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Results for “Embolic Stroke”

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PubMed1989

Embolic stroke from a carotid arterial source in the rat: pathology and clinical implications.

We developed a new animal model of stroke which resembles human stroke more closely than existing models. We described the pathology produced in the brain following platelet embolism, previously described only in the retina. The common carotid artery of the rat was irradiated for 6.5 minutes with an argon laser at 514.5 nm after intravenous injection of a photosensitizing agent, rose bengal. A retinal embolus was seen in 1 rat 5 minutes after irradiation. A nonocclusive platelet thrombus was present in the carotid artery 50 minutes after irradiation, with almost all the platelet thrombus being cleared 24 hours later. Acute (1 to 10 days) changes in the brain included 44 small infarcts in 12/13 rats, cortical arterioles occluded with platelets and thickening of small vessels in normotensive rats. Chronic (4 to 12 weeks) changes included lacunes in the brains of normotensive rats and intimal proliferation of smooth muscle in the carotid artery. This is the 1st animal model of (1) stroke with emboli produced in vivo rather than injected into the carotid, (2) intimal proliferation of smooth muscle without invasion of the vessel, and (3) lacunes. This model provides results important to the laboratory study of stroke.

Acute Disease↗
PubMed1995

Thrombus associated with mitral valve calcification. A possible mechanism for embolic stroke.

BACKGROUND: Several studies have demonstrated an association between mitral annular calcification and stroke; however, the pathophysiological explanation remains speculative. CASE DESCRIPTIONS: We describe two patients with cerebral embolism in whom mitral valve calcification was demonstrated by transthoracic echocardiography. In both patients, transesophageal echocardiography identified a mass that appeared to be thrombus on the calcified portion of the mitral apparatus. There was no evidence of a hypercoagulable state or endocarditis in either case. Repeated transesophageal echocardiography after anticoagulation demonstrated resolution of the masses in both patients. CONCLUSIONS: These cases support the hypothesis that thrombus formation may be a pathophysiological link between ischemic cerebral events and mitral annular calcification in some patients.

Aged↗
PubMed2000

Survival and histological evaluation of therapeutic window of post-ischemia treatment with magnesium sulfate in embolic stroke model of rat.

The neuroprotective window of magnesium for up to 8 h after ischemic insult was evaluated in a clinically relevant model of focal cerebral ischemia subjected to embolization of the right middle cerebral artery (MCA) with an autologous thrombus. The animals were treated with either vehicle or 5% magnesium sulfate (90 mg/kg) intravenously at 2, or 6, or 8 h after ischemic insult. Survival rate significantly increased only in animals treated with magnesium sulfate in treatment groups at 2 h after MCA embolization but improvement in neurological outcome was observed in all medicated groups. Compared with animals in control group, post-ischemia treatment with magnesium sulfate significantly reduced brain infarct volume (P<0.01) except the 8 h group. These data indicate that the therapeutic window for neuroprotection of magnesium can be extended up to 6 h in the focal cerebral ischemia model of this study. The long window of opportunity for effective dosing may be explained with the proposed multiple mechanisms of actions for magnesium.

Animals↗
PubMed2003

Adjuvant treatment with a glycoprotein IIb/IIIa receptor inhibitor increases the therapeutic window for low-dose tissue plasminogen activator administration in a rat model of embolic stroke.

BACKGROUND: Platelet aggregation and fibrin deposition are key events leading to microvascular thrombosis and progressive impairment of downstream microvascular perfusion after stroke. We tested the hypothesis that inhibition of platelet function with a GP IIb/IIIa receptor antagonist would increase the efficacy and safety and increase the time window for thrombolytic therapy for stroke with full- and half-dose tissue plasminogen activator (tPA). METHODS AND RESULTS: Rats were subjected to embolic middle cerebral artery occlusion. Four hours after ischemia, rats were treated with 7E3 F(ab')2 (6 mg/kg) in combination with tPA at doses of 10 and 5 mg/kg, tPA alone at a dose of 10 or 5 mg/kg, 7E3 F(ab')2 (6 mg/kg) alone, or saline. Combination treatment with 7E3 F(ab')2 and tPA (full- or half-dose) significantly (P<0.05) reduced infarct volume and neurological deficits compared with saline-treated rats. However, treatment with 7E3 F(ab')2 or tPA (full- or half-dose) alone did not reduce infarct volume. Quantitative measurements of cerebral microvessels perfused by FITC-dextran revealed that combination treatment with 7E3 F(ab')2 and full-dose tPA significantly (P<0.05) increased the percentage of FITC-dextran-perfused vessels compared with saline and full-dose tPA-treated rats. In addition, treatment with 7E3 F(ab')2 in combination with full-dose tPA significantly (P<0.05) decreased microvascular platelet accumulation and matrix metalloproteinase 9 immunoreactivity and protected against loss of collagen IV immunoreactivity. CONCLUSIONS: Combination treatment with 7E3 F(ab')2 with full- and half-dose tPA at 4 hours after ischemia significantly reduces infarct volume and improves neurological outcome. Enhancement of patency and integrity of cerebral microvessels most likely contributes to the benefits observed with this combination therapy.

Abciximab↗
PubMed2003

Effects of minocycline alone and in combination with mild hypothermia in embolic stroke.

Inflammatory reactions occurring in the brain after ischemia may contribute to secondary damage. In the present study effects of minocycline, an anti-inflammatory agent, alone or in combination with mild hypothermia, on focal embolic brain ischemia have been examined. Focal ischemic injury was induced by embolizing a preformed clot into the middle cerebral artery (MCA). Infarct volume was measured at 48 h after the injury. Administration of minocycline alone or minocycline plus mild hypothermia reduced infarct volume significantly. However, mild hypothermia in combination with minocycline did not show any additive effect. These results suggest that minocycline is beneficial in focal ischemic brain injury, and the lack of the enhanced neuroprotection may be due to the brief exposure to hypothermia.

Animals↗
PubMed2002

New method of embolus preparation for standardized embolic stroke in rabbits.

BACKGROUND AND PURPOSE: Although thromboembolic stroke is caused by red, white, or mixed clots, the emboli previously used in animal studies on thrombolysis were more often red than white. Because this might be one of the reasons why thrombolysis is less effective in patients than in experimental stroke, we developed a new method of preparing highly standardized red and fibrin-rich white emboli. METHODS: The middle cerebral artery of 20 rabbits was embolized with either red or fibrin-rich white autologous emboli. Cerebral perfusion was monitored by MRI. RESULTS: Red emboli consisted of closely packed erythrocytes within a sparse fibrin net and white emboli of a dense mass of fibrin with only few other blood cells. Infarct volumes were 26+/-4% (mean+/-SD) of the ischemic hemisphere with red and 27+/-6% with white emboli. The relative regional cerebral blood volume dropped below 50% 90 minutes after vascular occlusion with either type of embolus. Late spontaneous lysis and hemorrhagic complications occurred in 37.5% of red but not in white embolus cases. CONCLUSIONS: Emboli prepared by our technique result in standardized cerebral infarctions. Size and composition of the emboli continuously can be adjusted according to the experimental requirements.

Angiography, Digital Subtraction↗
PubMed2002

Delayed minocycline but not delayed mild hypothermia protects against embolic stroke.

BACKGROUND: Inflammatory reactions occurring in the brain after ischemia may contribute to secondary damage. In the present study, effects of minocycline, an anti-inflammatory agent, alone or in combination with mild hypothermia on focal embolic cerebral ischemia have been examined. METHODS: Focal ischemic injury was induced by embolizing a preformed clot into the middle cerebral artery (MCA). Infarction volume was measured at 48 h after the injury. Mortality was also recorded. RESULTS: Delayed administration of minocycline alone or delayed minocycline plus delayed mild hypothermia reduced the infarction volume significantly. However, delayed mild hypothermia alone was not protective and delayed mild hypothermia in combination with minocycline did not show any additive effect. CONCLUSIONS: These results suggest that minocycline is beneficial in focal ischemic brain injury, and the lack of the enhanced neuroprotection may be due to the brief exposure to hypothermia.

Animals↗
PubMed1990

Regression of intracardiac thrombus after embolic stroke.

Using two-dimensional echocardiography, we studied the pathophysiology of intracardiac thrombus regression accompanied by anticoagulant therapy in 82 consecutive patients with acute cardiogenic cerebral embolism. We noted intracardiac thrombus in 15 patients; nine of the 15 were started on anticoagulant therapy with warfarin potassium to maintain the prothrombin time between 2.5 and 3.5 (international normalized ratio). Serial two-dimensional echocardiograms were obtained for these nine patients before and after anticoagulation, with the plasma levels of fibrinopeptide A, fibrinopeptide B beta 15-42, and D-dimer measured at the same time. In eight of the nine patients the intracardiac thrombi gradually decreased in size while the plasma level of fibrinopeptide A fell to within the normal range and the plasma levels of fibrinopeptide B beta 15-42 and D-dimer remained above the normal ranges. In the other patient the thrombus disappeared, with embolization to the right arm immediately after starting anticoagulant therapy. Mobile or small thrombi regressed earlier than nonmobile or large ones. We conclude that regression of intracardiac thrombi after anticoagulation may be based on the relative predominance of plasma fibrinolytic activity over anticoagulation-inhibited thrombin activity.

Aged↗
PubMed1999

Brain hemorrhages after rt-PA treatment of embolic stroke in spontaneously hypertensive rats.

Intracerebral hemorrhage is a major complicating factor of thrombolytic therapy of stroke. To investigate the incidence of bleeding in animals with a diseased vascular system, thrombolysis was carried out in spontaneously hypertensive rats (SHR) after clot embolism of the right middle cerebral artery (MCA). Three hours after embolism SHR were treated with either recombinant tissue-plasminogen activator (rt-PA) or saline, and neurological deficits and intracerebral hemorrhages were evaluated after 3 days survival. Rt-PA-treated SHR exhibited a significantly higher incidence of hemorrhages than untreated rats but neurological deficits and survival rates showed a non-significant trend for improvement. This model offers the possibility of investigating the pathophysiology of post-thrombolytic complications in a clinically relevant small animal model.

Animals↗