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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There are racial differences in the prevalence and pattern of left ventricular (LV) hypertrophy in hypertension. This study was performed to determine whether racial differences also exist in LV hypertrophy among chronic cocaine users. We studied 112 chronic cocaine abusers < 45 years old in whom normal blood pressures (< or = 140/90 mm Hg) were recorded 3 times daily for 3 weeks. LV wall thickness and mass were measured echocardiographically. Technically adequate studies were obtained in 79 blacks and 33 whites. Self-reported cocaine use was higher in whites than in blacks (688 +/- 516 vs 431 +/- 468 $/week, p = 0.03). There were no group differences in terms of duration of cocaine use, age, height, weight, blood pressure, LV dimensions, or left atrial size. However, posterior wall thickness (1.13 +/- 0.17 vs 1.03 +/- 0.14 cm, p = 0.0035) and LV mass index (113 +/- 25 vs 94 +/- 19 g/m2, p = 0.0001) were significantly greater in blacks. LV hypertrophy, defined as an M-mode LV mass index > or = 134 g/m2, was present in 24 blacks (30%) and 2 whites (6%) (p = 0.011). When defined as a posterior wall thickness > or = 1.2 cm and a 2-dimensional echocardiographic LV mass index > or = 105 g/m2, LV hypertrophy was present in 37 of 79 blacks (47%) and in 6 of 33 whites (18%) (p = 0.0086). Cocaine-related LV hypertrophy is more prevalent in black men than in white men.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Racial differences in the prevalence of left ventricular hypertrophy among chronic cocaine abusers. 748 35

Cocaine is an extremely addictive local anesthetic which can produce stimulation of the sympathetic nervous system due to the inhibition of catecholamine reuptake at the synaptic junction. Because of the rapid metabolism of cocaine, the probability of a patient presenting to the operating room with acute intoxication is unlikely. However, the physiological effects of chronic cocaine abuse on various organ systems have an impact on anesthesia management. A preoperative review of major organ systems is essential. Selective beta 1 antagonists (i.e., esmolol) may need to be titrated with a direct vasodilator (i.e., nitroprusside) to manage hypertension and tachycardia. The nonselective beta antagonist effects of labetalol are much more potent than its alpha antagonist effects, which could result in unopposed alpha vasoconstriction. In addition, the equal affinity of the alpha adrenergic antagonist, phentolamine, for both alpha 1 and alpha 2 receptors may result in significant tachycardia. Nitroglycerin has also been used in management of hypertension associated with coronary vasoconstriction. There is controversy regarding management of ventricular dysrhythmias and asystole. Lidocaine is an amide local anesthetic that may have addictive effects, in the presence of cocaine, which may lower the seizure threshold. In addition, the use of epinephrine to treat asystole is controversial in the presence of a state of excess catecholamines induced by cocaine. General anesthesia may include barbiturates, nitrous oxide, and opioids. Inhalational agents may be used with caution due to their myocardial depressant effects. Regional anesthesia may be a good choice if coagulopathies and hypovolemia are corrected before the procedure.
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PMID:Anesthetic management of the cocaine abuse patient. 750 43

We studied hemodynamic responses to cocaine and two metabolites, cocaethylene (CE) and benzoylecgonine (BE), in five conscious ewes and fetuses, which were chronically instrumented to measure maternal and fetal aortic pressures, uterine artery blood flow (Qutr) and fetal common carotid artery blood flow (Qcar) to estimate cerebral blood flow. Conscious ewes of 121 to 128 days' (mean, 124 days) gestation received 1.0 mg/kg i.v. of cocaine (n = 12 doses), CE (n = 14) or BE (n = 12) and responses were compared to seven additional ewes and fetuses at 115 to 127 days' (mean, 122 days) gestation each given one 1.0 mg/kg i.v. of cocaine dose while anesthetized with halothane. In conscious ewes, cocaine, CE and BE all caused maternal and fetal hypertension. Qutr decreased 31% after cocaine, increased 37% after CE and was unaffected by BE. Cocaine induced fetal hypoxemia; fetal arterial blood gas tensions were unaffected by CE or BE. Fetal Qcar was reduced 51% at peak effect by cocaine (57 +/- 8 to 28 +/- 6 ml/min) and 46% by CE (65 +/- 7 to 33 +/- 6 ml/min), and was unaffected by BE because of variable subject response, although all three drugs increased calculated fetal cerebral vascular resistance. The cocaine-induced changes were attenuated or abolished in anesthetized sheep. Fetal/maternal peak serum concentrations were 100% for CE and only 2% for BE; amniotic fluid concentrations of CE were 10-fold higher than both fetal and maternal serum concentrations. Cocaine and cocaine metabolites have important effects on maternal and fetal hemodynamics and fetal cerebral blood flow which, for CE and BE, are not dependent on decreased uterine blood flow or fetal hypoxemia.
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PMID:Hemodynamic and cerebral blood flow effects of cocaine, cocaethylene and benzoylecgonine in conscious and anesthetized fetal lambs. 803 7

Industrial solvents mixed from thinner, used in paints, leathers, rubber, varnishes, have neurotoxic action. By laboral inhalation or spontaneously these are absorbed from the lungs, transported by blood and because of this high lipophilic section are retained within the lipid rich nervous system. Euphoric effects appear accompanied with visual and additive halucinations. In chronic abusers it produce schizophrenic-paranoid consequences with encephalic and peripheral neuronal and nervous fibers destruction, accompanied of blindness and paralysis. Cocaine is another neurotoxic drug. At first it produces euphoria, arterial hypertension and symptoms suggestive of underlying psychiatric diseases. The cocaine addicts often suffer depression, paranoia, hallucinations, seizures and suicidal ideation. The morphological base of the symptomatology is the encephalic and peripheral neuronal and nerve fibers destruction.
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PMID:[Clinico-pathologic correlation of dementia produced by thinner and cocaine]. 806 72

Acute drug-induced hypertension is known to have adverse consequences on the cerebral vasculature. Cocaine abuse has been reported to be associated with an increased frequency of hemorrhagic or ischemic stroke. The purpose of this study was to determine whether cocaine alters the blood pressure or cerebral blood flow response to exogenous norepinephrine. A craniectomy was made over the parietal cortex in rats and cortical blood flow changes were measured using laser-Doppler flowmetry. Ten minutes after cocaine (1 mg/kg, i.v.) or saline, increasing doses of norepinephrine (0.01-10 micrograms/kg, i.v.) were given by bolus injection and changes in blood pressure and flow were monitored. Cocaine produced a transient 27 +/- 5% increase in blood pressure and a 38 +/- 9% increase in blood flow. Cocaine significantly potentiated the blood pressure and cerebral blood flow responses produced by submaximal pressor doses of norepinephrine (0.01-0.6 microgram/kg, i.v.). In summary, cocaine causes a rapid, transient increase in blood pressure and cortical blood flow and potentiates the magnitude and duration of the pressure and flow response to norepinephrine. Repetitive blood pressure elevations in cocaine abusers is one of the proposed mechanisms leading to damage of cerebral vessels. These results may be relevant to an increased frequency of cerebrovascular accidents in cocaine-abusing individuals.
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PMID:Cocaine potentiates the blood pressure and cerebral blood flow response to norepinephrine in rats. 828 15

Cocaine abuse is widespread in North America. It is estimated that almost one in every four Americans has used cocaine at least once in his/her lifetime. In the past two decades, cocaine related cardiovascular complications have mushroomed because cocaine has become cheaper and more readily available. The fundamental effects of cocaine on cardiovascular system are similar to those observed following an intense, sympathetic stimulation. Cocaine intake results in marked increase in blood pressure, myocardial oxygen demand and heart rate. Coronary blood flow, which increases in response to exercise (endogenous sympathetic stimulation) however, is decreased by cocaine intake. Increased demand of oxygen by the myocardium in the face of decreased supply in subjects with cocaine use, leads to myocardial ischemia, which in turn forms a substrate for most of the cardiovascular complications, namely, myocardial infarction, cardiac arrhythmias and acute pulmonary edema. Hypertension related complications, dissection and rupture of aortic aneurysm, hemorrhagic stroke, in addition to infective endocarditis, myocarditis, cardiomyopathy all occur more frequently in cocaine addicts. In this review, pertinent clinical pharmacology and cardiovascular risks associated with cocaine abuse are presented.
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PMID:Cardiovascular effects of cocaine abuse. 829 63

Cocaine abuse has produced a major epidemic health problem in North America in the 1980s. The abuse of cocaine is maintained by the drug's effects on brain reward systems, mediated at least in part by its dopaminergic action. The patterns and consequences of use are best understood by considering the pharmacokinetics (rapid absorption and delivery to the brain, relatively short half-life) and the pharmacodynamics (intense central and peripheral neural stimulation). Cocaine is used therapeutically as a topical and local anaesthetic. Toxicity occurs primarily in cocaine abusers, but also occasionally after therapeutic dosing. Medical complications reflect primarily excessive central nervous system stimulation and excessive vasoconstriction, the latter resulting in severe hypertension and/or organ ischaemia with associated organ injury. Most deaths that result from medical complications of cocaine intoxication are sudden and occur before medical intervention is possible. Other complications of cocaine abuse with severe personal and social consequences include traumatic deaths and injuries, and reproductive disturbances, as well as transmission of infectious diseases, especially AIDS. Cocaine addiction is clearly a problem, although the number of addicts is unknown. Pharmacologic treatment of cocaine addiction has as yet been unsuccessful. Psychosocial approaches remain the mainstay of therapy.
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PMID:Clinical pharmacology and toxicology of cocaine. 844 38

Cocaine use, frequently associated with other substance abuse, is becoming more common in the pregnant patient. These patients are more likely to experience peripartum complications. A case of hypertension and pulmonary oedema in such a patient, possibly triggered by ketamine, is reported. A tumultuous course in the intensive care unit was resolved when the patient's hypertension and sympathetic reactivity were successfully treated with barbiturates. A number of factors supported a diagnosis of barbiturate withdrawal in this patient, its onset also was related temporally to ketamine administration. Hypertension should be considered a sign of acute barbiturate withdrawal. If a history of cocaine use, particularly crack cocaine, is elicited, one should suspect multiple substance abuse and be especially cautious when administering ketamine.
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PMID:Hypertension and pulmonary oedema associated with ketamine administration in a patient with a history of substance abuse. 844 55

Although cocaine abuse has been associated with an increased incidence of cerebrovascular accident, the underlying mechanisms are unknown. In this study we have investigated the effects of cocaine upon the autoregulation of local cortical blood flow (lCBF) during hypertension. Hypertension was induced in conscious rats by intravenous infusion of angiotensin-II (5 micrograms/ml; 0.5-2.5 ml/h), and animals were subsequently injected IV with either cocaine-HCl (5 mg/kg) or saline, prior to the measurement of lCBF of glucose utilization (lCGU) using [14C]-iodoantipyrine or [14C]-2-deoxyglucose quantitative autoradiography, respectively. Hypertension alone (< 155 mmHg) did not significantly alter lCBF in any cortical areas examined. However, at higher mean arterial blood pressure (MABP), lCBF increased focally (+265%) in parietal cortex. Cocaine did not alter lCBF in normotensive animals, but with increasing levels of hypertension (MABP > 145 mmHg), all cocaine-treated rats showed focal increases (200-400%) in lCBF in parietal cortex. Glucose use remained relatively unaffected in all treatment groups. This hyperaemia in cocaine-treated rats at MABP below the normal upper limit of autoregulation may provide a mechanism to explain haemorrhagic stroke in cocaine abusers.
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PMID:Acute cocaine alters cerebrovascular autoregulation in the rat neocortex. 849 81

Cocaine use is associated with a variety of serious neurological complications, including cerebral infarction, intracerebral and subarachnoid hemorrhage, transient ischemic attacks, migraines, and seizures. We report two cases of intracerebral hemorrhage with biopsy-proven cerebral vasculitis associated with the use of cocaine. The first case involved a 32-year-old man who presented with headache, left-sided hemiparesis, and severe hypertension and who was found to have a large right putaminal hemorrhage on cranial tomographic (CT) scan. Cerebral angiography did not show vasculitic changes, but brain tissue obtained during hematoma evacuation revealed a nonnecrotizing leukocytoclastic angiitis of the small vessels. The second case involved a 20-year-old man who presented with headache, agitation, and speech difficulty that progressed to disorientation and dysphasia. He had a large left temporoparietal hematoma seen on CT scan. Cerebral angiography was consistent with vasculitis, and brain tissue obtained during hematoma evacuation revealed a small vessel vasculitis. In both cases, thorough clinical and laboratory investigations found no evidence of systemic vasculitis or an etiologic agent other than cocaine. We also critically reviewed the previously reported cases of cocaine-associated cerebral vasculitis and the relevant medical literature to discuss the "cocaine-associated vasculitis syndrome" in the context of more established vasculitidies, including hypersensitivity vasculitis. In addition, we outline a diagnostic and therapeutic approach to patients with possible cocaine-associated vasculitis.
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PMID:Cocaine-associated cerebral vasculitis. 865 May 87


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