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

Between January 1978 and December 1979 23 consecutive patients aged under 40 years with acute ischemic brain infarction were admitted to the department of neurology, Meilahti University Hospital in Helsinki. In 10 patients (43%) the onset of symptoms was preceded within 24 hours by ethanol intoxication, and all but one symptom occurred at weekends when most liquor is consumed in Finland. Ethanol intoxication preceding the stroke was 4 times as common in female and 5 times as common in male patients as ethanol intoxication in the general Finnish population of the same age and sex. The present results support those of our previous study and suggest that occasional ethanol intoxication increases the risk of ischemic brain infarction both in adolescents and young adults.
Stroke
PMID:Ethanol intoxication: a risk factor for ischemic brain infarction in adolescents and young adults. 731 64

Acute ethanol exposure (8-570 mM) induced potent contractile responses of rings in both basilar and middle cerebral arteries, from dogs, sheep, piglets and baboons, in a dose-dependent manner. The contractions were reproducible and not tachyphylactic. The middle cerebral arteries were found to be more sensitive to ethanol than the basilar arteries. No known pharmacological antagonist, tested, exerted any effects on ethanol-induced contractions. No differences in responsiveness to ethanol in canine cerebral arteries were found between male and female animals or between the presence and the absence of endothelial cells. Removal of extracellular Ca2+ ([Ca2+]o) partially attenuated ethanol-induced contractions, while withdrawal of extracellular Mg2+ ([Mg2+]o) potentiated such contractions. In the complete absence of [Ca2+]o, caffeine and ethanol induced similar, transient contractions followed by relaxation in K(+)-depolarized cerebral vascular tissue. Ethanol-induced contractions were completely abolished by pretreatment of tissues with caffeine. Our results suggest that: (a) acute ethanol intoxication can induce direct contractions (independent of amine, prostanoid or opioid mediation) of diverse mammalian cerebral vascular tissues, including those from primates; (b) these contractile responses are heterogeneous along the cerebrovascular tree and independent of endothelial cells; (c) in addition to a need for [Ca2+]o, an intracellular release of Ca2+ is needed for ethanol to induce contractions; and (d) hypomagnesemia or Mg deficiency potentiates the contractile effects of ethanol on brain vessels and may be a risk factor for ethanol-related, ischemic stroke events.
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PMID:Ethanol-induced contraction of cerebral arteries in diverse mammals and its mechanism of action. 829 88

Exposure of primary astrocyte cultures to isosmotic ethanol from 10-100 mM led to both swelling of the cells and release of [3H]taurine and D-[3H]aspartate. Exposure to hyperosmotic ethanol, in the same concentration range, caused neither swelling nor release. Release was inhibited by the anion transport blocker L-644,711, already shown to inhibit amino acid release evoked by hypoosmotic or high-potassium medium, conditions that also cause astrocytic swelling. Ethanol-induced release generally showed a decline in response to successive exposures to ethanol, and release was not dependent on extracellular calcium. Thus, the characteristics of swelling-induced release of amino acids by isosmotic ethanol seem to correspond to those of swelling-induced release from astrocytes due to exposure to hypotonic or high-K+ media. We discuss whether such effects may contribute to CNS damage after head injury and stroke.
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PMID:Ethanol-induced aspartate and taurine release from primary astrocyte cultures. 847 90

Cocaethylene is a pharmacologically active cocaine metabolite that is produced in the liver by the transesterification of cocaine only in the presence of ethanol. The acute cardiovascular effects of cocaethylene are not known. We compared the acute cardiovascular effects of cocaethylene with cocaine and with cocaine plus ethanol in 18 dogs. We administered cocaethylene 7.5 mg/kg to 6 dogs, cocaine 7.5 mg/kg to 6 dogs, and cocaine 7.5 mg/kg plus ethanol 1 gm/kg to 6 dogs. The dose of each drug was chosen to produce in dogs the concentrations of cocaethylene or cocaine that have been measured in patients who have experienced cardiotoxic reactions to cocaine or cocaine plus ethanol. Arterial, left ventricular (LV), pulmonary artery wedge pressures (PAWP), the maximum rate of LV pressure rise [(dP/dt)max] and fall [(dP/dt)min], and heart rate (HR) were continuously measured. Stroke volume was determined 3 times during the first hour after drug administration then hourly for four hours. The concentrations of cocaethylene and cocaine peaked in the serum at 3717 +/- 651 ng/ml and 4140 +/- 459 ng/ml, respectively, two minutes after each bolus. The median half-life of cocaethylene was 144.3 minutes whereas the median half-life of cocaine was 96.7 minutes (p < 0.01). Cocaethylene maximally decreased (dP/dt)max by 44%, (dP/dt)min by 29%, and stroke volume by 28% (all p < 0.01) and increased the PAWP by 50% (p < 0.02) and the HR by 13% (p = NS) during the first hour. Cocaine maximally decreased (dP/dt)max by 40%, (dP/dt)min by 31%, and the stroke volume by 26% and increased the PAWP by 100% and the HR by 46% (all p < 0.01) during the first hour. Ethanol plus cocaine maximally decreased (dP/dt)max by 68%, (dP/dt)min by 78% and the stroke volume by 49% and increased the PAWP by 118% and the HR by 74% (all p < 0.01) during the first hour. In this last group, (dP/dt)max and stroke volume remained depressed by approximately 20% (p < 0.01) for five hours. We conclude that cocaethylene is as toxic as cocaine to the myocardium but is less toxic than ethanol plus cocaine.
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PMID:Cocaethylene is as cardiotoxic as cocaine but is less toxic than cocaine plus ethanol. 876 Oct 12

Our previous studies have shown that ethanol selectively counteracts centrally mediated hypotensive responses. This study investigated the role of cardiac output and peripheral resistance in the antagonistic interaction between ethanol and antihypertensive drugs. Changes in blood pressure, heart rate, cardiac index, stroke volume, and peripheral resistance elicited by clonidine and subsequent ethanol or saline administration were evaluated in conscious rats. The aortic barodenervated rat was employed because it exhibits greater hypotensive responses to clonidine compared with the intact rat. Aortic barodenervation elicited acute rises in blood pressure, heart rate, and peripheral resistance, whereas cardiac index and stroke volume were not altered. The blood pressure of conscious aortic barodenervated rats returned to sham-operated levels by 48 hours due to concomitant reductions in cardiac index and stroke volume; the peripheral resistance, however, remained significantly elevated. Clonidine (30 microg/kg, I.V.) elicited greater decreases in blood pressure in aortic barodenervated compared with sham-operated rats. The hypotension was caused by decreases in cardiac index and stroke volume because peripheral resistance did not change. Ethanol (1 g/kg, I.V.) counteracted the hypotensive effect of clonidine and raised blood pressure to levels higher than preclonidine values. Significant (P<.05) increases in cardiac index and stroke volume and decreases in peripheral resistance accompanied the pressor effect of ethanol. Additional control groups were included in the study to determine the selectivity of the interaction. A dose of hydralazine (0.5 mg/kg, I.V.) was used that produced similar hypotension to that evoked by clonidine in aortic barodenervated rats. Hydralazine-evoked hypotension was similar in denervated and control rats and resulted from significant reductions in peripheral resistance. Reflex increases in heart rate and stroke volume and hence cardiac output were observed. Ethanol given after hydralazine produced a short-lived pressor effect (<5 minutes versus 40 minutes in the case of clonidine) and counteracted the sympathetically mediated increases in cardiac output, stroke volume, and heart rate. These findings support our hypothesis that ethanol selectively counteracts hypotensive responses of central origin by reversing the reduction in cardiac output elicited by clonidine.
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PMID:Role of cardiac output in ethanol-evoked attenuation of centrally mediated hypotension in conscious rats. 926 Sep 94

Ethanol ingestion can cause irreversible neuronal and vascular damage in the brain and stroke-like events. Using an intact in vivo rat brain (pial) model, TV image-intensification, cultured cerebral vascular muscle cells, digital-image analysis, and a novel Mg2+ ion-selective electrode to measure extracellular ionized Mg2+, studies were designed to determine whether: 1) perivascular or systemic administration (i.v. or intra-arterial) of magnesium aspartate HCI (MgA) exert vasodilator effects on arterioles (65-130 microm o.d.) and venules (60-135 microm); 2) nonvasodilator doses of MgA could modify vascular spasms induced by BaCl2 and ethanol; 3) nonvasodilator doses of MgA could ameliorate or prevent the cerebral vascular damage induced by high doses of ethanol; and 4) ethanol depletes cerebral vascular muscle of intracellular Mg ions ([Mg2+]i). Perivascular application of MgA (0.01-100 micromol) produced dose-dependent vasodilatation of cerebral arterioles and venules; arterioles yielded greater vasodilator responses compared to venules. Nonvasodilator doses of Mg (1.0, 4.0 micromol/min), administered i.v. or intra-arterially, into a branch of the internal carotid artery, prevented: 1) the spasmogenic actions of ethanol and Ba2+; and 2) the vasculotoxic actions (rupture of postcapillary venules and focal hemorrhages) of ethanol. In addition, ethanol depleted cerebral vascular muscle cells of [Mg2+]i; blood levels of ionized Mg2+ rose after IP ethanol. Despite the fact that systemic infusion of low nonvasodilator doses did not result in dilatation of the pial arterioles and venules, plasma total and ionized Mg rose 18-230%, depending upon dose of MgA and time of plasma sampling. These data support the idea that Mg2+ can act as a local vasodilator on brain microvessels and possess antispasmodic properties on brain arterioles and venules. In addition, our results indicate that Mg may possess some unique cerebral vascular protective properties against the vasculotoxic effects of ethanol. Lastly, these findings suggest ethanol-induced cerebrovasospasm and vascular damage appear to be associated with a rapid loss of [Mg2+]i from cerebral vascular muscle cells.
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PMID:Alcohol-induced vascular damage of brain is ameliorated by administration of magnesium. 947 55

The N-methyl-d-aspartate (NMDA)-glutamate receptor could contribute to stroke, trauma, and alcohol-induced brain damage through activation of nitric oxide formation and excitotoxicity. In rat primary cortical cultures NMDA was more potent at activating nitric oxide formation than triggering excitotoxicity. Ethanol dose dependently inhibited both responses. In contrast, treatment of neuronal cultures with ethanol (100 mM) for 4 days significantly increased NMDA stimulated nitric oxide formation and excitotoxicity. These findings suggest that ethanol acutely inhibits but chronically causes supersensitivity to NMDA-induced excitotoxicity in neuronal cultures. To investigate ethanol's interaction with stroke induced damage models of global cerebral ischemia were studied. Transient global ischemia resulted in a loss of hippocampal CA1 pyramidal neurons over a 3- to 5-day period. Determinations of the NMDA receptor ligand binding stoichiometry or postischemic receptor binding changes did not show differences between neurons that undergo delayed neuronal death following ischemia and those that show no toxicity, for example, CA1 and dentate gyrus, respectively. Acute ethanol (3 g/kg) was found to protect against ischemia-induced CA1 hippocampal damage by lowering body temperature, but not under temperature controled conditions. These studies indicate that the factors contributing to stroke-induced brain damage are complex, although they are consistent with chronic ethanol increasing stroke-induced brain damage by increasing NMDA excitotoxicity.
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PMID:Ethanol, stroke, brain damage, and excitotoxicity. 958 59

Alcohol and tobacco consumption are correlated. Smokers consume more alcohol than do nonsmokers, and alcohol consumers smoke more than do teetotalers. The independent effects of alcohol and nicotine on the cardiovascular system are well documented, but combined effects of short-term administration are unknown. This experimental work was designed to study the effects due to short-term administration of alcohol and nicotine on cardiovascular system. In phase I, 30 experiments were performed to study the dose-response curve of both the drugs. In phases II and III, 15 dogs were subjected to 30 experiments. In phase II, ethanol, 400 mg/kg, was given i.v., followed by nicotine 50 microg/kg, i.v., and in phase III, sequence of drug administration was reversed to study the effects on hemodynamics and coronary artery blood flow. The dose-response curve established the i.v. dose of ethanol, 400 mg/kg, and nicotine, 50 microg/kg. Ethanol administration caused a nonsignificant increase in heart rate (HR), mean arterial pressure (MAP), left ventricular systolic pressure (LVS), and left ventricular mechanical work (LVMW), and a decrease in maximal rate of increase of LV pressure per second (dP/dt), stroke volume (SV), and systemic vascular resistance (SVR). Left ventricular end-diastolic pressure (LVEDP), pulmonary artery mean pressure (PAM), right atrial pressure (RAP), pulmonary vascular resistance (PVR), myocardial oxygen consumption (MVO2), and average peak velocity of coronary blood flow (APV) had mild significant increases as compared with controls. Nicotine significantly increased heart rate, mean arterial pressures, LVEDP, and pulmonary artery, pulmonary capillary wedge, and right atrial pressures. Nicotine increased dP/dt (2,062-3,188; p < 0.006) and decreased APV (9 to 8; p < 0.03). Combined ethanol followed by nicotine had synergistic increase in HR, SD, MAP, LVS, LVEDP, pulmonary pressures, CO, SV, dP/dt (2,184 > 5,206; p < 0.005), MVO2, and LVMW. However, the excitatory effects of nicotine were attenuated when ethanol was administered after nicotine (dP/dt, reduced from 2,058 to 1,653; p < 0.04, and APV increased from 10 to 12; p < 0.02). We conclude that ethanol increased APV but had nonsignificant effects on the hemodynamics, whereas nicotine reduced the APV and had significant excitatory responses. In combination (i.v.), ethanol + nicotine produced significant synergistic excitatory effects. On the other hand, the nicotine + ethanol combination increased APV and caused attenuation of the excitatory effects of nicotine in dogs.
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PMID:Combined effects of alcohol and nicotine on cardiovascular performance in a canine model. 964 79

Our recent findings have shown that ethanol selectively counteracts decreases in blood pressure (BP) evoked via activation of central I1-imidazoline receptors but not alpha-2 adrenoceptors in conscious spontaneously hypertensive rats (SHRs). This study investigated the role of sympathetic activity, cardiac output and total peripheral resistance (TPR) in the differential effect of ethanol on centrally mediated hypotension. Changes in plasma norepinephrine (NE), as index of sympathetic activity, BP, heart rate, cardiac index, stroke volume, and TPR elicited by rilmenidine or alpha-methylnorepinephrine (selective I1 and alpha-2 receptor agonists, respectively) and subsequent ethanol (0.5 or 1 g/kg) or saline, were evaluated in conscious SHRs. Intracisternal rilmenidine (25 microg) or alpha-methylnorepinephrine (alpha-MNE; 4 microg) elicited similar decreases in BP, TPR, and plasma NE, but cardiac index was not changed. Ethanol (0.5 g/kg i.v.) had no effect on hemodynamic responses to rilmenidine or alpha-MNE. The higher dose (1 g/kg i.v.) of ethanol counteracted the hypotensive response to rilmenidine and significantly (P <.05) elevated TPR and plasma NE. In contrast, ethanol (1 g/kg) had no effect on the hypotensive responses to alpha-MNE but significantly (P <.05) elevated plasma NE. However, this increase in NE was approximately one third of the increase evoked by ethanol when given after rilmenidine. These findings suggest that the selective counteraction by ethanol of the hypotension evoked via activation of central I1 but not alpha-2 receptors may relate, at least in part, to its greater ability to reverse the sympathoinhibition and the associated decrease in vascular resistance mediated by I1 receptors.
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PMID:Ethanol counteraction of I1-imidazoline but not alpha-2 adrenergic receptor-mediated reduction in vascular resistance in conscious spontaneously hypertensive rats. 991 45

This study investigated the differential hemodynamic effects of small to high doses of ethanol in conscious age-matched spontaneously hypertensive rats (SHRs) and Wistar Kyoto rats (WKYs). Changes evoked by ethanol (0.25, 0.5, or 1 g/kg, i.v.) or equal volume of saline in mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), stroke volume (SV), and total peripheral resistance (TPR) were followed for 90 min in the two rat strains. The baseline MAP (163 +/- 4 vs. 113 +/- 2 mm Hg) of SHRs was significantly (p < 0.05) higher, compared with WKYs due mainly to the presence of an elevated TPR 13.82 +/- 0.12 vs. 2.51 +/- 0.09 mm Hg/ml/min/100 g, p < 0.05) in SHRs. In both rat strains, all doses of ethanol produced immediate increases in MAP at 1 min, after which the MAP responses varied and depended on the rat strain and dose of ethanol used. In WKYs, 0.25 g/kg ethanol had no effect on MAP, but caused significant decreases in CO and SV and increased HR. Ethanol (0.5 and 1 g/kg) produced a short-lived (10 min) and dose-related increase in MAP. The higher dose (1 g/kg) of ethanol elicited significant (p < 0.05) increases in TPR that were counterbalanced by concomitant decreases in CO and SV. In SHRs, the two higher doses (0.5 and 1 g/kg) of ethanol elicited significant (p < 0.05) decreases and increases in MAP, respectively, compared with control (saline-treated) values. The pressor response to the 1 g/kg dose of ethanol was associated with an increase in TPR that achieved a statistical significance (p < 0.05) at 50 and 80 min after ethanol administration. HR was significantly (p < 0.05) reduced by the two higher doses of ethanol, whereas SV and CO were not changed. Blood ethanol concentrations measured 10, 30, and 60 min after ethanol administration were similar in SHRs and WKYs. These findings suggest that acute administration of ethanol to conscious rats elicits hemodynamic responses that are strain- and dose-dependent. In contrast to a short-lived and dose-related pressor response in WKYs, ethanol (0.5 and 1 g/kg) elicited opposite and longer lasting effects on MAP (decreases and increases, respectively) in SHRs. In both rat strains, the pressor response to the higher dose of ethanol was associated with an increase in TPR; an effect that was compromised by a concomitant decrease in CO in WKYs but not SHRs.
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PMID:Acute hemodynamic effects of ethanol in conscious spontaneously hypertensive and normotensive rats. 1006 58


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