Alcohol and drug abuse in trauma

Hadfield, R.J.; Mercer, Mary Catherine; Parr, Michael

doi:10.1016/s0300-9572(00)00315-4

Cited by 25 publications

(17 citation statements)

References 84 publications

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“…Almost 50% of trauma victims have positive blood alcohol concentrations (BACs), among them 35% with a BAC greater than 1 mg·mL -1 (Reyna et al, 1985;Rivara et al, 1993;Madan et al, 1999;Hadfield et al, 2001). Alcohol-intoxicated BJP British Journal of Pharmacology DOI:10.1111DOI:10.…”

Section: Introductionmentioning

confidence: 99%

Acute alcohol intoxication reduces mortality, inflammatory responses and hepatic injury after haemorrhage and resuscitationin vivo

Relja

Höhn

Bormann

et al. 2012

British J Pharmacology

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BACKGROUND AND PURPOSEHaemorrhagic shock and resuscitation (H/R) induces hepatic injury, strong inflammatory changes and death. Alcohol intoxication is assumed to worsen pathophysiological derangements after H/R. Here, we studied the effects of acute alcohol intoxication on survival, liver injury and inflammation after H/R, in rats. EXPERIMENTAL APPROACHRats were given a single oral dose of ethanol (5 g·kg -1 , 30%) or saline (control), 12 h before they were haemorrhaged for 60 min and resuscitated (H/R). Sham groups received the same procedures without H/R. Measurements were made 2, 24 and 72 h after resuscitation. Survival was assessed 72 h after H/R. KEY RESULTSEthanol increased survival after H/R three-fold and also induced fatty changes in the liver. H/R-induced liver injury was amplified by ethanol at 2 h but inhibited 24 h after H/R. Elevated serum IL-6 levels as well as hepatic IL-6 and TNF-a gene expression 2 h after H/R were reduced by ethanol. Ethanol enhanced serum IL-1b at 2 h, but did not affect increased hepatic IL-1b expression at 72 h after H/R. Local inflammatory markers, hepatic infiltration with polymorphonuclear leukocytes and intercellular adhesion molecule 1 expression decreased after ethanol compared with saline, following H/R. Ethanol reduced H/R-induced IkBa activation 2 h after H/R, and NF-kB-dependent gene expression of MMP9. CONCLUSIONS AND IMPLICATIONSEthanol reduced H/R-induced mortality at 72 h, accompanied by a suppression of proinflammatory changes after H/R in ethanol-treated animals. Binge-like ethanol exposure modulated the inflammatory response after H/R, an effect that was associated with NF-kB activity. AbbreviationsALT, alanine aminotransferase; BAC, blood alcohol concentrations; H/R:, haemorrhagic shock and resuscitation; ICAM-1, intercellular adhesion molecule 1; MODS, multiple organ dysfunction syndrome; MOF, multiple organ failure; PMNL, polymorphonuclear leukocytes IntroductionAlcohol consumption is associated with one-third of all traumatic injury deaths each year (Li et al., 1997;Rehm et al., 2003). Almost 50% of trauma victims have positive blood alcohol concentrations (BACs), among them 35% with a BAC greater than 1 mg·mL -1 (Reyna et al., 1985;Rivara et al., 1993;Madan et al., 1999;Hadfield et al., 2001). Alcohol-intoxicated BJP British Journal of Pharmacology DOI:10.1111DOI:10. /j.1476DOI:10. -5381.2011 1188 British Journal of Pharmacology (2012) 165 1188-1199The Authors British Journal of Pharmacology © 2011 The British Pharmacological Society trauma victims have an increased risk for subsequent complications such as pneumonia, sepsis or multiple organ failure (MOF); some studies report a greater morbidity and mortality in these patients (Faunce et al., 1997;Bagby et al., 1998;Ruiz et al., 1999;Boe et al., 2001;Messingham et al., 2002;Zhang et al., 2002). Other studies report divergent results showing that acute alcohol intoxication does not affect the outcome and is even associated with decreased 24 h mortality after trauma (own unpublished data). The source ...

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Section: Introductionmentioning

confidence: 99%

Acute alcohol intoxication reduces mortality, inflammatory responses and hepatic injury after haemorrhage and resuscitationin vivo

Relja

Höhn

Bormann

et al. 2012

British J Pharmacology

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“…[12][13][14] Given the role of collecting lymphatics in the transport of gut-derived bacterial products, cytokines, and inflammatory mediators, it is possible that disrupted pumping of mesenteric collecting lymphatics in intoxicated trauma victims may contribute to the greater prevalence of morbidity and mortality from traumatic injury in the alcohol-abusing population. 15 Contractility of lymphatic smooth muscle can be modulated by extrinsic (neural and humoral) and intrinsic (myogenic) factors. Calcium transport across the sarcolemma via L-type channel contributes significantly to the contractile activity of collecting lymphatics.…”

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confidence: 99%

Mechanisms of Acute Alcohol Intoxication-Induced Modulation of Cyclic Mobilization of [Ca²⁺] in Rat Mesenteric Lymphatic Vessels

Souza‐Smith

Kerut

Breslin

et al. 2015

Lymphatic Research and Biology

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“…Nearly half of all injured patients that enter emergency departments across the United States test positive for blood alcohol (6,24,38), with blood alcohol levels frequently Ͼ80 mg/dl, the legal limit in most states (14,24,37,38). Alcohol-intoxicated trauma patients enter the emergency department more hypotensive than their sober counterparts (41).…”

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confidence: 99%

Central acetylcholinesterase inhibition improves hemodynamic counterregulation to severe blood loss in alcohol-intoxicated rats

Mathis¹,

Molina²

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Acute alcohol intoxication results in impaired hemodynamic counterregulation to blood loss and is associated with an attenuated hemorrhage-induced release of catecholamines and AVP. We speculated that restoration of the neuroendocrine response to hemorrhage would improve mean arterial blood pressure (MABP) recovery during acute alcohol intoxication. Previously, we demonstrated that intracerebroventricular (i.c.v.) choline, a precursor of acetylcholine, transiently increases sympathetic nervous system (SNS) outflow but is not capable of improving neuroendocrine and hemodynamic compensation to hemorrhage in alcohol-treated rats. We hypothesized that prolongation of the observed effect via i.c.v. neostigmine, an acetylcholinesterase inhibitor, would enhance SNS outflow, restore the neuroendocrine response, and in turn improve hemodynamic responses to hemorrhage during acute alcohol intoxication. I.c.v. neostigmine (1 microg) increased MABP, catecholamines, and AVP within 5 min and reversed hypotension due to 40% hemorrhage and intragastric alcohol (30% wt/vol, 2.5 g/kg) administration in chronically catheterized male Sprague-Dawley rats (225-250 g body wt). Acute alcohol intoxication before 50% hemorrhage decreased basal MABP, accentuated hypotension midhemorrhage, suppressed the hemorrhage-induced release of norepinephrine and AVP, and prevented restoration of MABP to basal levels after fluid resuscitation with lactated Ringer solution. I.c.v. neostigmine (0.5 microg) produced a sustained increase in MABP beginning at 30 min of hemorrhage that persisted throughout fluid resuscitation in control and alcohol-treated animals. I.c.v. neostigmine enhanced epinephrine responses and restored the hemorrhage-induced release of norepinephrine and AVP in alcohol-treated rats. These results demonstrate that inhibition of acetylcholinesterase in the central nervous system enhances SNS outflow, restores the neuroendocrine response to severe blood loss, and thereby improves hemodynamic counterregulation during acute alcohol intoxication. This study provides evidence for a central (and not peripheral) role of alcohol in impairing hemodynamic stability during hemorrhagic shock.

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Alcohol and drug abuse in trauma

Cited by 25 publications

References 84 publications

Acute alcohol intoxication reduces mortality, inflammatory responses and hepatic injury after haemorrhage and resuscitationin vivo

Acute alcohol intoxication reduces mortality, inflammatory responses and hepatic injury after haemorrhage and resuscitationin vivo

Mechanisms of Acute Alcohol Intoxication-Induced Modulation of Cyclic Mobilization of [Ca²⁺] in Rat Mesenteric Lymphatic Vessels

Central acetylcholinesterase inhibition improves hemodynamic counterregulation to severe blood loss in alcohol-intoxicated rats

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Alcohol and drug abuse in trauma

Cited by 25 publications

References 84 publications

Acute alcohol intoxication reduces mortality, inflammatory responses and hepatic injury after haemorrhage and resuscitationin vivo

Acute alcohol intoxication reduces mortality, inflammatory responses and hepatic injury after haemorrhage and resuscitationin vivo

Mechanisms of Acute Alcohol Intoxication-Induced Modulation of Cyclic Mobilization of [Ca2+] in Rat Mesenteric Lymphatic Vessels

Central acetylcholinesterase inhibition improves hemodynamic counterregulation to severe blood loss in alcohol-intoxicated rats

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Mechanisms of Acute Alcohol Intoxication-Induced Modulation of Cyclic Mobilization of [Ca²⁺] in Rat Mesenteric Lymphatic Vessels