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

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

Progressive bleeding is uncommon in spontaneous intracerebral hemorrhage. We describe two cases of spontaneous thalamic hemorrhage with evidence of active bleeding or rebleeding detected by noncontrast CT. The first patient was a 47-year-old man with a history of hypertension and cocaine abuse. The second patient, a 73-year-old man, had no valuable risk factors. It is noteworthy that most well-documented instances of continued bleeding or rebleeding in spontaneous intracerebral hemorrhage occur in the thalamus. The natural evolution of spontaneous intracerebral hemorrhage after the first hours of stroke remains to be elucidated.
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PMID:Progressive bleeding in spontaneous thalamic hemorrhage. 780 55

Cocaine abuse is widespread, and it is possible that its two main pharmacological actions, sympathomimetic and local anesthetic, could influence the blood pressure and cerebral blood flow response to brain injury, which occurs with increased frequency in drug abusers. We tested this hypothesis in ventilated barbiturate-anesthetized rats. Brain injury was induced using the fluid-percussion method, and cortical blood flow was measured using laser-Doppler flowmetry. Saline, cocaine, methamphetamine, or lidocaine was administered 10 min before injury. Upon injury, both cocaine- and saline-pretreated rats showed a similar acute hypertensive phase, which was followed by a period of more pronounced hypotension in the cocaine group (68 +/- 4 vs. 100 +/- 6 mmHg). Cortical blood flow increased dramatically 3-15 s following injury-induced hypertension in both the cocaine and saline groups (approximately 230-260%), but then fell below preinjury values within minutes. At 1 h postinjury, the blood flow in the saline group was 53 +/- 6% of the preinjury value, while in the cocaine group, flow was 74 +/- 7% of preinjury baseline. Similar to the cocaine-treated animals, methamphetamine also caused a more pronounced hypotensive event, but blood flow was not significantly different from saline controls. Lidocaine did not alter posttraumatic blood pressure but did significantly elevate blood flow throughout the 1-h postinjury period. At 60 min posttrauma, blood flow in the lidocaine group was 80 +/- 10% of the preinjury value. The mechanism by which cocaine alters blood pressure and blood flow after injury is not entirely certain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute cocaine administration alters posttraumatic blood pressure and cerebral blood flow in rats. 784 Mar 3

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

After decades of focus on the effects of cocaine abuse on the central nervous system (CNS), the cardiovascular toxicity of cocaine is just beginning to be appreciated. The most common cardiovascular pathologies associated with cocaine use include: cardiomyopathy, left ventricular dysfunction, myocarditis, arrhythmia, hypertension, myocardial infarction, stroke, arterial thrombosis, deep vein thrombosis, and gastrointestinal, renal, and skeletal muscle ischemia. This article reviews the above pathologies with speculations on the mechanisms by which cocaine produces cardiovascular tissue damage.
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PMID:Cardiovascular and thrombosis pathology associated with cocaine use. 829 12

Maternal cocaine abuse has been associated with neonatal neurological and neurobehavioral problems of unknown pathogenesis. We administered a single intravenous dose of cocaine (2 mg/kg) to 12 unanesthetized pregnant sheep; their fetuses had been catheterized in utero 2 days before the study. We measured fetal cerebral blood flow (CBF), cerebral metabolic rate of O2 (CMRO2), mean arterial blood pressure (MAP), and blood gases before and 2, 5, 15, and 30 min after maternal cocaine injection. Fetal CBF increased by 37 +/- 33% (mean +/- SD) at 5 min and returned to baseline by 15 min. Regional brain blood flow changes paralleled CBF changes with the greatest increases occurring in cerebellum (54 +/- 43%) and brain stem (54 +/- 52%). Cerebral vascular resistance was decreased for cerebellum (22%) and brain stem (19%) but was unchanged for cerebral hemispheres and caudate. Increased CBF at 5 min was associated with a 20 +/- 9% increase in fetal MAP and a 38 +/- 13% decrease in fetal arterial O2 content. Fetal CMRO2 was unchanged. There was a decrease in fetal intestinal blood flow at 2 min, an increase in myocardial, adrenal, and renal blood flow at 5 min, and no change in placental blood flow. Maternal cocaine injection causes fetal hypoxemia, hypertension, and increased CBF. Possible mechanisms for cerebral vasodilation (in some areas) include hypoxemia, impaired autoregulatory response to increased blood pressure, and/or direct or indirect vascular effects of cocaine or its metabolites.
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PMID:Fetal responses to acute maternal cocaine injection in sheep. 834 69

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

Recent statistics from the National Institute on Drug Abuse indicate that cocaine abuse continues to be a significant public health problem. Between 1988 and 1990 at Grady Memorial Hospital in metropolitan Atlanta, Georgia, we identified 12 patients in whom subarachnoid hemorrhage was temporally related to cocaine abuse. All 12 patients had underlying cerebral aneurysms that had ruptured. Currently, the incidence of ruptured intracranial aneurysms in patients with cocaine-induced subarachnoid hemorrhage is 84.9% (mean age, 31.1 years; overall mortality, 60.5%). Hypertension is the likely precursive factor in cocaine-induced aneurysmal rupture. Cocaine abuse appears to be a significant negative factor in the natural history of cerebral aneurysms, especially in young adults. We review the epidemiology of cocaine-induced subarachnoid hemorrhage and its effects on the cerebral circulation, and suggest guidelines for patient management.
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PMID:Cocaine-induced aneurysmal rupture: an emergent negative factor in the natural history of intracranial aneurysms? 847 41

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


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