Alcohol-Induced Spasms of Cerebral Blood Vessels: Relation to Cerebrovascular Accidents and Sudden Death

Altura, Burton M.; Altura, Bella T.; Gebrewold, Asefa

doi:10.1126/science.6836278

Cited by 217 publications

(90 citation statements)

References 25 publications

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“…Alcohol consumption is associated with an increased incidence of hypertension [4][5][6] and stroke. [1][2][3] Although many factors have been implicated in the pathogenesis of alcohol-induced cardiovascular complications, 1,25 sympathetic activation could conceivably trigger acute events by promoting short-term increases in blood pressure and platelet aggregation. 26,27 Whether sympathetic activation also contributes to long-term elevation of arterial pressure in persons who drink alcohol every day needs further investigation, but results from studies of rats suggest that this could be the case.…”

Section: Discussionmentioning

confidence: 99%

Suppression of Alcohol-Induced Hypertension by Dexamethasone

et al. 1995

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Section: Discussionmentioning

confidence: 99%

Suppression of Alcohol-Induced Hypertension by Dexamethasone

et al. 1995

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“…Moreover, the idea that ethanol causes vasoconstriction through actions of two mediators, endothelin-1 and nitric oxide, may be applied to other organs, such as heart and brain, where ethanol is also known to induce vasoconstriction (2)(3)(4).…”

Section: Discussionmentioning

confidence: 99%

“…Ethanol causes serious health problems ( 1 ) including ethanolinduced microcirculatory disturbances in many organs such as heart and brain (2)(3)(4). In the liver, infusion ofethanol into the portal vein elicits vasoconstriction in the hepatic microvasculature, leading to hepatic tissue hypoxia and eventually hepatocellular necrosis (5,6).…”

Section: Introductionmentioning

confidence: 99%

Roles of endothelin-1 and nitric oxide in the mechanism for ethanol-induced vasoconstriction in rat liver.

Oshita¹,

Takei²,

Kawano³

et al. 1993

J. Clin. Invest.

112

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This study was designed to investigate the mechanism for ethanol-induced hepatic vasoconstriction in isolated perfused rat liver. Upon initiation of ethanol infusion into the portal vein at concentrations ranging from 25 to 100 mM, portal pressure began to increase in a concentration-dependent manner and reached maximal levels in 2-5 min (initial phase), followed by a gradual decrease over the period of ethanol infusion (escape phenomenon). Endothelin-1 antiserum significantly inhibited this ethanol-induced hepatic vasoconstriction by 45-80%. Cessation of infusion of endothelin-1 antiserum was followed by a subsequent increase in portal pressure. On the other hand, when a nitric oxide synthesis inhibitor, NG-monomethyl-L-arginine (L-NMMA), was infused into the portal vein simultaneously with ethanol, the initial phase of the response of portal pressure to ethanol was not altered and the peak values of portal pressure remained unchanged. However, after the peak increase in portal pressure, the rate of decrease was less than in the absence of L-NMMA. Thus, L-NMMA diminished the escape phenomenon and sustained the vasoconstriction. This study supports the hypothesis that two endothelium-derived vasoactive factors, endothelin-1 and nitric oxide, regulate hepatic vascular tone in the presence of ethanol. (J. Clin. Invest.

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“…Several of these investigators have reported that alcohol constricts umbilical and cerebral blood vessels (9)(10)(11)(12). Alcohol is generally regarded as a "depressant," and several studies have demonstrated that alcohol intoxication is associated with decreased CMR02 and CMRglu, presumably reflecting decreased functional activity (5,10,(13)(14)(15) sheep but found an increase in CBF during alcohol intoxication.…”

Section: Discussionmentioning

confidence: 99%

Cerebral Responses to Acute Maternal Alcohol Intoxication in Immature Fetal Sheep

Gleason

Hotchkiss

1992

Pediatr Res

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ABSTRACT. Previous studies in mature fetal sheep have and behavioral problems (3). Several of these neurologic abnorshown that alcohol depresses cerebral blood flow (CBF), malities have been produced in animals exposed to alcohol in cerebral O2 consumption (CMR02), and cerebral glucose utero (4). However, the mechanism(s) by which alcohol produces consumption (CMRglu). This effect earlier in gestation brain damage and the vulnerable developmental period (if any) might contribute to the pathogenesis of fetal alcohol syn-during which damage occurs are unknown. The depressant efdrome. Physiologic studies of immature fetal sheep have fects of alcohol on CBF and CMR02 have been previously demonstrated lower CBF, CMR02, and CMRglu as well reported in several adult animal models as well as in mature fetal as a blunted vasodilatory response to hypoxia compared sheep. Richardson et al. (5) studied the physiologic responses of with mature fetal sheep. The purpose of this study was to term fetal sheep to acute maternal alcohol intoxication and noted determine whether immature fetal responses to alcohol are a significant decrease in both CBF and CMRO1. In addition, blunted compared with near-term fetal responses. We stud-they noted significant fetal hypoglycemia and a decrease in ied seven immature fetal sheep in utero at 92 f 1 d CMRglu. The fetal sheep brain is very mature near term, both gestation (term = 147 d) 2 d after placement of vascular structurally and functionally. Studies of immature fetal sheep catheters. Pure ethanol (1 g/kg) was infused i.v. to the have shown significantly lower CBF, CMR02, and CMRglu mother over 1 h. We measured CBF and myocardial blood compared with mature fetal sheep (6). Furthermore, the cerebral flow by radioactive microspheres and calculated CMROz vasodilatory response to hypoxemia is "blunted," reflecting either and CMRglu using arterial and sagittal sinus O2 and immature regulatory mechanisms or an inability of cerebral glucose concentrations. At a fetal ethanol concentration of vessels to respond to the usual stimuli (7). We theorized that 33 + 8 mmol/L (150 f 37 mg/dL), there were no significant cerebral responses to acute maternal alcohol intoxication may changes in CBF, CMR02, or CMRglu. There was mild be similarly blunted or absent in immature fetal sheep, and we hypoglycemia (glucose concentration = 1.05 f 0.2 versus therefore compared the physiologic responses to acute alcohol Subjects. Before initiating these studies, all surgical and experMild hypoglycemia and lactic acidemia did develop. The imental procedures were approved by the Animal Care and Use reason for the developmental differences in response to Committee at the University of California, San Francisco. Seven alcohol and their relationship to fetal alcohol syndrome mixed-breed fetal sheep were obtained from time-dated pregnanremain to be elucidated. (Pediatr Res 31: 645-648, 1992) cies.Surgiculpreparation. One d before surgery, food was withheld Abbreviations from the ewe, although she was allowed free access to ...

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Alcohol-Induced Spasms of Cerebral Blood Vessels: Relation to Cerebrovascular Accidents and Sudden Death

Cited by 217 publications

References 25 publications

Suppression of Alcohol-Induced Hypertension by Dexamethasone

Suppression of Alcohol-Induced Hypertension by Dexamethasone

Roles of endothelin-1 and nitric oxide in the mechanism for ethanol-induced vasoconstriction in rat liver.

Cerebral Responses to Acute Maternal Alcohol Intoxication in Immature Fetal Sheep

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