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)

: Cocaine is the most commonly used recreational drug among young adults with levels reaching epidemics proportions. This accelerated rate of use is due mainly to easy access and administration, reduced cost, and, importantly, underestimation of the drug risks. Cocaine, instead, is responsible of endothelial dysfunction and accelerated atherosclerosis with consequent organ damage. Cocaine abuse is not only associated with central necrotizing vasculitis, but it is also appeared to play a role in the development of peripheral vasoconstriction with symptoms similar to Buerger's disease. The current study reports a middle-aged man addicted to cocaine for 20 years. The patient presents several cardiovascular disease risk factors and manifestations, including diabetes mellitus and hypertension. Additionally, arteriography showed complete left posterior tibial artery obstruction with distal collateral vessels and severe leftfoot ischemia. For clinical worsening 1 month later, the patient underwent another arteriography. Although angioplasty of posterior tibial artery showed recovery of blood flow, immediately after treatment (selective percutaneous transluminal angioplasty of posterior tibial artery, dilation with balloon without stenting), a return to pretreatment blood flow 2 min later was observed. This transient change was mediated by severe vasospasm resulting in a complete re-obstruction of the vessel. The poor vascular manifestations are most probably due to cocaine-necrotizing vasculitis subsequent to endothelial dysfunction and accelerated atherosclerosis usually associated with cardiovascular risk factors. Therefore, treatments of young cocaine addicts presenting many cardiovascular risk factors and manifestations should always be carefully investigated and cautiously approached, especially in those with poor outcomes.
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PMID:Lower limb ischemia due to long-term abuse of cocaine. 2483 35

Cocaine constriction of the cerebral vasculature is thought to contribute to the ischemia associated with cocaine use. However, the mechanisms whereby cocaine elicits relevant vasoconstriction remain elusive. Indeed, proposed intra- and intercellular mechanisms based on over 3 decades of ex vivo vascular studies are, for the most part, of questionable relevancy due to the generally low contractile efficacy of cocaine combined with the use of nonresistance-type vessels. Furthermore, the significance attached to mechanisms derived from in vivo animal studies may be limited by the inability to demonstrate cocaine-induced decreased cerebral blood flow, as observed in (awake) humans. Despite these apparent limitations, we surmise that the vasoconstriction relevant to cocaine-induced ischemia is elicited by inhibition of dilator and activation of constrictor pathways because of cocaine action on the neurovascular unit (neuron, astrocyte, and vessel) and on vessels outside the unit. Furthermore, previous cocaine exposure, that is, conditions present in human subjects, downregulates and sensitizes these dilator and constrictor pathways, respectively, thereby enhancing constriction to acute cocaine. Identification of specific intra- and intercellular mechanisms requires investigations in the isolated microvasculature and the neurovascular unit from species chronically exposed to cocaine and in which cocaine decreases cerebral blood flow.
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PMID:Cocaine Constrictor Mechanisms of the Cerebral Vasculature. 2677 Nov 52

Cocaine, a natural alkaloid derived from the coca plant, is one of the most commonly used illicit drugs. Cocaine abuse causes systemic adverse effects like stroke, myocardic infarction, arterial dissection, vascular thrombosis and rhabdomyolysis. Cocaine use is, also, associated with renal complications such as acute kidney injury, vasculitis, acute interstitial nephritis, chronic kidney disease, malignant hypertension with thrombotic microangiopathy. Acute kidney injury may or may be not associated to rhabdomyolysis. Rhabdomyolysis caused by cocaine abuse is multifactorial, involving tissue ischemia secondary to vasoconstriction and cellular damage caused by the drug. We report a 50-year-old man with history of chronic hepatitis C and substance abuse admitted to our unit with severe rhabdomyolysis and acute kidney failure after nasal insufflation of cocaine overdose. Renal function recovered after several treatments of dialysis. We conclude that cocaine adversely impacts kidney function ; in addition cocaine and rhabdomyolysis are the double danger for acute kidney injury. Medical management of cocaine toxicity requires a multisystem approach, with close monitoring cardiac, neurological and renal function.
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PMID:[Acute kidney injury and rhabdomyolysis after cocaine overdose: case report and literature review]. 2958 60

Cocaine is a well-known factor of tissue ischemia and may be related to thinning of the inner retinal layers. The present study aimed to evaluate and determine whether cocaine users show retinal nerve fiber layer (RNFL) thinning by means of spectral-domain optical coherence tomography. A group of 17 cocaine users and 18 non-users were recruited for complete ophthalmologic examination. Spectral domain optical coherence tomography (Cirrus OCT) was used to evaluate peripapillary RNFL and macular thickness. The average RNFL measurement in the cocaine users group was significantly thinner compared to the control group. Subjects in the cocaine users group showed significant thinning in the nasal, superior and inferior quadrant. There were no significant differences in macular thickness or in the temporal quadrant between the two groups. This study supports further research with larger sample sizes to precisely determine the effect of cocaine on the RNFL.
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PMID:Retinal nerve fiber layer analysis in cocaine users. 3050 59

Cocaine toxicity can result in myocardial infarction from coronary vasospasm. The current treatment algorithm includes intravenous and/or intracoronary vasodilator administration with an expectantly quick resolution of symptoms and signs of ischemia. However, in situations in which myocardial injury persists, the optimal management is uncertain. We present a case in which extracorporeal membrane oxygenation effectively stabilized a patient with ongoing hemodynamic instability who experienced repeated episodes of myocardial injury and ventricular tachyarrhythmias due to cocaine toxicity. <Learning objective: In many urban settings, cocaine-induced angina is not uncommon. The pathogenesis of its manifestation includes coronary artery vasospasm and decreased left ventricular function. Treatment typically involves systemic vasodilators, such as nitrates and calcium channel blockers. However, in patients with substantial hemodynamic instability, these agents might result in a worsening of systemic perfusion. Accordingly, extracorporeal membrane oxygenation should be considered in such cases to promote myocardial recovery.>.
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PMID:Extracorporeal membrane oxygenation for profound cardiogenic shock due to cocaine toxicity. 3054 30

Cocaine-regulated and amphetamine-regulated transcript (CART) is a neuropeptide with reported neuroprotective effects in ischemic cerebral injury. However, its mechanism has not yet been elucidated. Herein, we investigated the role and mechanism of CART in synaptic plasticity in neurons after ischemic cerebral stroke. We found that the survival rate of the oxygen-glucose deprivation (OGD) neurons was increased after CART treatment. Moreover, CART treatment significantly attenuated ischemia-induced neuronal synaptic damage and increased synaptophysin expression. In addition, the number of presynaptic vesicles was increased and the postsynaptic density (PSD) was thickened after CART treatment. Mechanistically, CART treatment enhanced the expression of Arc mRNA in a cAMP response element binding protein (CREB) dependent manner in OGD neurons, and blockade of CREB by KG-501 eliminated the protective effect of CART. Collectively, CART protected the synaptic structure in neurons after ischemic cerebral injury by increasing the Arc expression via upregulating p-CREB.
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PMID:Cocaine- and amphetamine-regulated transcript protects synaptic structures in neurons after ischemic cerebral injury. 3200


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