Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Cardiac effects of ethanol ingestion (1.75 g/kg within 3 hours) were examined in 8 healthy males by echocardiography and systolic time intervals in a controlled study. Heart rate (HR) was increased by 15% (p less than 0.05) during intoxication when blood ethanol (mean +/- SD) was 33.7 +/- 4.1 mmol/l. Left ventricular (LV) end-diastolic dimension was simultaneously shortened by 4% (p less than 0.01) and LV end-systolic dimension by 3% (p less than 0.05). Stroke volume was reduced by 12% (p less than 0.05). Most subjects experienced hangover symptoms 12 hours after the beginning of ethanol intake; blood ethanol was 8.8 +/- 4.0 mmol/l. At this time, HR was raised by 17% (p less than 0.05), ejection fraction by 7% (p less than 0.05), and circumferential fiber shortening velocity by 19% (p less than 0.01); total peripheral resistance was decreased by 17% (p less than 0.001). The resultant increase in cardiac output amounted to 22% (p less than 0.01). In short, the main effect of ethanol at modest blood concentrations was to reduce LV preload without detectably impairing myocardial performance. Hangover was characterized by vasodilation as well as intensified LV myocardial and pump performances.
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PMID:Drunkenness, hangover, and the heart. 683 36

Although there is general agreement that chronic ingestion of alcohol poses great risks for normal cardiovascular functions and peripheral-vascular homeostasis, a direct cause and effect between the real phenomena of alcohol-induced headache and risk of brain injury and stroke is not appreciated. "Binge drinking" of alcohol is associated with an ever-growing number of strokes and sudden death. It is becoming clear that alcohol ingestion can result in profoundly different actions on the cerebral circulation (e.g., vasodilation, vasoconstriction-spasm, vessel rupture), depending upon dose and physiologic state of host. Using rats, it has been demonstrated that acute, high doses of ethanol can result in stroke-like events concomitant with alterations in brain bioenergetics. We review recent in vivo findings obtained with 31P-NMR spectroscopy, optical reflectance spectroscopy, and direct in vivo microcirculatory studies on the intact brain. Alcohol-induced hemorrhagic stroke is preceded by a rapid fall in brain intracellular free magnesium ions ([Mg2+]i) followed by cerebrovasospasm and reductions in phosphocreatine (PCr)/ATP ratio, intracellular pH, and the cytosolic phosphorylation potential (CPP) with concomitant rises in deoxyhemoglobin (DH), mitochondrial reduced cytochrome oxidase aa3 (rCOaa3), blood volume, and intracellular inorganic phosphate (Pi). Using osmotic mini-pumps implanted in the third cerebral ventricle, containing 30% ethanol, it was found that brain [Mg2+]i is reduced 30% after 14 days; brain PCr fell 15%, whereas the CPP fell 40%. Such animals became susceptible to stroke from nonlethal doses of ethanol. Human subjects with mild head injury have been found to exhibit early deficits in serum ionized Mg (IMg2+); the greater the degree of early head injury (30 min-8 h), the greater and more profound the deficit in serum IMg2+ and the greater the ionized Ca (ICa2+) to IMg2+ ratio. Patients with histories of alcohol abuse or ingestion of alcohol prior to head injury exhibited greater deficits in IMg2+ (and higher ICa2+/IMg2+ ratios) and, unlike the subjects without alcohol, did not leave the hospital for at least several days. Women, for some unknown reason, exhibit a much higher incidence of morbidity and mortality from subarachnoid hemorrhage (SAH) than men. Data on 105 men and women with different types of stroke indicate that, on the average, a 20% deficit in serum IMg2+ is seen; total Mg (TMg) or blood pH is usually near normal. Women with SAH, however, exhibit much lower IMg2+ and higher ICa2+/IMg2+ ratios; the presence of ethanol in the blood is associated with even more depression in IMg2+ in SAH in women. It is possible that prior alcohol ingestion is, in large measure, responsible for a great deal of this unexplained higher incidence of SAH in women. It has recently been reported that the cyclical changes in estrogenic hormones appear to control the serum IMg2+ level in young women. A surge in estrogenic levels prior to SAH could thus precipitate, in part, the SAH. In other human studies, it has been shown that migraines and headache, dizziness, and hangover, which accompany ethanol ingestion, are associated with rapid deficits in serum IMg2+ but not in TMg. The former, and the alcohol-associated headache, can be ameliorated with IV administration of MgSO4. Premenstrual tension-headache (PTH) and its exacerbation by alcohol in women is also accompanied by deficits in IMg2+, and elevation in serum ICa2+/IMg2+; IV MgSO4 corrects the PTH and the serum deficit in IMg2+. Animal experiments show that IV Mg2+ can prevent alcohol-induced hemorrhagic stroke and the subsequent fall in brain [Mg2+]i, [PCr], pHi, and CPP. Other recent data indicate that alcohol-induced cellular loss of [Mg2+]i is associated with cellular Ca2+ overload and generation of oxygen-derived free radicals; chronic pretreatment with vitamin E prevents alcohol-induced vascular injury and pathology in the brain. (ABSTRACT TRUNCATED)
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PMID:Association of alcohol in brain injury, headaches, and stroke with brain-tissue and serum levels of ionized magnesium: a review of recent findings and mechanisms of action. 1054 55