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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cocaine, derived from the leaves of the shrub Erythroxylon coca, which grows on the slopes of the Andes, remains one of the most widely abused illicit drugs (Johnson et al., 1993). Its abuse appears to be increasing and as a result, so is its trafficking across borders, with ever-increasing sophistication of concealment (Rouse, 1992). Over the past few years, cases of cocaine intoxication have been reported, resulting from ruptured packets of cocaine that have been swallowed, or inserted into the vagina or rectum by couriers (drug smugglers), so called 'body packers' or 'mules' (Westli and Mittleman, 1981; Ricaurte and Langston, 1995). Cocaine is a powerful sympathomimetic and central nervous system stimulant, an overdose of which causes primarily cardiac, neurological and psychiatric effects (Ricaurte and Langston, 1995). Acute toxicity is dose-related and is characterized in the first place by its sympathomimetic effects, which include tachycardia, hypertension and hyperthermia arrythmias, followed by seizures. Brainstem depression and cardio-respiratory collapse, stroke, coma, intracranial vasculitis, myocardial infarction and sudden death have all been reported in cocaine abuse (Ricaurte and Langston, 1995). We present a fatal case with neurological and psychiatric symptoms, but without the usual cardiac and systemic signs.
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PMID:Body packer: cocaine intoxication, causing death, masked by concomitant administration of major tranquilizers. 1105 42

Cocaine use has increased considerably during the last twenty years and several related complications can be identified. Clinical features of cocaine intoxication are variable, but predominantly involve cardiovascular events. Chest pain is the most main complaint; myocardial ischemia must be ruled out. Other cardiovascular manifestations are left ventricular dysfunction, arrhythmia, endocarditis and aortic dissection. Non-cardiac complications include neurological (seizures, stroke, cerebral hemorrhage), respiratory (asthma, interstitial pneumonitis, pulmonary edema), renal (acute renal failure, rhabdomyolysis) and obstetrical disorders. Detection of cocaine in the urine provides the diagnosis. Symptomatic treatment is generally given, combining conventional treatment of the complication and broad use of benzodiazepines.
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PMID:[Acute complications in cocaine users]. 1221 80

Cocaine produces a pressor response associated with an initial hindquarters vasoconstriction followed by a prolonged vasodilation in conscious rats. Propranolol pretreatment prevented the vasodilation and enhanced the pressor response, whereas atropine methylbromide pretreatment reduced the increase in systemic vascular resistance. We studied the role of selective muscarinic and beta-adrenoceptor antagonists on responses to cocaine in rats with an increase in systemic vascular resistance to cocaine (vascular responders). Arterial blood pressure and ascending aortic and distal descending aortic blood flow using pulsed Doppler flowmetry were measured. In conscious rats, cocaine (5 mg/kg i.v.) elicited consistent pressor responses but variable systemic and hindquarters vascular resistance responses that were directly correlated, suggesting that skeletal muscle resistance responses comprise an important component of systemic vascular resistance. ICI 118551 [(+/-)-1-[2,3-(dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)-amino]-2-butanol] (0.5 mg/kg i.v.) pretreatment prevented the hindquarters vasodilation, enhancing the increase in systemic vascular resistance and the pressor response while further depressing the cardiac output response, similar to the effects of propranolol. Atenolol (1 mg/kg) pretreatment attenuated the stroke volume and cardiac output responses while enhancing the increase in systemic vascular resistance without affecting the hindquarters responses. In contrast, M2 antagonist methoctramine (0.3 mg/kg) pretreatment had similar effects as atropine in reducing the decrease in cardiac output by reducing the increase in systemic vascular resistance, whereas the M1 antagonist pirenzipine (0.02 mg/kg) did not alter responses. Therefore, the cocaine-induced pressor response is ameliorated by beta2-adrenoceptor mediated skeletal muscle vasodilation, whereas the decrease in cardiac output and the increase in systemic vascular resistance are dependent on M2-cholinoceptor activation.
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PMID:Muscarinic cholinergic and beta-adrenergic contribution to hindquarters vasodilation and cardiac responses to cocaine. 1273 Feb 77

Cocaine abuse is known to induce different types of brain-microvascular damage and many adverse cerebrovascular effects, including cerebral vasculitis, intracranial hemorrhage, cerebral infarction and stroke. A major physiological event leading to these pathophysiological actions of cocaine could be apoptosis. Whether cocaine can cause brain-microvascular pathology and vascular toxicity by inducing apoptosis of cerebral vascular smooth muscle cells is not known. This study, using several different methods to discern apoptosis, was designed to investigate if primary cultured canine cerebral vascular smooth muscle cells can undergo apoptosis when treated with cocaine. After treatment with cocaine (10(-6)-10(-3) M) for 12-24 h, the death rates of cerebral vascular smooth muscle cells increased in a concentration-dependent manner compared with controls. Morphological analysis of cerebral vascular smooth muscle cells using confocal fluoresence microscopy showed that the percentage of apoptotic cerebral vascular smooth muscle cells increased after cocaine (10(-6)-10(-3) M) treatment in a concentration-dependent manner. TUNEL assays also showed positive results for cerebral vascular smooth muscle cells treated with cocaine. These results clearly demonstrate that cerebral vascular smooth muscle cells can undergo rapid apoptosis in response to cocaine in a concentration-dependent manner. Cocaine-induced apoptosis may thus play a major role in brain-microvascular damage, cerebral vascular toxicity and strokes.
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PMID:Cocaine induces apoptosis in cerebral vascular muscle cells: potential roles in strokes and brain damage. 1466 5

The National Association of Medical Examiners Committee on Cocaine-related Deaths recommends that the following guidelines be applied in the process of documenting, interpreting, and certifying potential cocaine-related fatalities. The committee cautions that the investigation of any drug-related death requires a complete investigation of the circumstances of death, the death scene, and past medical history. It is also necessary to have the results of the forensic toxicological analysis and those of a complete forensic autopsy examination prior to formulating an opinion as to the cause and manner of death. Cocaine should be considered the underlying cause of the death when 1 or more of the following is true: (1). the circumstances surrounding the death can be associated with an acute cocaine exposure and there are no supervening causes of death; (2). the immediate cause of death is directly due to a readily identifiable mechanism or disease such as a gunshot wound or a stroke, yet the acute use of cocaine was the direct underlying cause of the trauma or the disease process; and (3). chronic cocaine use leads to a disease that results in an ultimately fatal pathologic process leading to organ injury and death. The committee further cautions that reported drug levels may not directly relate to the toxic or lethal effects of the drug upon the patient. These guidelines are intended for use by practicing medical examiners and physicians who certify drug deaths, as well as providing education tools for students.
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PMID:National Association of Medical Examiners position paper on the certification of cocaine-related deaths. 1557 31

Cocaine use in North America has reached epidemic proportions becoming one of the top causes of drug-related visits to US emergency rooms. The number of users has increased due to the popularity and accessibility of crack cocaine. The pharmacokinetic properties and effects of cocaine on the cardiovascular system can lead to serious complications. Cocaine is known to induce angina and precipitate myocardial infarction. Cocaine use has been associated with the development of dilated cardiomyopathy, left ventricular dysfunction, and can also predispose a patient to a variety of cardiac arrhythmias including sudden cardiac death. Additionally, cocaine use has been associated with spontaneous aortic and coronary dissection, mesenteric ischemia, stroke, venous thrombosis, and a variety of pulmonary complications. This review article focuses on the effects and complications of cocaine upon the cardiovascular system.
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PMID:Cardiovascular complications associated with cocaine use. 1568 70

Cocaine-induced hypoperfusion, a risk factor for ischemic stroke, has not been fully characterized during experimental drug-taking among individuals with cocaine use disorder. We sought to examine cocaine's dose-dependent, time-related effects on cerebral blood flow. In a double-blind, randomized human laboratory study with a counterbalanced order of drug administration, 31 male and female subjects with cocaine use disorder were divided into two groups receiving either (a) low-dose cocaine (0.325 mg/kg intravenously) or placebo (N=15) or (b) high-dose cocaine (0.650 mg/kg intravenously) or placebo (N=16). The different dose conditions were administered on test days separated by a rest period of >or=48 h. Cerebral blood flow was assessed quantitatively using H(2)O(15) positron emission tomography. Experimentally administered low- and high-dose cocaine conditions versus their corresponding placebo conditions were associated with global and regional hypoperfusion. The trend for high- versus low-dose cocaine to be associated with greater hypoperfusion achieved statistical significance only for the dopamine-rich sublobar and midbrain regions. Cocaine's hypoperfusion effects were maximal at 8 mins after infusion (i.e., at about the expected peak of intravenous cocaine levels) and had mostly dissipated by 32 mins after infusion. Although hypoperfusion occurred throughout the brain, the left hemispheric dopamine-rich sublobar region was the most severely affected. Cocaine-induced cerebral hypoperfusion is associated with the time course of its pharmacological effects, and dopamine-rich areas, particularly in the left hemisphere, may be most vulnerable. Increasingly larger doses of cocaine may be associated with greater risk for ischemic stroke.
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PMID:Acute intravenous low- and high-dose cocaine reduces quantitative global and regional cerebral blood flow in recently abstinent subjects with cocaine use disorder. 1575 48

Alcohol and stimulant abuse represents a major cause of cerebrovascular and cardiovascular disease in young adults. Although mild-to-moderate alcohol consumption has been linked to a decreased risk for stroke and CVD, excessive use is associated with an increased risk for intracranial hemorrhage and cardiomyopathy. Cocaine represents the single largest,cause of medical complications related to illegal drug use. Cocaine has been associated with cerebral infarction, intracranial hemorrhage, myocardial infarction, cardiomyopathy, and cardiac arrhythmias. Abuse of amphetamines is associated with complications similar to those of cocaine. The complications associated with stimulant abuse are thought to be primarily mediated through excess catecholamines, resulting in acute arterial hypertension, vasospasm, thrombosis, and accelerated atherosclerosis. Because many complications of alcohol and stimulant abuse are preventable and reversible, it is important to screen for these in patients with cerebrovascular and cardiovascular disease.
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PMID:Cerebrovascular and cardiovascular complications of alcohol and sympathomimetic drug abuse. 1622 66

Three relatively young patients, men aged 29 and 38 years and a woman aged 40 years, developed ischaemic stroke shortly after cocaine use. All three had used cigarettes or alcohol as well, and suffered from neurologic deficits with CT and MRI lesions. They recovered, but neurologic sequelae remained. Cocaine may induce haemorrhagic as well as ischaemic stroke. Different vascular complications of cocaine may be involved. The pathophysiologic mechanisms of cocaine-induced ischaemic stroke include vasoconstriction due to cerebrovascular spasms and serotoninergic action, and enhanced thrombocyte aggregation. Over the last years, the use of cocaine is rising, so that the number of cocaine-related stroke patients can be expected to increase. Cocaine use as a cause of ischaemic stroke is important to recognise because discontinuation of cocaine can prevent a recurrent stroke.
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PMID:[Cerebral infarction after cocaine use]. 1721 25

Oxidative stress is involved in the pathogenesis of cocaine-induced cardiomyopathy. In the present study, we aimed to determine the enzymatic sources of reactive oxygen species (ROS) production, namely NADPH oxidase and xanthine oxidoreductase (XOR) in male Wistar rats treated for 7 days with cocaine (2x7.5 mg/kg/day, ip) or cocaine with a NADPH oxidase inhibitor (apocynin, 50 mg/kg/day, po) or a XOR inhibitor (allopurinol, 50 mg/kg/day, po). Cocaine-induced cardiac dysfunction is associated with an increase in NADPH oxidase and XOR activities (59% and 29%, respectively) and a decrease in catalase activity. Apocynin or allopurinol treatment prevents the cocaine-induced cardiac alteration by restoration of cardiac output, stroke volume and fractional shortening. This is associated with a reduction of the myocardial production of superoxide anions and an enhancement of catalase activity. Surprisingly, apocynin treatment prevents XOR up-regulation supporting the hypothesis that NADPH oxidase-derived ROS play a role in modulating ROS production by XOR. These data suggest that NADPH and xanthine oxidase act synergically to form myocardial ROS and clearly demonstrate that their inhibition may be critical in preventing the initiation and progression of cocaine-induced LV dysfunction.
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PMID:NADPH oxidase inhibition prevents cocaine-induced up-regulation of xanthine oxidoreductase and cardiac dysfunction. 1721 56


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