Extravasation of blood is associated with intracerebral hemorrhage and head trauma. The mechanism of brain cell injury associated with hemorrhage differs from that due to pure ischemia. The purpose of this study was to investigate the acute changes after intracerebral injections of proteins that are involved in blood clotting and clot lysis. Sixty-eight adult rats were subjected to stereotaxic intrastriatal injections of normal saline (5 microL), low- (2.5 U/5 microL) and high-dose (25 U/5 microL) thrombin, low- (0.1 microgram/5 microL) and high-dose (1 microgram/5 microL) tissue plasminogen activator, low- (0.05 U/5 microL) and high-dose (0.5 U/5 microL) plasminogen, and low- (0.335 U/5 microL) and high-dose (3.35 U/5 microL) plasmin. Forty-eight hours later rats were perfusion fixed. Brain damage area, eosinophilic neurons, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL)-positive cells, infiltrating neutrophils, CD8a immunoreactive leukocytes, and reactive microglia were quantified. Damage area in striatum, dying cells, inflammatory cells, and microglial reaction were significantly greater after the high-dose plasminogen, plasmin, and thrombin injections. Tissue plasmi...Continue Reading
A specific histochemical marker (lectin Ricinus communis agglutinin-1) for normal human microglia, and application to routine histopathology
Stereotactic puncture and lysis of spontaneous intracerebral hemorrhage using recombinant tissue-plasminogen activator
Mechanisms of edema formation after intracerebral hemorrhage: effects of thrombin on cerebral blood flow, blood-brain barrier permeability, and cell survival in a rat model
Tissue plasminogen activator (tPA) increases neuronal damage after focal cerebral ischemia in wild-type and tPA-deficient mice
The protease thrombin is an endogenous mediator of hippocampal neuroprotection against ischemia at low concentrations but causes degeneration at high concentrations
Thrombin inhibitor ameliorates secondary damage in rat brain injury: suppression of inflammatory cells and vimentin-positive astrocytes
Intracerebral injection of autologous whole blood in rats: time course of inflammation and cell death
Experimental study on the PAR-1 expression around hemotoma following intracerebral hemorrhage in rats
Treadmill exercise decreases intrastriatal hemorrhage-induced neuronal cell death via suppression on caspase-3 expression in rats
Thrombin induces nigral dopaminergic neurodegeneration in vivo by altering expression of death-related proteins
Comparison of brain cell death and inflammatory reaction in three models of intracerebral hemorrhage in adult rats
The serine protease plasmin cleaves the amino-terminal domain of the NR2A subunit to relieve zinc inhibition of the N-methyl-D-aspartate receptors.
Safety of direct administration of AAV2(CU)hCLN2, a candidate treatment for the central nervous system manifestations of late infantile neuronal ceroid lipofuscinosis, to the brain of rats and nonhuman primates
Age-associated increases in poor outcomes after traumatic brain injury: a report from the Japan Neurotrauma Data Bank
Plasmin inhibitors prevent leukocyte accumulation and remodeling events in the postischemic microvasculature
Neutrophil depletion reduces blood-brain barrier breakdown, axon injury, and inflammation after intracerebral hemorrhage
Plasminogen potentiates thrombin cytotoxicity and contributes to pathology of intracerebral hemorrhage in rats
15d-Prostaglandin J2 activates peroxisome proliferator-activated receptor-gamma, promotes expression of catalase, and reduces inflammation, behavioral dysfunction, and neuronal loss after intracerebral hemorrhage in rats
Mast cells as early responders in the regulation of acute blood-brain barrier changes after cerebral ischemia and hemorrhage.
Plasmin-dependent modulation of the blood-brain barrier: a major consideration during tPA-induced thrombolysis?
Proinflammatory cytokine production by cultured neonatal rat microglia after exposure to blood products
Interaction of inflammation, thrombosis, aspirin and enoxaparin in CNS experimental antiphospholipid syndrome
Injections of blood, thrombin, and plasminogen more severely damage neonatal mouse brain than mature mouse brain.
Protease-activated receptor dependent and independent signaling by kallikreins 1 and 6 in CNS neuron and astroglial cell lines.
Glial responses, neuron death and lesion resolution after intracerebral hemorrhage in young vs. aged rats
Neutrophils contribute to intracerebral haemorrhages after treatment with recombinant tissue plasminogen activator following cerebral ischaemia.
The intrastriatal injection of thrombin in rat induced a retrograde apoptotic degeneration of nigral dopaminergic neurons through synaptic elimination
Ratiometric activatable cell-penetrating peptides provide rapid in vivo readout of thrombin activation
The injury response of oligodendrocyte precursor cells is induced by platelets, macrophages and inflammation-associated cytokines.
Thrombin-induced delayed injury involves multiple and distinct signaling pathways in the cerebral cortex and the striatum in organotypic slice cultures
Thrombin induces striatal neurotoxicity depending on mitogen-activated protein kinase pathways in vivo
The action of thrombin in intracerebral hemorrhage induced brain damage is mediated via PKCα/PKCδ signaling
Impaired adult hippocampal neurogenesis and cognitive ability in a mouse model of intrastriatal hemorrhage
Thrombin Activity and Thrombin Receptor in Rat Glioblastoma Model: Possible Markers and Targets for Intervention?
Basal Ganglia are a group of subcortical nuclei in the brain associated with control of voluntary motor movements, procedural and habit learning, emotion, and cognition. Here is the latest research.
Blood Clotting Disorders
Thrombophilia includes conditions with increased tendency for excessive blood clotting. Blood clotting occurs when the body has insufficient amounts of specialized proteins that make blood clot and stop bleeding. Here is the latest research on blood clotting disorders.