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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 alcohol on the central nervous system can be subdivided into three main categories: the effects of acute intoxication (drunkenness, acute encephalopathy, stroke), the effects of tolerance and ethanol withdrawal (delirium tremens, seizures) and the delayed manifestations of chronic alcohol consumption (cerebellar degeneration, Wernicke's encephalopathy, dementia).
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PMID:[Main involvement of the central nervous system in alcoholism]. 141 Sep 80

Intracerebroventricular (ivt) angiotensin II (ANG II) at 0.4, 2, 10, and 50 ng.kg-1.min-1 increased arterial pressure in conscious sheep in a dose-related manner (26 mmHg, P less than 0.05, at 50 ng.kg-1.min-1). Total peripheral resistance (TPR) and right atrial pressure also increased. Heart rate, stroke volume, and cardiac output did not change. Pressor responses to ivt ANG II were not caused by leakage of ANG II into the periphery, because plasma concentrations of ANG II did not change from control (31 +/- 7 pg/ml) at the highest dose of ANG II infused. In contrast, intravenous (iv) ANG II, 10 and 50 ng.kg-1.min-1, increased arterial pressure 29 and 47 mmHg, respectively (P less than 0.05), and decreased heart rate. ANG II, 10 ng.kg-1.min-1 iv, increased plasma ANG II levels from 36 +/- 6 to 354 +/- 69 pg/ml (P less than 0.05). Intracarotid (ic) ANG II, 10 ng.kg-1.min-1, increased arterial pressure 31 mmHg (P less than 0.05) but did not alter heart rate. ANG II ivt caused a dose-related drinking response, with a positive correlation between the amount of water drunk during ivt ANG II infusion and the increase in arterial pressure. Infusions of ANG II at 50 ng.kg-1.min-1 ivt were associated with decreased plasma osmolality and potassium concentration and increased plasma vasopressin concentration.
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PMID:Hemodynamic and behavioral effects of angiotensin II in conscious sheep. 233

Alcohol-related minor accidents such as sprains and burns are common in sauna, but more serious accidents also take place--head contusions, heat stroke after passing out in sauna and drownings while swimming. The exact number of these accidents is not known, but in Finland (population 4.8 million) the consumption of alcohol has been estimated to be a contributing factor in some 20 to 25 sauna-related deaths every year. The scientific information on the interaction of sauna and alcohol on human physiology is totally lacking. Thus our discussion on the physiological and medical consequences of this interaction relies merely on presumptions. Ingestion of large amounts of alcohol while sauna bathing may affect the body's ability to maintain blood pressure. In particular, the risk of an orthostatic hypotensive reaction is increased with concomitant faintings and accidents. Alcohol intoxication and particularly the hangover phase exposes a person to cardiac arrhythmias, and sauna may further increase the arrhythmia-risk due to enhanced adrenergic activity. Sauna bathing and heavy drinking, and also sauna bathing during hangover phase undoubtedly create real health risks.
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PMID:The sauna and alcohol. 321 3

For more than 30 years, clinical observations to link alcohol abuse and stroke have accumulated in several countries. Studies of general populations have indicated that the risk for stroke increases with increasing alcohol consumption. Studies of young victims of stroke where the classical risk factors of stroke are uncommon, have demonstrated that even occasional heavy drinking carries an increased risk for stroke. In particular, the increased occurrence of strokes during weekends, the very time of heavy alcohol consumption in non-alcoholics, supports this notion. Alcoholics seem to get their strokes at an earlier age than non-alcoholics. Paradoxically, the published evidence has implicated drinking in both ischemic and hemorrhagic strokes, which suggests that there may be more than one mechanism by which alcohol can increase the risk. Strokes seem to be precipitated during the alcohol intoxication itself rather than the following withdrawal syndrome, but the contributing mechanisms, except for bleedings caused by external violence, are unknown. Alcohol can produce fluctuations in platelet reactivity and untoward interactions with certain drugs, but it remains to be demonstrated that such effects are temporally related to the onset of ischemic and hemorrhagic strokes.
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PMID:What supports the role of alcohol as a risk factor for stroke? 331 65

The hemodynamic effects of acute alcohol intoxication were studied at rest and during upright exercise in 28 patients with coronary artery disease by right-sided heart catheterization and radionuclide cardiography. The mean arterial blood pressure at rest was reduced by 5% and the left ventricular ejection fraction at rest decreased 2% because of end-systolic dilation during intoxication (serum ethanol 21 mmol/liter). No changes were observed in heart rate, stroke volume, pulmonary artery pressure, pulmonary artery wedge pressure or total peripheral resistance. No significant changes occurred in plasma catecholamines, and no changes occurred in any variable during mild exercise corresponding to a 30 to 40% heart rate increase. Thus, alcohol ingested in moderate doses causes slight impairment of left ventricular emptying and a reduction in the arterial blood pressure at rest in patients with coronary artery disease. A mild exercise load can be tolerated during alcohol intoxication without hemodynamic changes.
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PMID:Hemodynamic effects of alcohol at rest and during upright exercise in coronary artery disease. 333 17

Thirty male patients with ischemic heart disease and cardiomyopathy entered a controlled study of the acute effects of alcohol on cardiac function evaluated by right heart catheterization. Twenty patients, nine with angina pectoris and 11 with congestive heart failure, were studied during alcohol intoxication, and ten patients, five with angina pectoris and five with heart failure, served as a control group. The mean serum ethanol concentration in the alcohol group was 93 mg/100 ml (S.D. 17). The systemic arterial blood pressure was reduced by 6% in the alcohol group, P less than 0.05 compared with the control group. No significant changes occurred in the central venous pressure, the pulmonary artery pressure, the pulmonary capillary wedge pressure, or in cardiac output, stroke volume and total peripheral resistance. Alcohol intake in moderate doses has no measurable effect on pulmonary blood pressures or cardiac output in patients with ischemic heart disease and cardiomyopathy. Such an effect may, however, be masked by a reduction of afterload.
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PMID:Cardiac function after alcohol ingestion in patients with ischemic heart disease and cardiomyopathy: a controlled study. 335 19

Seven healthy men, aged 21 to 30 years, were investigated by radionuclide cardiography at rest and during submaximal exercise at heavy (early) and during declining (late) alcohol intoxication. Control studies, in which alcohol was substituted by an isocaloric, isovolumic drink, were performed on a different day. The left ventricular ejection fraction at rest decreased from 59 to 56% during early intoxication (serum ethanol 35 +/- 6 mmol/l), whereas no change was observed in the ejection fraction during exercise. No significant change was recorded in stroke volume after alcohol consumption as opposed to a small increase after ingestion of the caloric drink. Plasma noradrenaline concentrations were elevated during exercise and early intoxication. During late intoxication (serum ethanol 21 +/- 5 mmol/l) the left ventricular ejection fraction at rest was increased by 7% compared with the baseline value. At rest the heart rate was increased from 68 +/- 7 to 84 +/- 15 beats/min, whereas cardiac output had reverted to the baseline value. Plasma noradrenaline at late intoxication was increased both at rest and during exercise compared with the baseline values. Apart from tachycardia and a reduction in left ventricular volumes during late intoxication no alcohol induced hemodynamic changes occurred during exercise.
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PMID:Cardiac function at rest and during exercise in early and late alcohol intoxication. 336 May 22

Previous experimental studies found that acute intoxication may alter the long-term outcome of standardized spinal cord injury resulting in increased spinal cord necrosis and impaired functional recovery. We examined the effects of acute intoxication (blood alcohol concentration of 100 mg/dl) on hemorrhage and axonal conduction three hours after moderate severity spinal cord contusion induced by a constrained stroke pneumatic impactor. The hemorrhagic spinal cord lesion resulting from standardized injury was significantly increased by acute intoxication. Both local hemorrhage at the injury site and rostro-caudal and total extent of hemorrhage were increased. Also, the ability of nerve axons to recover function during the first three hours post-contusion was impaired by intoxication. These findings confirm that increased post-contusion hemorrhage results when spinal cord contusion injury occurs in the presence of acute intoxication, and suggest that increased intramedullary hemorrhage may contribute to previously observed increases in anatomic damage and impaired functional recovery with alcohol intoxication.
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PMID:Effects of acute alcohol intoxication on spinal cord vascular injury. 380 21

Alcohol might contribute to stroke in several ways: induction of cardiac arrhythmias and cardiac wall motion abnormalities which predispose to cerebral embolism, induction of hypertension, enhancement of platelet aggregation and activation of the clotting cascade, and reduction of cerebral blood flow by stimulation of cerebral vascular smooth muscle contraction or by altering cerebral metabolism. While these pathophysiological mechanisms have gained enthusiastic experimental and theoretical support, the findings are preliminary and will require further large-scale clinical and epidemiological analyses to substantiate their roles as causal factors or potentiators of stroke. Documentation of measurable platelet and coagulation cascade abnormalities reported in healthy volunteers who have ingested alcohol will need to be confirmed on a broader scale in stroke patients with recent ethanol consumption. The risk of stroke in those with alcohol-induced atrial fibrillation and cardiomyopathy must be ascertained for the general population. While the experimental evidence is exciting and provocative, epidemiological evidence also suggests a link between alcohol consumption and stroke. Regular alcohol ingestion is associated with hypertension, fatal and nonfatal intracranial hemorrhage, cerebral infarction, and increased risk of death from stroke. Recent, less stringently controlled studies suggest that alcohol consumption is a risk factor for cerebral infarction in young adults with occasional ethanol intoxication and middle-aged women and young men with occasional alcohol intoxication and regular heavy drinking. Alcohol may also be a risk factor for subarachnoid hemorrhage.
Stroke
PMID:Alcohol and stroke. 381 Jul 63

Current drinking, alcoholic binges, and a history of alcohol intoxication differentiated young stroke patients from older stroke patients and young medical control subjects. Acute heavy alcohol consumption may be an important element in the development of strokes among young adults.
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PMID:Alcohol and strokes in young adults. 396 70


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