Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acetylcholine (ACh) is the neurotransmitter related to learning and memory. The activity of its metabolic enzyme - choline acetyltransferase (CAT) is found to be remarkably decreased at autopsy. We consider that there is some relationship between ACh and cerebrovascular dementia such as dementia in ischemia and forgetfulness after ischemia. So we studied the relationship between ischemia and cholinergic neuron. We examined changes of muscarinic cholinergic receptor (m-ChR) in experimental ischemia by binding assay and autoradiography, and performed immunohistochemical study of CAT that is, acetylcholine synthetase, by PAP method. We also studied delayed neuronal death from the aspect of cholinergic system because the hippocampus receives ACh pathway arising from the basal nucleus. Materials used include: Pulsinelli's 4 vessel occluded rats, Tamura's MCA occluded rats and forebrain ischemia mongolian gerbils. In ischemia, the number of m-ChR decreased and binding affinity of m-ChR increased, and recirculation caused increased the number of m-ChR. While m-ChR changed immediately after ischemia, it was not until the fourth day that CAT positive cells decreased in hippocampus. In other words, at first m-ChR in postsynaptic membrane changed in ischemia, and with the progress of neuronal damage, CAT also changed. After m-ChR decreased in the thalamus, stria terminalis and Meynert nucleus 1 day following ischemia, it decreased in hippocampus after 7 days. We can consider receptor changed corresponding to the pathway of cholinergic neuron. Our study suggested that the receptor change in cholinergic system plays some role in the delayed neuronal death in the hippocampus.
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PMID:[Changes in muscarinic cholinergic receptor and choline acetyltransferase in experimental ischemic brain]. 267 78

A case of dural arteriovenous malformation of the transverse sinus, is presented, with dural sinus occlusion imaged with gadolinium diethylenetriamine pentaacetic acid (Gd-DTPA). The patient, a 59-year-old man, had developed easy forgetfulness and frequent misreading over a four-month period; he had had episodic vertiginous attacks since 3 January 1992. Magnetic resonance (MR) imaging done on 21 January 1992 showed abnormally dilated subcortical vessels and a non-hemorrhagic venous ischemia in the subcortical white matter of the left posterior temporal lobe. Thrombosis of the left sigmoid sinus was seen. After administration of intravenous Gd-DTPA, dense enhancement in the left sigmoid sinus and abnormal serpiginous enhancement in the left temporal lobe were revealed. Left carotid angiography showed dural arteriovenous malformation in the posterior fossa, with non-opacification of the left transverse and sigmoid sinuses, plus forward venous drainage into left superior petrosal sinus. The focal neurologic deficits in this case from non-hemorrhagic venous ischemia in the subcortical white matter of the left posterior temporal lobe, and were secondary to venous hypertension.
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PMID:Gadolinium-DTPA enhanced magnetic resonance imaging of dural sinus occlusion in dural arteriovenous malformation: a case report. 829 43

Huperzine A (HupA), isolated from Chinese herb Huperzia serrata, is a potent, highly specific and reversible inhibitor of acetylcholinesterase. It has been found to reverse or attenuate cognitive deficits in a broad range of animal models. Clinical trials in China have demonstrated that HupA significantly relieves memory deficits in aged subjects, patients with benign senescent forgetfulness, Alzheimer's disease (AD) and vascular dementia (VD), with minimal peripheral cholinergic side effects compared with other AChEIs in use. HupA possesses the ability to protect cells against hydrogen peroxide, beta-amyloid protein (or peptide), glutamate, ischemia and staurosporine-induced cytotoxicity and apoptosis. These protective effects are related to its ability to attenuate oxidative stress, regulate the expression of apoptotic proteins Bcl-2, Bax, P53 and caspase-3, protect mitochondria, and interfere with APP metabolism. Antagonizing effects on NMDA receptors and potassium currents may contribute to the neuroprotection as well. It is also possible that the non-catalytic function of AChE is involved in neuroprotective effects of HupA. The therapeutic effects of HupA on AD or VD are probably exerted via a multi-target mechanism.
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PMID:Neuroprotective effects of huperzine A. A natural cholinesterase inhibitor for the treatment of Alzheimer's disease. 1595 16

Huperzine A (HupA), a novel alkaloid isolated from the Chinese herb Huperzia serrata, is a potent, highly specific and reversible inhibitor of acetylcholinesterase(AChE). Compared with tacrine, donepezil, and rivastigmine, HupA has better penetration through the blood-brain barrier, higher oral bioavailability, and longer duration of AChE inhibitory action. HupA has been found to improve cognitive deficits in a broad range of animal models. HupA possesses the ability to protect cells against hydrogen peroxide, beta-amyloid protein (or peptide), glutamate, ischemia and staurosporine-induced cytotoxicity and apoptosis. These protective effects are related to its ability to attenuate oxidative stress, regulate the expression of apoptotic proteins Bcl-2, Bax, P53, and caspase-3, protect mitochondria, upregulate nerve growth factor and its receptors, and interfere with amyloid precursor protein metabolism. Antagonizing effects of HupA on N-methyl-D-aspartate receptors and potassium currents may also contribute to its neuroprotection as well. Pharmacokinetic studies in rodents, canines, and healthy human volunteers indicated that HupA was absorbed rapidly, distributed widely in the body, and eliminated at a moderate rate with the property of slow and prolonged release after oral administration. Animal and clinical safety tests showed that HupA had no unexpected toxicity, particularly the dose-limiting hepatotoxicity induced by tacrine. The phase IV clinical trials in China have demonstrated that HupA significantly improved memory deficits in elderly people with benign senescent forgetfulness, and patients with Alzheimer disease and vascular dementia, with minimal peripheral cholinergic side effects and no unexpected toxicity. HupA can also be used as a protective agent against organophosphate intoxication.
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PMID:Progress in studies of huperzine A, a natural cholinesterase inhibitor from Chinese herbal medicine. 1636 7

Carbon monoxide (CO) is a colorless, odorless, nonirritant gas that accounts for numerous cases of CO poisoning every year from a variety of sources of incomplete combustion of hydrocarbons. These include poorly functioning heating systems, indoor propane-powered forklifts, indoor burning of charcoal burning briquettes, riding in the back of pick-up trucks, ice skating rinks using propane-powered resurfacing machines, and gasoline-powered generators that are not in correct locations. Once CO is inhaled it binds with hemoglobin to form carboxyhemoglobin (COHb) with an affinity 200 times greater than oxygen that leads to decreased oxygen-carrying capacity and decreased release of oxygen to tissues leading to tissue hypoxia. Ischemia occurs with CO poisoning when there is loss of consciousness that is accompanied by hypotension and ischemia in the arterial border zones of the brain. Besides binding to many heme-containing proteins, CO disrupts oxidative metabolism leading to the formation of free radicals. Once hypotension and unconsciousness occur with CO poisoning, lipid peroxidation and apoptosis follow. Because COHb has a short half-life, examination of other biomarkers of CO neurotoxicity that reflect inflammation or neuronal damage has not demonstrated consistent results. The initial symptoms with CO exposure when COHb is 15-30% are nonspecific, namely, headache, dizziness, nausea, fatigue, and impaired manual dexterity. However individuals with ischemic heart disease may experience chest pain and decreased exercise duration at COHb levels between 1% and 9%. COHb levels between 30% and 70% lead to loss of consciousness and eventually death. Following resolution of acute symptoms there may be a lucid interval of 2-40 days before the development of delayed neurologic sequelae (DNS), with diffuse demyelination in the brain accompanied by lethargy, behavior changes, forgetfulness, memory loss, and parkinsonian features. Seventy-five percent of patients with DNS recover within 1 year. Neuropsychologic abnormalities with chronic CO exposure are found even when magnetic resonance imaging (MRI) and magnetic resonance spectroscopy are normal. White-matter damage in the centrum semiovale and periventricular area and abnormalities in the globus pallidus are most commonly seen on MRI following CO exposure. Though not as common, toxic or ischemic peripheral neuropathies are associated with CO exposure in humans and animals. The cornerstone for treatment for CO poisoning is 100% oxygen using a tight-fitting mask for greater than 6 hours. The indications for treatment with hyperbaric oxygen to decrease the half-life of COHb remain controversial.
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PMID:Carbon monoxide intoxication. 2656 90