Hemodynamic actions of acute ethanol after resuscitation from traumatic brain injury

Matthew J. Fabian, Kenneth G Proctor

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Background: The purposes of this study were to determine how clinically relevant levels of acute ethanol (EtOH) influence cerebral perfusion pressure (CPP), cerebral venous O2 saturation (Scvo2), and systemic hemodynamics after fluid resuscitation from traumatic brain injury (TBI); and to test the hypothesis that the actions of EtOH on these variables are mediated by adenosine. Methods: Anesthetized swine were ventilated (F102 = 0.4) and instrumented. In protocol 1, EtOH (3.5 g/kg, n = 11) or its vehicle (n = 17) was administered orally before TBI + 40% hemorrhage. At 90 minutes post-TBI, resuscitation consisted of shed blood + saline. In protocol 2, either saline (n = 15) or an adenosine-regulating agent (5-amino-4-imidazolecarboxamide riboside) in saline (1 mg/kg bolus + 12 mg/kg/h intravenously [i.v.]) (n = 5), was administered i.v. before TBI + 45% hemorrhage. At 90 minutes post-TBI, resuscitation consisted of saline only (three times shed blood volume). In protocol 3, EtOH was administered i.v. (1 g/kg; 20% vol/vol in saline) followed by either an adenosine receptor antagonist (theophylline, 10 mg/kg) or an adenosine uptake inhibitor (dipyridamole, 0.25 mg/kg). Results: In protocol 1, with no EtOH, 11 of 17 (65%) survived post-TBI hypotension. Mean arterial blood pressure, cardiac index, and mixed venous oxygen saturation were stable for 1 hour at 40% to 60% below their respective baselines, whereas lactate increased three- to four-fold (all p < 0.05). After fluid resuscitation, most variables rapidly corrected, but intracranial pressure was increased 10 to 15 mm Hg (p < 0.05). With EtOH, 9 of 11 (82%) survived post-TBI hypotension (p = 0.42 vs. no EtOH). After resuscitation from TBI, there were significant effects of EtOH on systemic hemodynamics (mean arterial pressure, cardiac index, mixed venous oxygen saturation), on CPP, on lactate, and on Scvo2 at normo- and hypercapnia (all p < 0.05). The data from protocol 2 showed that essentially none of these changes were duplicated with an adenosine-regulating agent. In protocol 3, i.v EtOH produced small but significant changes in Scvo2, intracranial pressure, and lactate, at normo-, hyper-, and hypocapnia. Dipyridamole and theophylline tended to have opposite, albeit small and not statistically significant, effects on these variables relative to EtOH alone. Conclusion: Acute EtOH (200-300 mg/dL) did not increase mortality after TBI + secondary hypotension, as long as cardiopulmonary support was provided. With EtOH, CPP was maintained and cerebral blood flow appeared to be adequate, if not excessive, with respect to cerebral metabolic demand, as judged by changes in Scvo2 at normo-, hyper-, and hypocapnia. These changes were probably not mediated, but might have been modulated, by increases in endogenous adenosine.

Original languageEnglish
Pages (from-to)864-875
Number of pages12
JournalJournal of Trauma - Injury, Infection and Critical Care
Volume53
Issue number5
StatePublished - Nov 1 2002

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Resuscitation
Ethanol
Hemodynamics
Cerebrovascular Circulation
Adenosine
Hypercapnia
Hypotension
Hypocapnia
Lactic Acid
Arterial Pressure
Dipyridamole
Intracranial Pressure
Theophylline
Hemorrhage
Oxygen
Purinergic P1 Receptor Antagonists
Traumatic Brain Injury
Blood Volume
Swine
Mortality

Keywords

  • Adenosine
  • Dipyridamole
  • Intracranial pressure
  • Jugular bulb oximetry
  • Swine
  • Theophylline

ASJC Scopus subject areas

  • Surgery

Cite this

Hemodynamic actions of acute ethanol after resuscitation from traumatic brain injury. / Fabian, Matthew J.; Proctor, Kenneth G.

In: Journal of Trauma - Injury, Infection and Critical Care, Vol. 53, No. 5, 01.11.2002, p. 864-875.

Research output: Contribution to journalArticle

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title = "Hemodynamic actions of acute ethanol after resuscitation from traumatic brain injury",
abstract = "Background: The purposes of this study were to determine how clinically relevant levels of acute ethanol (EtOH) influence cerebral perfusion pressure (CPP), cerebral venous O2 saturation (Scvo2), and systemic hemodynamics after fluid resuscitation from traumatic brain injury (TBI); and to test the hypothesis that the actions of EtOH on these variables are mediated by adenosine. Methods: Anesthetized swine were ventilated (F102 = 0.4) and instrumented. In protocol 1, EtOH (3.5 g/kg, n = 11) or its vehicle (n = 17) was administered orally before TBI + 40{\%} hemorrhage. At 90 minutes post-TBI, resuscitation consisted of shed blood + saline. In protocol 2, either saline (n = 15) or an adenosine-regulating agent (5-amino-4-imidazolecarboxamide riboside) in saline (1 mg/kg bolus + 12 mg/kg/h intravenously [i.v.]) (n = 5), was administered i.v. before TBI + 45{\%} hemorrhage. At 90 minutes post-TBI, resuscitation consisted of saline only (three times shed blood volume). In protocol 3, EtOH was administered i.v. (1 g/kg; 20{\%} vol/vol in saline) followed by either an adenosine receptor antagonist (theophylline, 10 mg/kg) or an adenosine uptake inhibitor (dipyridamole, 0.25 mg/kg). Results: In protocol 1, with no EtOH, 11 of 17 (65{\%}) survived post-TBI hypotension. Mean arterial blood pressure, cardiac index, and mixed venous oxygen saturation were stable for 1 hour at 40{\%} to 60{\%} below their respective baselines, whereas lactate increased three- to four-fold (all p < 0.05). After fluid resuscitation, most variables rapidly corrected, but intracranial pressure was increased 10 to 15 mm Hg (p < 0.05). With EtOH, 9 of 11 (82{\%}) survived post-TBI hypotension (p = 0.42 vs. no EtOH). After resuscitation from TBI, there were significant effects of EtOH on systemic hemodynamics (mean arterial pressure, cardiac index, mixed venous oxygen saturation), on CPP, on lactate, and on Scvo2 at normo- and hypercapnia (all p < 0.05). The data from protocol 2 showed that essentially none of these changes were duplicated with an adenosine-regulating agent. In protocol 3, i.v EtOH produced small but significant changes in Scvo2, intracranial pressure, and lactate, at normo-, hyper-, and hypocapnia. Dipyridamole and theophylline tended to have opposite, albeit small and not statistically significant, effects on these variables relative to EtOH alone. Conclusion: Acute EtOH (200-300 mg/dL) did not increase mortality after TBI + secondary hypotension, as long as cardiopulmonary support was provided. With EtOH, CPP was maintained and cerebral blood flow appeared to be adequate, if not excessive, with respect to cerebral metabolic demand, as judged by changes in Scvo2 at normo-, hyper-, and hypocapnia. These changes were probably not mediated, but might have been modulated, by increases in endogenous adenosine.",
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T1 - Hemodynamic actions of acute ethanol after resuscitation from traumatic brain injury

AU - Fabian, Matthew J.

AU - Proctor, Kenneth G

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N2 - Background: The purposes of this study were to determine how clinically relevant levels of acute ethanol (EtOH) influence cerebral perfusion pressure (CPP), cerebral venous O2 saturation (Scvo2), and systemic hemodynamics after fluid resuscitation from traumatic brain injury (TBI); and to test the hypothesis that the actions of EtOH on these variables are mediated by adenosine. Methods: Anesthetized swine were ventilated (F102 = 0.4) and instrumented. In protocol 1, EtOH (3.5 g/kg, n = 11) or its vehicle (n = 17) was administered orally before TBI + 40% hemorrhage. At 90 minutes post-TBI, resuscitation consisted of shed blood + saline. In protocol 2, either saline (n = 15) or an adenosine-regulating agent (5-amino-4-imidazolecarboxamide riboside) in saline (1 mg/kg bolus + 12 mg/kg/h intravenously [i.v.]) (n = 5), was administered i.v. before TBI + 45% hemorrhage. At 90 minutes post-TBI, resuscitation consisted of saline only (three times shed blood volume). In protocol 3, EtOH was administered i.v. (1 g/kg; 20% vol/vol in saline) followed by either an adenosine receptor antagonist (theophylline, 10 mg/kg) or an adenosine uptake inhibitor (dipyridamole, 0.25 mg/kg). Results: In protocol 1, with no EtOH, 11 of 17 (65%) survived post-TBI hypotension. Mean arterial blood pressure, cardiac index, and mixed venous oxygen saturation were stable for 1 hour at 40% to 60% below their respective baselines, whereas lactate increased three- to four-fold (all p < 0.05). After fluid resuscitation, most variables rapidly corrected, but intracranial pressure was increased 10 to 15 mm Hg (p < 0.05). With EtOH, 9 of 11 (82%) survived post-TBI hypotension (p = 0.42 vs. no EtOH). After resuscitation from TBI, there were significant effects of EtOH on systemic hemodynamics (mean arterial pressure, cardiac index, mixed venous oxygen saturation), on CPP, on lactate, and on Scvo2 at normo- and hypercapnia (all p < 0.05). The data from protocol 2 showed that essentially none of these changes were duplicated with an adenosine-regulating agent. In protocol 3, i.v EtOH produced small but significant changes in Scvo2, intracranial pressure, and lactate, at normo-, hyper-, and hypocapnia. Dipyridamole and theophylline tended to have opposite, albeit small and not statistically significant, effects on these variables relative to EtOH alone. Conclusion: Acute EtOH (200-300 mg/dL) did not increase mortality after TBI + secondary hypotension, as long as cardiopulmonary support was provided. With EtOH, CPP was maintained and cerebral blood flow appeared to be adequate, if not excessive, with respect to cerebral metabolic demand, as judged by changes in Scvo2 at normo-, hyper-, and hypocapnia. These changes were probably not mediated, but might have been modulated, by increases in endogenous adenosine.

AB - Background: The purposes of this study were to determine how clinically relevant levels of acute ethanol (EtOH) influence cerebral perfusion pressure (CPP), cerebral venous O2 saturation (Scvo2), and systemic hemodynamics after fluid resuscitation from traumatic brain injury (TBI); and to test the hypothesis that the actions of EtOH on these variables are mediated by adenosine. Methods: Anesthetized swine were ventilated (F102 = 0.4) and instrumented. In protocol 1, EtOH (3.5 g/kg, n = 11) or its vehicle (n = 17) was administered orally before TBI + 40% hemorrhage. At 90 minutes post-TBI, resuscitation consisted of shed blood + saline. In protocol 2, either saline (n = 15) or an adenosine-regulating agent (5-amino-4-imidazolecarboxamide riboside) in saline (1 mg/kg bolus + 12 mg/kg/h intravenously [i.v.]) (n = 5), was administered i.v. before TBI + 45% hemorrhage. At 90 minutes post-TBI, resuscitation consisted of saline only (three times shed blood volume). In protocol 3, EtOH was administered i.v. (1 g/kg; 20% vol/vol in saline) followed by either an adenosine receptor antagonist (theophylline, 10 mg/kg) or an adenosine uptake inhibitor (dipyridamole, 0.25 mg/kg). Results: In protocol 1, with no EtOH, 11 of 17 (65%) survived post-TBI hypotension. Mean arterial blood pressure, cardiac index, and mixed venous oxygen saturation were stable for 1 hour at 40% to 60% below their respective baselines, whereas lactate increased three- to four-fold (all p < 0.05). After fluid resuscitation, most variables rapidly corrected, but intracranial pressure was increased 10 to 15 mm Hg (p < 0.05). With EtOH, 9 of 11 (82%) survived post-TBI hypotension (p = 0.42 vs. no EtOH). After resuscitation from TBI, there were significant effects of EtOH on systemic hemodynamics (mean arterial pressure, cardiac index, mixed venous oxygen saturation), on CPP, on lactate, and on Scvo2 at normo- and hypercapnia (all p < 0.05). The data from protocol 2 showed that essentially none of these changes were duplicated with an adenosine-regulating agent. In protocol 3, i.v EtOH produced small but significant changes in Scvo2, intracranial pressure, and lactate, at normo-, hyper-, and hypocapnia. Dipyridamole and theophylline tended to have opposite, albeit small and not statistically significant, effects on these variables relative to EtOH alone. Conclusion: Acute EtOH (200-300 mg/dL) did not increase mortality after TBI + secondary hypotension, as long as cardiopulmonary support was provided. With EtOH, CPP was maintained and cerebral blood flow appeared to be adequate, if not excessive, with respect to cerebral metabolic demand, as judged by changes in Scvo2 at normo-, hyper-, and hypocapnia. These changes were probably not mediated, but might have been modulated, by increases in endogenous adenosine.

KW - Adenosine

KW - Dipyridamole

KW - Intracranial pressure

KW - Jugular bulb oximetry

KW - Swine

KW - Theophylline

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