Mode of ethanol administration influences the severity of hemorrhage-induced lactic acidemia in conscious guinea pigs.

Mechanisms that limit metabolic acidemia during shock are limited by ethanol (EtOH). This may be due to (1) loss of respiratory compensation, (2) a greater fall in cardiac output, (3) altered removal of plasma lactate by the liver, and (4) alterations in central nervous system orchestration of compensatory responses. We have previously shown that loss of metabolic compensation during hemorrhage is correlated with plasma EtOH concentrations. The present study determines if the mode of ethanol administration influences compensation during hemorrhage. Male guinea pigs were administered EtOH (1 g/kg, 30% wt/vol) via intraperitoneal (IP) or intragastric (IG) routes. After 30 minutes, 60% of the estimated blood volume was removed. Animals remained in shock for 30 minutes were resuscitated with lactated Ringer solution and monitored for 3 hours. Plasma EtOH levels were similar in the 2 groups at the initiation of, and during, hemorrhage and resuscitation. Animals given EtOH IP exhibited more severe acidemia. The mode of EtOH administration may affect hepatic ethanol and lactate metabolism, thus exacerbating acidemia. An altered central nervous system response may impact compensatory responses during shock. Our results indicate that the "history" of the EtOH episode may be an important determinant in the compensation for hemorrhage and resuscitation.

Ethanol intoxication and lactated Ringer's resuscitation prolong hemorrhage-induced lactic acidosis.

Ethanol (EtOH) blunts the respiratory and metabolic compensation during hemorrhage, resulting in a more severe lactic acidemia. We hypothesized that lactated Ringer's (LR) resuscitation may exacerbate this lactic acidemia. Male guinea pigs were implanted with arterial and venous catheters. Two days after catheter placement, conscious animals were injected intraperitoneally with 1 g/kg EtOH, 0.3 g/kg EtOH, or an equal volume of water 30 min before hemorrhage (60% of estimated blood volume). After 30 min of hemorrhagic shock, animals were resuscitated with isotonic saline (S) or LR at 1 mL/min (three times shed blood volume). Mean arterial blood pressure (MABP) was not affected by pretreatment with either dose of EtOH, but was significantly decreased by hemorrhage in all groups. Both S and LR resuscitation slightly increased MABP, but neither restored it to prehemorrhage values. Blood lactate levels increased in all groups during hemorrhage and remained elevated for 3 h in animals pretreated with 1 g/kg EtOH. In the group pretreated with 0.3 g/kg EtOH, pH decreased during shock but returned to prehemorrhage levels during the resuscitation period. Resuscitation with S returned pH to prehemorrhage values in animals pretreated with 1.0 g/kg EtOH. Resuscitation with LR did not exacerbate, but did prolong, the lactic acidemia after shock in animals pretreated with 1.0 g/kg EtOH. Administration of additional lactate during intoxication and hypovolemia for hemodynamic stabilization before blood transfusion may exacerbate a metabolic stress.

Low-dose ethanol alters the cardiovascular, metabolic, and respiratory compensation for severe blood loss.

BACKGROUND: Compensation for hemorrhage and shock requires coordination of responses and sufficient physiologic reserve capacity of the cardiovascular, respiratory, renal, and neuroendocrine systems. Intake of ethanol (EtOH) is known to degrade physiologic response to stress. The purpose of this study was to investigate how acute EtOH exposure changes responses to severe blood loss, shock, and resuscitation. METHODS: Conscious male Duncan Hartley guinea pigs were given an intraperitoneal injection of either EtOH (1 g/kg) or an equal volume of water 30 minutes before controlled hemorrhage (60% blood volume), resuscitated after 30 minutes of hypovolemia with a lactated Ringer's solution volume equal to that of the shed blood volume, and observed for 24 hours. Hemodynamic (heart rate, arterial blood pressure), clinical laboratory (arterial blood gases, glucose, lactate, hematocrit), and metabolic gas exchange (oxygen consumption, carbon dioxide production) indicators of shock were monitored. RESULTS: Of the animals that survived 24 hours, changes in arterial pH and lactate were significantly greater in the experiment group than in the control group. Mortality at 24 hours was 77% in the experiment group (EtOH-treated) and 42% (p = 0.39) in the control group (water-treated). CONCLUSION: Acute EtOH exposure, with blood EtOH concentration similar to legal intoxication levels, limits physiologic reserve during hemorrhagic shock and resuscitation. In survivors of shock and resuscitation, compensation is compromised and physiologic reserve is adversely affected by acute EtOH intake.