Quantitative Evaluation of Vascular Permeability in the Gerbil Brain after Transient Ischemia Using Evans Blue Fluorescence

Uyama, Osamu; Okamura, Nobutaka; Yanase, Masahiro; Narita, Mitsuhiro; Kawabata, Keita; Sugita, Minoru

doi:10.1038/jcbfm.1988.59

Cited by 251 publications

(159 citation statements)

References 7 publications

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“…26 Four additional animals per group were operated as described above with 2-hour MCAO. Animals were briefly reanesthetized 22 hours after MCAO and 1% Evans Blue in phosphatebuffered saline (80 mg/kg; Sigma-Aldrich) was injected into the femoral vein.…”

Section: Blood-brain Barrier Permeability For Evans Bluementioning

confidence: 99%

Rivaroxaban Does Not Increase Hemorrhage after Thrombolysis in Experimental Ischemic Stroke

Ploen

Sun

Zhou

et al. 2013

J Cereb Blood Flow Metab

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The management of acute ischemic stroke during anticoagulation with a novel oral anticoagulant (NOAC) is challenging because intravenous thrombolysis is contraindicated because of a putative increased risk of intracerebral hemorrhagic complications. We examined the risk of secondary postischemic hemorrhage after thrombolysis in rodents pretreated with rivaroxaban or warfarin. Mice were pretreated with either rivaroxaban (30 mg/kg), warfarin (target international normalized ratio 2 to 3) or vehicle. After 2 or 3 hours, middle cerebral artery occlusion (MCAO), mice received 9 mg/kg recombinant tissue plasminogen activator. Twenty-four hours after MCAO, secondary hemorrhage was quantified using a macroscopic hemorrhage score and hemoglobin spectrophotometry. Blood-brain barrier (BBB) permeability was measured by Evans Blue spectrofluorometry. To increase the validity of our findings, experiments were also performed using a thromboembolic model in anticoagulated rats. Infarct size did not differ among groups. Pretreatment with warfarin led to significantly more secondary hemorrhage compared with rivaroxaban and nonanticoagulated controls after 2-and 3-hour ischemia in mice as well as in rats. Blood-brain barrier permeability was significantly higher in the warfarin group compared with rivaroxaban and control. Thus, rivaroxaban in contrast to warfarin does not increase secondary hemorrhage after thrombolysis in experimental cerebral ischemia. Less effects of rivaroxaban on postischemic BBB permeability may account for this difference.

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Section: Blood-brain Barrier Permeability For Evans Bluementioning

confidence: 99%

Rivaroxaban Does Not Increase Hemorrhage after Thrombolysis in Experimental Ischemic Stroke

Ploen

Sun

Zhou

et al. 2013

J Cereb Blood Flow Metab

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show abstract

“…The permeability of the BBB was determined according to the protocol described by Uyama et al (12), by the detection of EB fluorescence. Twenty-three hours following reperfusion, rats were anesthetized with 10% chloral hydrate and 2% EB (3 ml/kg) was injected into the femoral vein.…”

Section: Detection Of Ebmentioning

confidence: 99%

“…The absorbency of the supernatant at 620 nm was determined using a Hitachi U2001 (Hitachi, Ltd, Tokyo, Japan). The content of EB (µg/g) was subsequently calculated according to the standard curve method (12).…”

Section: Detection Of Ebmentioning

confidence: 99%

Propofol post-conditioning protects the blood brain barrier by decreasing matrix metalloproteinase-9 and aquaporin-4 expression and improves the neurobehavioral outcome in a rat model of focal cerebral ischemia-reperfusion injury

Liang

Miao

et al. 2015

Molecular Medicine Reports

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Abstract. Propofol, an intravenous anesthetic, inhibits neuronal apoptosis induced by ischemic stroke, protects the brain from ischemia/reperfusion injury and improves neuronal function. However, whether propofol is able to protect the blood brain barrier (BBB) and the underlying mechanisms have remained to be elucidated. In the present study, a rat model of cerebral ischemia/reperfusion was established, using a thread embolism to achieve middle cerebral artery occlusion. Rats were treated with propofol (propofol post-conditioning) or physiological saline (control) administered by intravenous injection 30 min following reperfusion. Twenty-four hours following reperfusion, neurobehavioral manifestations were assessed. The levels of cephaloedema, damage to the BBB and expression levels of matrix metalloproteinase-9 (MMP-9), aquaporin-4 (AQP-4) and phosphorylated c-Jun N-terminal kinase (pJNK) were determined in order to evaluate the effects of propofol on the BBB. In comparison to the cerebral ischemia/reperfusion group, the levels of brain water content and Evans blue content, as well as the expression levels of MMP-9, AQP-4 and pJNK were significantly reduced in the propofol post-conditioning group. These results indicated that propofol post-conditioning improved the neurobehavioral manifestations and attenuated the BBB damage and cephaloedema induced following cerebral ischemia/reperfusion. This effect may be due to the inhibition of MMP-9 and AQP-4 expression, and the concurrent decrease in JNK phosphorylation.

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“…19 A 2% solution of EB (Sigma-Aldrich, St Louis, MO, USA) was injected (4 mL/kg) into the femoral vein. Twenty-four hours later, 0.4 mL of blood was obtained by cardiac puncture, then the mouse was transcardially perfused with phosphate-buffered saline (100 mm Hg) for 5 minutes.…”

Section: Blood-brain Barrier Dysfunctionmentioning

confidence: 99%

Mild Hypercholesterolemia Blunts the Proinflammatory and Prothrombotic Effects of Hypertension on the Cerebral Microcirculation

Rodrigues

Vital

Granger

2013

J Cereb Blood Flow Metab

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Although an increased leukocyte and platelet adhesion is observed in cerebral venules of mice with either hypertension (HTN) or hypercholesterolemia (HCh), it remains unclear whether the combination of HTN and HCh exerts a comparable effect on leukocyte and platelet recruitment in the cerebral microvasculature. Thus, we examined whether HCh alters platelet and leukocyte adhesion, and blood-brain barrier (BBB) permeability, in cerebral venules in two models of murine HTN: DOCA salt-induced and angiotensin II (Ang II) induced. In both models, the mice were placed on either a normal or cholesterol-enriched diet. An enhanced recruitment of adherent leukocytes and platelets in cerebral venules was noted in both HTN models in the absence of HCh, but not in its presence. The Ang II-induced increase in BBB permeability was attenuated by HCh as well. Both total and high-density lipoprotein (HDL) cholesterol levels were elevated in the HCh mice. The HTN-induced increase in leukocyte and platelet adhesion was attenuated in apolipoprotein A-I transgenic mice (ApoA1-Tg) and blunted in wild-type mice treated with the ApoA1 mimetic peptide, 4F. Our findings indicate that mild HCh significantly blunts the cerebral microvascular responses to HTN and that HDL may have a role in mediating this beneficial effect of HCh.

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Quantitative Evaluation of Vascular Permeability in the Gerbil Brain after Transient Ischemia Using Evans Blue Fluorescence

Cited by 251 publications

References 7 publications

Rivaroxaban Does Not Increase Hemorrhage after Thrombolysis in Experimental Ischemic Stroke

Rivaroxaban Does Not Increase Hemorrhage after Thrombolysis in Experimental Ischemic Stroke

Propofol post-conditioning protects the blood brain barrier by decreasing matrix metalloproteinase-9 and aquaporin-4 expression and improves the neurobehavioral outcome in a rat model of focal cerebral ischemia-reperfusion injury

Mild Hypercholesterolemia Blunts the Proinflammatory and Prothrombotic Effects of Hypertension on the Cerebral Microcirculation

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