Publications by authors named "Aliza T Brown"

Introduction: Time delay is the key obstacle for receiving successful stroke treatment. Alteplase therapy must start within 4.5 hours from stroke occurrence.

View Article and Find Full Text PDF

The pathophysiology of posterior reversible encephalopathy syndrome (PRES) is incompletely understood; however, an underlying state of immune dysregulation and endothelial dysfunction has been proposed. We examined alterations of serum lactate dehydrogenase (LDH), a marker of endothelial dysfunction, relative to the development of PRES in patients receiving chemotherapy. A retrospective Institutional Review Board approved database of 88 PRES patients was examined.

View Article and Find Full Text PDF

Purpose: To develop angiographic models of embolic stroke in the rabbit using pre-formed clot or microspheres to model clinical situations ranging from transient ischemic events to severe ischemic stroke.

Materials And Methods: New Zealand White rabbits (N=151) received angiographic access to the internal carotid artery (ICA) from a femoral approach. Variations of emboli type and quantity of emboli were tested by injection into the ICA.

View Article and Find Full Text PDF

Oxidative stress and mitochondrial permeability transition (MPT) are important mechanisms in acetaminophen (APAP) toxicity. The MPT inhibitor trifluoperazine (TFP) reduced MPT, oxidative stress, and toxicity in freshly isolated hepatocytes treated with APAP. Since hypoxia inducible factor-one alpha (HIF-1α) is induced very early in APAP toxicity, a role for oxidative stress in the induction has been postulated.

View Article and Find Full Text PDF

Background: To investigate whether estrogen may attenuate neointima formation in hyperhomocysteinemic rat carotid endarterectomy.

Methods: Rats were divided into 6 groups: ovariectomized estradiol-treated homocysteine or chow; ovariectomized placebo-treated homocysteine or chow; intact placebo-treated homocysteine or chow. Chow served as controls while homocysteine served as exaggerated intimal hyperplasia.

View Article and Find Full Text PDF

Purpose: To assess the efficacy of dodecafluoropentane emulsion (DDFPe), a nanodroplet emulsion with significant oxygen transport potential, in decreasing infarct volume in an insoluble-emboli rabbit stroke model.

Materials And Methods: New Zealand White rabbits (N = 64; weight, 5.1 ± 0.

View Article and Find Full Text PDF

Acetaminophen (APAP) toxicity is responsible for approximately half of all cases of acute liver failure in the United States. The mouse model of APAP toxicity is widely used to examine mechanisms of APAP toxicity. Noninvasive approaches would allow for serial measurements in a single animal to study the effects of experimental interventions on the development and resolution of hepatocellular necrosis.

View Article and Find Full Text PDF

Background And Purpose: Microbubbles (MB) combined with ultrasound (US) have been shown to lyse clots without tissue-type plasminogen activator (tPA) both in vitro and in vivo. We evaluated sonothrombolysis with 3 types of MB using a rabbit embolic stroke model.

Methods: New Zealand White rabbits (n=74) received internal carotid angiographic embolization of single 3-day-old cylindrical clots (0.

View Article and Find Full Text PDF

Purpose: The New Zealand White rabbit (NZWR) serves an important role as an experimental model for vascular research, specifically in the area of stroke. Here the authors document vascular variations in the circle of Willis (COW).

Materials And Methods: Subselective internal carotid digital subtraction angiography was performed in 100 NZWRs.

View Article and Find Full Text PDF

Objectives: Increasing evidence confirms that microbubble (MB)-augmented ultrasound (US) thrombolysis enhances clot lysis with or without tissue plasminogen activator (tPA). Intracranial hemorrhage (ICH) is a major complication militating against tPA use in acute ischemic stroke. We quantified the incidence of ICH associated with tPA thrombolysis and MB + US therapy and compared infarct volumes in a rabbit model of acute ischemic stroke.

View Article and Find Full Text PDF
Article Synopsis
  • Tissue plasminogen activator (tPA) is the standard treatment for acute ischemic stroke, but its use can lead to intracerebral hemorrhage (ICH), making it necessary to explore alternative methods to enhance its effectiveness and safety.
  • Researchers used ultrasound (US) and microbubbles (MBs) in experiments with blood clots to determine if these techniques could help reduce the dosage of tPA while still effectively dissolving clots.
  • Results showed that combining tPA with MBs led to significant clot loss and lower infarct volumes in animal models, suggesting that this approach may minimize the risks of ICH and reduce tPA requirements in potential human stroke treatments.
View Article and Find Full Text PDF

Background: Increased carotid restenosis due to revascularization therapy is associated with insulin resistance. We hypothesize that glucose control using acarbose may attenuate intimal hyperplasia in rat carotid endarterectomy model of diet-induced insulin resistance.

Methods: Rats were fed low-fat complex carbohydrate (control) or high-fat sucrose (insulin resistance) for 4 months.

View Article and Find Full Text PDF

Purpose: Current rabbit stroke models often depend on symptoms as endpoints for embolization and produce wide variation in location, size, and severity of strokes. In a further refinement of an angiographic embolic stroke model, localized infarctions were correlated to neurologic deficits with the goal to create a rabbit model for long-term studies of therapies after stroke.

Materials And Methods: New Zealand White rabbits (4-5 kg; N = 71) had selective internal carotid artery (ICA) angiography and a single clot was injected.

View Article and Find Full Text PDF
Article Synopsis
  • Carotid endarterectomy (CEA) and carotid artery stenting are key treatments for atherosclerotic disease, but early restenosis due to neointimal hyperplasia poses challenges.
  • Researchers hypothesized that administering ketorolac tromethamine (Toradol), a nonsteroidal anti-inflammatory drug, could reduce oxidative stress and thus lower intimal hyperplasia in a rat model of CEA.
  • The study found that both doses of Toradol significantly decreased platelet activity, oxidative stress markers, and intimal hyperplasia without increasing bleeding, suggesting its potential effectiveness in improving surgical outcomes.
View Article and Find Full Text PDF

Development of new therapies for stroke requires animal models with well-defined intracranial vasculature. The rabbit as a small animal model has many desirable traits; however, a modern atlas of rabbit angiographic anatomy is not readily available. Improved digital subtraction magnification angiography and superselective small-catheter techniques now allow excellent anatomical definition.

View Article and Find Full Text PDF

Intimal hyperplasia, resulting from a complex cascade of events involving platelets, leukocytes, and smooth muscle cells, may be inhibited by the HMG-CoA reductase inhibitor pravastatin, which demonstrates inhibition of platelet activity and leukocyte adhesion and may be associated with inhibition of vascular smooth muscle cell proliferation and migration. Clopidogrel, an adenosine diphosphate (ADP) receptor inhibitor, was shown to decrease platelet activity and aggregation but not intimal hyperplasia (IH). We postulated that the combination of both pravastatin and clopidogrel would significantly decrease IH in a rat carotid endarterectomy model.

View Article and Find Full Text PDF

Elevated plasma homocysteine accelerates myointimal hyperplasia and luminal narrowing after carotid endarterectomy. N-methyl D aspartate receptors (NMDAr) in rat cerebrovascular cells are involved in homocysteine uptake and receptor-mediated stimulation. In the vasculature, NMDAr subunits (NR1, 2A-2D) have been identified by sequence homology in rat aortic endothelial cells.

View Article and Find Full Text PDF

Intimal hyperplasia results in significant morbidity and mortality following vascular intervention. Both platelets and elevated homocysteine have been implicated in the development of intimal hyperplasia. We previously demonstrated that a locally applied antiplatelet agent decreases the development of intimal hyperplasia.

View Article and Find Full Text PDF

Background: Homocysteine, a risk factor for atherosclerosis, increases intimal hyperplasia after carotid endarterectomy with associated smooth muscle cell proliferation and modulation of cytokines. The N-methyl-D-aspartate receptor (NMDAr), a glutamate-gated ion channel receptor, is associated with homocysteine-induced cerebrovascular injury; however, the receptor has not been identified in peripheral vascular cells, nor has any interaction with homocysteine been clarified. Our objectives were first, to identify NMDAr in rat carotid artery and rat aorta endothelial cells (RAEC); and second, to determine whether homocysteine activates NMDAr in the endothelium.

View Article and Find Full Text PDF

Background: This study investigated Saratin's (Merck KGaA, Darmstadt, Germany) prevention of platelet adhesion and intimal hyperplasia at different doses and in the hyperhomocystinemia rat carotid endarterectomy (CEA) model.

Methods: Rats were divided into two groups: (1) platelet adhesion or (2) luminal stenosis because of intimal hyperplasia. At CEA, rats received 0, 0.

View Article and Find Full Text PDF

Objective: The effect of a rat carotid endarterectomy (CEA) on homocysteine and the metabolic enzymes methylenetetrahydrofolate reductase (MTHFR) and cystathionine beta-synthase (CBS) was studied.

Methods: Rats were placed into 7 groups: (1) no anesthesia (NA), (2) anesthesia only (AO), (3) skin opened and closed (O/C), (4) skin opened with exposure of the carotid artery and closed (O/E/C), (5) carotid isolated and clamped (CO), (6) open CEA, and (7) open femoral endarterectomy (FEA). End points included homocysteine, hepatic MTHFR, and CBS activity.

View Article and Find Full Text PDF

Background: Homocysteine and smoking are independent risks for CVD; however their importance in post-CEA intimal hyperplasia is unclear. We performed a CEA in rats exposed to cigarette smoke with the hypothesis that smoking would increase intimal hyperplasia that may be associated with an elevated serum homocysteine. Folic acid (FA) and the homocysteine metabolic enzymes MTHFR and CBS were used to test for the significance of homocysteine elevation.

View Article and Find Full Text PDF

Vein diameter measurements using B-mode Doppler ultrasound (US) are used to assess the greater saphenous vein (GSV) for bypass operations; a 2.5-3.0 mm diameter is suggested as a minimum.

View Article and Find Full Text PDF

Prosthetic dialysis access thrombosis and/or stenosis is the most common cause of graft impairment or loss and is primarily attributed to venous outflow stenosis due to intimal hyperplasia. Intimal hyperplasia is thought to result from interactions between areas of exposed subendothelial collagen in an injured vessel and platelets, resulting in platelet adhesion. Saratin, an inhibitor of the vWF-dependent binding of platelet to collagen interaction, has been shown in vitro to reduce the adhesion of platelets to collagen.

View Article and Find Full Text PDF