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Acute Alcohol Binge Deteriorates Metabolic and Respiratory Compensation Capability After Blunt Chest Trauma Followed by Hemorrhagic Shock—A New Research Model
Author(s) -
Wagner Nils,
Franz Niklas,
Dieteren Scott,
Perl Mario,
Mörs Katharina,
Marzi Ingo,
Relja Borna
Publication year - 2017
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/acer.13446
Subject(s) - medicine , resuscitation , base excess , pco2 , shock (circulatory) , anesthesia , saline , blood pressure , traumatic shock , alcohol , biochemistry , chemistry
Background The clinical relevance of blunt (thoracic) chest trauma (TxT) and hemorrhagic shock is indisputable due to the high prevalence of this injury type, as well as its close association with mortality and/or preventable deaths. Furthermore, there is an ongoing discussion about the influence of alcohol in trauma patients. Thus, we established a model of TxT followed by hemorrhagic shock with resuscitation (H/R) in alcohol‐intoxicated rats. Methods Depending on group allocation, 12 (subacute) or 2 (acute) hours before experimentation, the animals received a single oral dose of alcohol (ethanol [Et OH ]) or saline (NaCl) followed by TxT, hemorrhagic shock (35 ± 3 mm Hg), and resuscitation (TxT + H/R). Arterial blood gas analyses and continuous monitoring of blood pressure were performed during the experimentation period. Survival during the experimentation procedure was determined. Results Subacute and acute Et OH group exhibited lower baseline mean arterial blood pressure values compared with the corresponding NaCl group, respectively. Both Et OH groups showed lower maximal bleed‐out volume, which was necessary to induce hemorrhagic shock compared to NaCl groups, and the recovery during the resuscitation period was attenuated. During the experimentation in all groups, a trend to acidic pH was observed. Acute Et OH group showed lowest pH values compared to all other groups. Higher pCO 2 values were observed in both Et OH groups. All groups developed negative base excess and decreasing HCO 3 − values until the end of hemorrhagic shock and showed increasing base excess and HCO 3 − values during resuscitation. Significantly higher mortality rate was found in the acute Et OH group. Conclusions This study indicates that alcohol limits the metabolic and respiratory compensation capability, thereby promoting mortality.