Cerebral blood flow and cerebrovascular response to acetazolamide in patients with chronic alcoholism

Oishi, Minoru; Mochizuki, Yoko; Takasu, Toshiaki

doi:10.1136/jnnp.63.1.100

Cited by 10 publications

(5 citation statements)

References 14 publications

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“…This is consistent with current theory that the depressive disorder is a functional disease and the patients have no cerebrovascular disease [1]. Osihi performed brain SPECT and intravenous acetazolamide brain SPECT tests on patients with chronic alcoholism [15]. It was found that the cerebral blood flow perfusion decreased for base state SPECT while it increased obviously after intravenous injection of acetazolamide, which showed that the decrease of cerebral blood flow perfusion of the patients with chronic alcoholism was not due to the pathological changes of the vessel itself but due to the decrease of brain metabolism.…”

Section: Discussionsupporting

confidence: 88%

Acetazolamide Stress SPECT Test on Cerebral Blood Flow in Patients with Depressive Disorder

Xu¹,

Gong²,

Xu³

2016

AAP

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The regional cerebral blood flow (rCBF) and the cerebral vasoreactivity of the patients with depressive disorder were observed by SPECT and acetazolamide stress SPECT test respectively. Eighteen unmedicated depressed patients and nineteen healthy control subjects were included. Baseline SPECT was performed in both patients and control subjects. Acetazolamide stress SPECT test was performed two days later in patients two hours after taking 2g acetazolamide orally. It was found that there was significant difference between the untreated depressed patients and the controls, because there was relatively reduced perfusion in frontal lobe, temporal lobe, left parietal lobe and right basal ganglia in depressed patients. After acetazolamide stress SPECT test, the perfusion of decreased regions in baseline step was increased. No potential ischemic lesion was found. The perfusion of some specific regions of the depressed patients decreased. Acetazolamide stress SPECT test could not reveal silent brain ischemia in the depressed patients. The perfusion of decreased regions in the baseline imaging was increased in acetazolamide stress SPECT test.

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Section: Discussionsupporting

confidence: 88%

Acetazolamide Stress SPECT Test on Cerebral Blood Flow in Patients with Depressive Disorder

Xu¹,

Gong²,

Xu³

2016

AAP

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“…They demonstrated that blood flows in the cerebral cortex, thalamus, and putamen were significantly lower in the chronic alcoholic group than in the healthy control group. The increase in blood flow in response to Acz was not significantly different between the two groups (Oishi et al, 1997). However, they did not demonstrate blood flows in the cerebellum and brain stem in the subtentorial region.…”

Section: Discussionmentioning

confidence: 90%

“…Oishi et al (1997) performed a xenon CT study in 12 chronic alcoholics and 12 age-matched healthy controls. They demonstrated that blood flows in the cerebral cortex, thalamus, and putamen were significantly lower in the chronic alcoholic group than in the healthy control group.…”

Section: Discussionmentioning

confidence: 99%

Regional Cerebral Blood Flow Measured by the Resting and Vascular Reserve (RVR) Method in Chronic Alcoholics

Suzuki

Oishi

Mizutani

et al. 2002

Alcoholism Clin & Exp Res

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It has been reported that cerebral blood flow is decreased in chronic alcoholics without neurological diseases. We performed SPECT by the resting and vascular reserve (RVR) method in 11 chronic alcoholics (mean age 59.1 Ϯ 10.4, all males) and 11 age-matched healthy controls (mean age 58.8 Ϯ 10.1, all males). The resting and vascular reserve (RVR) method is a consecutive 99m Tc-ECD SPECT study before and after acetazolamide administration with adjunctive radionuclide angiography, which is easy to perform for a routine clinical study and quite useful for evaluating regional cerebral blood flow and the cerebrovascular response to acetazolamide. Regional cerebral blood flows in almost all regions in the alcoholic group were lower than those in the control group. However, there were no significant differences in increased rates of blood flow in response to acetazolamide in almost all regions between the chronic alcoholic group and the control group. In both groups, the increased rates of blood flow in response to acetazolamide in the supratentorial region, cerebellum, and brain stem were 30 -40%, 20 -25%, and 42-48%, respectively. The cerebrovascular response to acetazolamide in chronic alcoholics was not impaired, therefore the reduction of brain metabolism may be one of the important factors causing the decreased cerebral blood flow in chronic alcoholics.

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“…The vast majority of studies that addressed the alcohol-cerebral vessel interaction have focused on chronic EtOH exposure (10,(44)(45)(46). However, binge drinking, in which cerebral vessels are acutely exposed to moderate-heavy [EtOH], is the dominant style of drinking in Western societies (47) and most closely associated with deaths from ischemic stroke (3,42,43).…”

Section: Discussionmentioning

confidence: 99%

Essential role for smooth muscle BK channels in alcohol-induced cerebrovascular constriction

Liu

Xi²,

Ahmed³

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

171

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Binge drinking is associated with increased risk for cerebrovascular spasm and stroke. Acute exposure to ethanol at concentrations obtained during binge drinking constricts cerebral arteries in several species, including humans, but the mechanisms underlying this action are largely unknown. In a rodent model, we used fluorescence microscopy, patch-clamp electrophysiology, and pharmacological studies in intact cerebral arteries to pinpoint the molecular effectors of ethanol cerebrovascular constriction. Clinically relevant concentrations of ethanol elevated wall intracellular Ca 2؉ concentration and caused a reversible constriction of cerebral arteries (EC50 ‫؍‬ 27 mM; Emax ‫؍‬ 100 mM) that depended on voltage-gated Ca 2؉ entry into myocytes. However, ethanol did not directly increase voltage-dependent Ca 2؉ currents in isolated myocytes. Constriction occurred because of an ethanol reduction in the frequency (؊53%) and amplitude (؊32%) of transient Ca 2؉ -activated K ؉ (BK) currents. Ethanol inhibition of BK transients was caused by a reduction in Ca 2؉ spark frequency (؊49%), a subsarcolemmal Ca 2؉ signal that evokes the BK transients, and a direct inhibition of BK channel steady-state activity (؊44%). In contrast, ethanol failed to modify Ca 2؉ waves, a major vasoconstrictor mechanism. Selective block of BK channels largely prevented ethanol constriction in pressurized arteries. This study pinpoints the Ca 2؉ spark͞BK channel negative-feedback mechanism as the primary effector of ethanol vasoconstriction.M oderate-heavy episodic alcohol intake, such as in binge drinking, remains a major public health problem (1, 2). Moderate-heavy drinking is associated, independently of any other factor, with an increased risk for stroke and deaths from ischemic stroke (3, 4). Binge drinkers are significantly predisposed to brain hemorrhage, cerebrovascular spasm, and stroke (3, 5).Cerebrovascular disease associated with moderate-heavy alcohol intake is independent of beverage type and alcohol metabolism but linked to ethanol (EtOH) itself (6, 7). Strong evidence for a dose-response relationship between EtOH intake and risk for stroke suggests causality (8). EtOH cerebral artery constriction is considered responsible for cerebral vasospasm, ischemia, and stroke in moderate-heavy drinkers (6, 9). Acute EtOH at legally intoxicating (Ն20 mM) blood levels in naive subjects constricts cerebral arteries in several species, including humans (7, 9).Rats are excellent models to study EtOH cerebral artery constriction and stroke (7,10,11). Evidence from this and other species indicates that EtOH constricts cerebral arteries by acting primarily on the smooth muscle (7,11,12). However, the molecular mechanisms mediating EtOH cerebral artery constriction remain largely unidentified.In cerebrovascular smooth muscle, an elevation in global intracellular Ca 2ϩ ([Ca 2ϩ ] ic ) leads to contraction (13). Ca 2ϩ mobilization in response to EtOH may result from direct potentiation of mechanisms leading to Ca 2ϩ influx͞release from internal organel...

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Cerebral blood flow and cerebrovascular response to acetazolamide in patients with chronic alcoholism

Cited by 10 publications

References 14 publications

Acetazolamide Stress SPECT Test on Cerebral Blood Flow in Patients with Depressive Disorder

Acetazolamide Stress SPECT Test on Cerebral Blood Flow in Patients with Depressive Disorder

Regional Cerebral Blood Flow Measured by the Resting and Vascular Reserve (RVR) Method in Chronic Alcoholics

Essential role for smooth muscle BK channels in alcohol-induced cerebrovascular constriction

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