Cerebral Hemorrhage and Alcohol Exposure: A Review

Jialing Peng; Hongxuan Wang; Xiaoming Rong; Lei He; L Xiangpen; Qingy Shen; Ying Peng

Disclosures

Alcohol Alcohol. 2020;55(1):20-27. 

In This Article

Chronic Alcohol Abuse and Hypertensive ICH

It is well established chronic alcohol abuse elevates blood pressure; the probable mechanisms are that alcohol increases the activity of sympathetic nervous system and renin-angiotensin-aldosterone system (Passaglia et al., 2015) and enhances the contractile response to vasoconstrictor agents (Tirapelli et al., 2008a), for example, noradrenaline (Ladipo et al., 2002), phenylephrine and endothelin-1. Meanwhile, the vascular sensitivity to vasodilator-like acetylcholine is impaired (Husain et al., 2008). Alcohol increases the generation of reactive oxygen species (ROS) and promotes the oxidative stress, which results in endothelial dysfunction (Husain, 2007; Yeligar et al., 2012), leads to alterations in Ca2+ levels in vascular smooth muscle cells (Marchi et al., 2014) and causes a reduction in NO generation or release and so on (Tirapelli et al., 2008b). Hypertension is the most important risk factor for ICH, and hypertensive ICH (HICH) is the most common type of ICH accounting for 75% primary ICH (Elliott and Smith, 2010). Heavy drinkers tend to have severe hypertension, and vasoconstriction caused by episodic binge alcohol intoxication might trigger HICH. Thus, chronic alcohol abuse could increase the incidence of HICH (Ding et al., 2015). In parallel, chronic alcohol abuse might exaggerate HICH-contributed brain injury. The possible mechanisms underlying the observed relationship between chronic alcohol abuse and HICH are as follows: fluctuating and uncontrolled blood pressure caused by alcohol abuse might promote the rupture of cerebral small vessels (Altura et al., 1983; Matti Hillbom et al., 2011; Ding et al., 2015); dysfunction of vascular endothelial cells causes incident cerebral microbleeds (Ding et al., 2015); the abnormalities of liver function and malabsorption of vitamin K as well as inhibition of platelet aggregation and increase of fibrolysis, which promote tendency of bleeding (Relja et al., 2015). Lin et al. 2019 demonstrated the relation between alcoholic cirrhosis and cerebral hemorrhage in the Taiwanese; degradation of basement membrane linked to remarkable activation of detrimental agents like MMPs, which causes breakdown of blood vessels and blood leak (Haorah et al., 2008); disruption of BBB integrity via alterations of BBB tight junction proteins occludin, zonula occludens-1 and claudin-5, and the malfunction of BBB contributes to occurrence of HICH, enlargement of ICH volume and exaggeration of cerebral edema (Abdul Muneer et al., 2011). Up-regulation of microglia activities and increase of inflammatory mediators in parallel with neuroinflammation might contribute to neuronal apoptosis and brain edema, leading to brain damage post-HICH (Aschner et al., 2001; Mayfield et al., 2013; Wilhelm and Guizzetti, 2016); the increase of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, generation of ROS and reactive nitrogen species might accelerate HICH-derived cerebral injury (Zheng and Peng, 2014). Although the association between chronic alcohol abuse and HICH is observed in studies, further experimental and clinical studies are still needed to clarify the mechanisms.

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