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

The effects of ethanol ingestion on ADP-induced platelet aggregation and associated thromboxane formation were studied in the platelet-rich plasma of 10 healthy male volunteers, each serving as his own control. Ethanol caused a transient decrease in threshold concentration of ADP to produce irreversible aggregation. Over a wide range of ADP total platelet aggregation was increased. In the presence of irreversible aggregation, formation of thromboxane B2 rose from 303 +/- 56 to 950 +/- 212 fmol per 10(7) platelets (p less than 0.01). The effects lasted as long as ethanol was present in blood, did not significantly correlate to blood ethanol levels and exhibited great individual variation. It remains to be proved, whether these observations could contribute to the increased risk of ischemic brain infarction associated with acute ethanol ingestion.
Stroke
PMID:Acute ethanol ingestion increases platelet reactivity: is there a relationship to stroke? 396 61

Risk factors for the development and rupture of intracranial saccular (berry) aneurysms were identified in a case-control study of autopsy subjects. The development of berry aneurysms was positively correlated with increased frequencies of systemic arterial hypertension (p less than 0.001), cerebral artery atherosclerosis (p less than 0.05), and marked asymmetry of the cerebral vessels comprising the circle of Willis (p less than 0.005). In addition, patients with berry aneurysms more frequently had histories of persistent headache (p less than 0.001), pregnancy-induced hypertension (p less than 0.01), long-term use of analgesics (p less than 0.001), especially aspirin (p less than 0.05), and a family history of stroke (p less than 0.05). Factors associated with a decreased risk of berry aneurysms included treatment with insulin to control diabetes mellitus (p less than 0.005), leanness (p less than 0.05), chronic pancreatitis (p less than 0.001), malignant tumors (p less than 0.001), and moderate or severe coronary or renal atherosclerosis (p less than 0.05). Rupture of berry aneurysms was positively correlated with size (p less than 0.05) and the presence of multiple aneurysms (p less than 0.005), but also with long-term analgesic usage (p less than 0.05), excessive ethanol consumption (p less than 0.01), and fatty metamorphosis of the liver (p less than 0.01). The factors that predispose to rupture of berry aneurysms are interrelated in the sense that several of them are known to cause a decrease in the synthesis of prostaglandin E, whereas one of the factors that appears to be protective has the opposite effect. Marked and abrupt lowering of serum prostaglandin levels would cause dilatation of cerebral vasculature and increased cerebral blood flow; in the setting of hypertension, focal defects in cerebral arteries could develop, leading to the formation and subsequent rupture of berry aneurysms.
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PMID:Risk factors for the development and rupture of intracranial berry aneurysms. 401 70

The influence of chronic alcohol consumption on blood pressure was examined in normotensive Wistar/Kyoto rats (WKY) and in stroke-prone spontaneously hypertensive rats (SHR-SP). Ethanol, administered in drinking water from 5 weeks of age to produce moderate blood alcohol levels, substantially retarded the development of hypertension in SHR-SP and caused a mild reduction of blood pressure in WKY. Alcohol withdrawal caused an acute rise in blood pressure in both strains, followed by a reduction to the subnormal levels previously induced by alcohol treatment. This sustained antihypertensive effect of alcohol was not attributable to reductions of body weight or fluid intake.
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PMID:Retarded development of hypertension in stroke-prone spontaneously hypertensive rats following chronic alcohol consumption. 404 Aug 26

Since many patients with cardiomyopathy have a history of chronic ethanolism often associated with malnutrition, we have evaluated left ventricular (LV) function in alcoholics with fatty liver, who had no clinical evidence of cardiac or nutritional disease. During an afterload test of LV function the pressor response to angiotensin evoked a threefold rise of enddiastolic pressure in the alcoholic group which was substantially greater than the 4 mm Hg rise in control subjects. The stroke volume and stroke work response in the noncardiac alcoholic was significantly less than in controls. Diminished LV function was corroborated in the noncardiac alcoholic at rest, using a contractility index. To evaluate the dose-response relationship of ethanol in the production of cardiac malfunction, two groups of noncardiac alcoholic subjects were studied acutely at low and moderate dose levels. After 6 oz, ventricular function, myocardial blood flow, and metabolism were not significantly affected. After 12 oz, there was a progressive rise of end-diastolic pressure and decrease of stroke output at a mean blood alcohol level of 150 mg/100 ml, reverting toward control by 4 hr. The coronary effluent transiently evidenced leakage of cell constituents, despite an increase of coronary blood flow, suggesting a direct but reversible cardiac injury. Myocardial extraction of triglyceride was enhanced, whereas FFA uptake was reduced. A possible role of myocardial triglyceride accumulation in heart muscle was considered in pathogenesis. Chronic ingestion of 16 oz of Scotch daily by an alcoholic subject while on a normal diet produced, after 12 wk, a progressive increase of heart rate and size, circulation time, and venous pressure, and a ventricular diastolic gallop. Normal values were restored within 7 wk after interrupting alcohol. These several studies suggest that the cumulative effects of repeated ingestion of ethanol in intoxicating doses can produce diminished LV function before clinical evidence of cardiac abnormality, or heart disease not necessarily related to malnutrition.
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PMID:Ventricular function in noncardiacs with alcoholic fatty liver: role of ethanol in the production of cardiomyopathy. 430 60

In view of the variables that obscure the pathogenesis of cardiomyopathy, a study was undertaken in mongrel dogs fed ethanol as 36% of calories for up to 22 mo. Both the experimental and control groups maintained body weight, hematocrit, plasma vitamin, and protein levels. Left ventricular function was evaluated in the intact anesthetized dog using indicator dilution for end-diastolic and stroke volume determinations. During increased afterload with angiotensin, the ethanol group exhibited a larger rise of end-diastolic pressure (P<0.01), whereas end-diastolic and stroke volume responses were significantly less than in controls. Preload increments with saline elicited a significantly higher end-diastolic pressure rise in the ethanol group (P<0.01). No hypertrophy, inflammation, or fibrosis was present and it was postulated that the enhanced diastolic stiffness was related to accumulation of Alcian Blue-positive material in the ventricular interstitium. To evaluate myocardial lipid metabolism, [1-(14)C]oleic acid was infused systemically. Plasma specific activity and myocardial lipid uptake were similar in both groups. There was a significantly increased incorporation of label into triglyceride, associated with a reduced (14)CO(2) production, considered the basis for a twofold increment of triglyceride content. In addition, diminished incorporation of [(14)C]oleic acid into phospholipid was observed accompanied by morphologic abnormalities of cardiac cell membranes. Potassium loss and sodium gain, like the lipid alteration, was more prominent in the subendocardium. Thus, chronic ethanol ingestion in this animal model is associated with abnormalities of ventricular function without evident malnutrition, analogous to the preclinical malfunction described in the human alcoholic.
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PMID:Myocardial function and lipid metabolism in the chronic alcoholic animal. 436 46

Naloxone, an opiate antagonist, has recently been reported to temporarily reverse neurologic deficits associated with subarachnoid hemorrhage. To determine if this unexpected effect of naloxone might also occur in other forms of cerebrovascular diseases, 13 patients who presented with acute neurologic deficits were administered intravenous naloxone. In 3 of these patients, coincidental improvement in neurologic status was seen. In one patient the improvement was permanent. Ten of the 11 patients with non fatal neurologic damage improved later in their hospital course--7 of them to their pre-admission state. The only side effect noted was the temporally related onset of a single focal seizure in an ethanol intoxicated patient with an intracerebral hemorrhage.
Stroke
PMID:Naloxone administration to patients with acute stroke. 636 63

The authors compared the drinking habits of stroke patients and controls who were matched for the variables of age, sex, race, and day of the week admitted to the hospital. Rates of alcoholism were similar in the two groups. However, stroke patients were more likely to be current drinkers than controls, and were more likely to have been drinking within 24 hr of admission to the hospital, most of them rather heavily. Among the stroke patients, alcoholism was associated with hypertension, with being a current drinker, and with drinking at index, i.e., within 24 hr of the first symptoms of stroke. Of those stroke patients who were drinking at index, there were significant associations with being black, alcoholic, and hypertensive. The implications of these findings are discussed.
Alcohol Clin Exp Res
PMID:Alcohol, hypertension, and stroke. 637 45

Inasmuch as ethanol is thought to exert its major effects on the CNS, it is important to determine whether this abused substance can exert any direct action on cerebral blood vessels. Since chronic ingestion of alcohol: (1) can produce a loss (and degeneration) of neurons and glial cells in the brain, and (2) is associated, often, with hallucinations in human subjects particularly those undergoing withdrawal, it is possible that ethanol could produce hypoxia in select regions of the brain. The available indirect evidence in man and animals, albeit equivocal, does indicate that ethanol in certain concentrations might produce deficits in cerebral blood flow in select regions of the brain. Direct in-situ observations on the rat brain, using high-resolution, quantitative TV image-intensification microscopy, indicates that administration of ethanol, irrespective of the route of administration (e.g., perivascularly, intraarterially or systemically), produces graded concentration-dependent spasms of arterioles and venules. Concentrations of ethanol approximately greater than 250 mg/dl produce intense spasms resulting in rupture of these vessels. Recent in-situ studies in conscious dogs, using radiolabelled microspheres, also indicate that ethanol can produce deficits in regional brain blood flow. Studies with isolated canine middle cerebral and basilar arteries clearly demonstrate that low concentrations of ethanol (e.g., (less than 10 mM) can produce concentration-dependent spasms by a direct vascular action. Collectively, these new findings could be used to support the concept that heavy use of alcohol or binge-drinking can produce stroke-like effects. Specific calcium antagonists prevented or reversed the alcohol-induced cerebrovasospasms in rats and may prove valuable in treating the hypertension and strokes observed in heavy users of alcohol.
Alcohol
PMID:Alcohol, the cerebral circulation and strokes. 639 12

A variety of mechanisms may cause intravascular coagulation. Fibrinolysis is nearly always secondary to the initial clotting. In the acute form, ICF is characterized by depletion of platelets and several coagulation factors together with active fibrinolysis. There is a decrease in Factors V and VIII because they are sensitive to coagulation. The stable coagulation factors may be decreased as well because after activation they are removed from the circulation by the liver and reticuloendothelial system. Severe bleeding is the usual accompaniment of the acute syndrome, which may also occur in cancer and infection of all types. The acute syndrome may also occur in prolonged, extensive operations, after transfusion of incompatible blood, heat stroke, acute injury, certain snake bites, and with the administration of certain drugs. The chronic syndrome of intravascular coagulation is much more common and is associated with many diseases, including collagen diseases or immune diseases and malignancy. Many patients with chronic intravascular coagulation have normal or even increased levels of coagulation factors, and these patients have no unusual bleeding. The diagnosis depends on the demonstration of circulating complex of "soluble" fibrin revealed by the ethanol gel and protamine sulfate gelation tests. The secondary fibrinolysis results in elevation of FSP. Many laboratories are investigating the use of other procedures in the diagnosis of intravascular coagulation, including fibrinopeptides A and B, the VIII:C VIIIR:AG ratio, antithrombin III, PF 4, beta-thromboglobulin, D dimer, urinary FSP, and fibrinogen chromatography.
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PMID:The clinical pathology of intravascular coagulation. 642 Dec 71

Reovirus 3 in the presence of foetal bovine serum was exposed to six disinfectants for times of 10, 20 and 30 sec. At the end of such exposure times the addition of skim milk terminated disinfectant activity, and residual virus was assayed using the plaque technique. The six disinfectants considered were Javex (a sodium hypochlorite disinfectant), sodium hydroxide, ethanol, Wescodyne, One Stroke Ves-Phene, and Sonacide. Ethanol (95% v/v) and 1/75 Javex (800 ppm chlorine) were the most effective virucides. Both of these agents inactivated 10(5) plaque forming units (PFU) in 30 sec. Undiluted Sonacide, 0.25% (w/v) sodium hydroxide and 1/200 Wescodyne each inactivated between 10(2) and 10(3) PFU in 30 sec. Javex at a dilution of 1/100 (600 ppm chlorine) was next in effectiveness, inactivating 10(1.5) PFU in 30 sec and was more effective than 1/50 Ves-Phene which inactivated 10(1) PFU in 30 sec. Ethanol in 70% (v/v) solution was totally ineffective in inactivating reovirus 3. Ethanol (95% v/v) after dilution in the test system was 76% (v/v) and ethanol (70% v/v) was really 56% (v/v).
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PMID:The effectiveness of six disinfectants in inactivation of reovirus 3. 652 63


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