared with a control group, which agreed with results from previous reports on the action of thrombolytic agents.…”

Section: Therapeutic Management Of Strokesupporting

confidence: 81%

Drug Therapy in Stroke: From Preclinical to Clinical Studies

Kaur¹,

Prakash²,

Medhi³

2013

Pharmacology

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Background: Stroke is one of the major challenges to health and the reason for increasing disability-adjusted life years. Despite tremendous progress in preclinical studies, none of the treatment options has proven efficacious in clinical studies. The basic aim of neuroprotection is to interfere with the events of the ischemic cascade, halt the pathological processes and prevent the death of vulnerable nerve cells in the ischemic penumbra. Summary: This review will provide a brief overview of the current understanding of stroke, including the global epidemiology of stroke, its pathophysiology, the targeting of specific pathways and the success and failure of preclinical as well as clinical studies, and it will discuss the emerging targets for novel therapeutic strategies under investigation. Key Messages: New advancing investigational drugs for the prevention and treatment of stroke are on the way and may someday give hope to neuroscientists and clinicians. A novel approach should adopt preclinical testing, advance the understanding of the pathophysiology of stroke and make it possible to translate it from bench to bedside. We should learn from the past failures and move on with more enthusiasm.

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Section: Therapeutic Management Of Strokesupporting

confidence: 81%

Drug Therapy in Stroke: From Preclinical to Clinical Studies

Kaur¹,

Prakash²,

Medhi³

2013

Pharmacology

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“…Our previous study showed that intra-arterial administration of UK at a dose of 170 000 IU/kg (infusion at 4000 IU/min) induced neuroprotection in the rat MCAO stroke model. 10 In the present study, we observed that a neuroprotective dose of ethanol (1.5 g/kg) did not promote hemorrhage with or without thrombolytic therapy in the rat.…”

Section: Discussionsupporting

confidence: 50%

Neuroprotective Effect of Acute Ethanol Administration in a Rat With Transient Cerebral Ischemia

Wang

et al. 2012

Stroke

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Background and Purpose-Ethanol consumption is inversely associated with the risk of ischemic stroke, suggesting a neuroprotective effect. In a rat model of transient cerebral ischemia, we identified ethanol as a possible treatment for acute ischemic stroke. Methods-Sprague-Dawley rats were subjected to middle cerebral artery occlusion for 2 hours. Five sets of experiments were conducted: to determine the dose-response effect of ethanol on brain infarction and functional outcome; to determine whether combining ethanol and hypothermia produces synergistic neuroprotection; to determine the therapeutic windows of opportunity for ethanol in stroke; to test whether ethanol promotes intracerebral hemorrhage in a hemorrhagic or ischemic stroke or after administration of thrombolytics; and to test the affect of ethanol on hypoxia-inducible factor-1␣ protein expression. Results-Ethanol at 1.5 g/kg reduced infarct volume and behavioral dysfunction when administered at 2, 3, or 4 hours after middle cerebral artery occlusion. The protective effect of ethanol was not improved when paired with hypothermia. Ethanol did not promote cerebral hemorrhage in hemorrhagic or ischemic stroke in combination with recombinant tissue-type plasminogen activator or urokinase. Ethanol treatment (1.5 g/kg) increased protein levels of hypoxiainducible factor-1␣ at 3 hours postreperfusion. Conclusions-Ethanol exerts a strong neuroprotective effect when administered up to 4 hours after ischemia, increases expression of hypoxia-inducible factor-1␣, and does not promote intracerebral hemorrhage when used with thrombolytics. Ethanol is a potential neuroprotectant for acute ischemic stroke. (Stroke. 2012;43:205-210.)

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“…Neurological deficits were assessed before surgery and 0.5h, 24h, 48h, and 72h after brain reperfusion by an investigator blinded to experimental groups. Longa scoring system [ 18 ] (0 = no deficit, 1 = failure to extend left forepaw, 2 = circling to the left, 3 = falling to the left, 4 = failure to walk spontaneously and loss of consciousness, 5 = death) was used.…”

Section: Methodsmentioning

confidence: 99%

Splenectomy Fails to Provide Long-Term Protection Against Ischemic Stroke

et al. 2018

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Splenectomy before or immediately after stroke provides early brain protection. This study aims to explore the effect of splenectomy on long-term neurological recovery after stroke, which is currently lacking in the field. Adult male rats were randomized into splenectomy or sham groups and then subjected to 90 min of middle cerebral artery occlusion (MCAO). Spleen was removed right upon reperfusion or 3d after MCAO. Infarct volume, neurological functions, and peripheral immune cell populations were assessed up to 28d after stroke. The results show that delayed removal of spleen did not reduce brain tissue loss and showed no effect on sensorimotor function (Rotarod, beam balance, forelimb placing, grid walk, and adhesive removal tests) or cognitive function (Morris water maze). Spleen removal immediately upon reperfusion, although significantly reduced the infarct size and immune cell infiltration 3d after MCAO, also failed to promote long-term recovery. Flow cytometry analysis demonstrated that immediate splenectomy after MCAO resulted in a prolonged decrease in the percentage of CD3+CD4+ and CD3+CD8+ T cells in total lymphocytes as compared to non-splenectomy MCAO rats. In contrast, the percentage of CD3-CD45RA+ B cells was significantly elevated after splenectomy. As a result, the ratio of T/B cells was significantly reduced in stroke rats with splenectomy. In conclusion, delayed splenectomy failed to provide long-term protection to the ischemic brain or improve functional recovery. The acute neuroprotective effect achieved by early splenectomy after stroke cannot last for long term. This loss of neuroprotection might be related to the prolonged disturbance in the T cell to B cell ratio.

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Outcome in Acute Stroke with Different Intra-Arterial Infusion Rate of Urokinase on Thrombolysis

Cited by 10 publications

References 17 publications

Drug Therapy in Stroke: From Preclinical to Clinical Studies

Drug Therapy in Stroke: From Preclinical to Clinical Studies

Neuroprotective Effect of Acute Ethanol Administration in a Rat With Transient Cerebral Ischemia

Splenectomy Fails to Provide Long-Term Protection Against Ischemic Stroke

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