Resuscitation from traumatic brain injury (TBI) and secondary hypotension with a hemoglobin-based oxygen carrying solution (HBOC)

Jeffrey B. Gibson, Robert A. Maxwell, John B. Schweitzer, Timothy C. Fabian, Kenneth G Proctor

Research output: Contribution to journalArticle

Abstract

Introduction: We have observed that early transfusion with shed blood vs saline improved cerebral perfusion pressure (CPP) and cerebral venous outflow saturation (CvO2) when hypotension was superimposed on TBI. In patients, it may be difficult to transfuse within the "golden hour", which has led to searches for blood substitutes. HBOCs have shown promise in many different models, and are now in phase III clinical trials. However, the potential benefits may be outweighed by vasoconstriction due to NO scavenging. Methods: Anesthetized, ventilated swine (37±1kg) received a fluid-percussion injury and 30% hemorrhage. After 1 hr, resuscitation consisted of 500ml of Baxter's first generation HBOC (DCLHb, n=6) or saline (SAL, n=5), followed by supplemental fluid. To test cerebral vasoreactivity, FiCO 2 = 0.05 and hyperventilation were administered for 10 minutes pre- and post-resuscitation. At 72 hrs, the brains were removed for histopathology. Results: CPP (table) and arterial lactate were significantly higher following DCLHb vs. SAL resuscitation (lactate: 3.3±0.5 vs 1.2±0.2, p<0.05). CvO2changes to the CO2 challenge were similar (table). Histologic findings included subarachnoid hemorrhage, diffuse axonal injury, and infarcts. DCLHb did not aggravate these changes. Conclusions: 1) Initial resuscitation with DCLHb improved CPP but increased systemic lactate, both manifestations of systemic vasoconstriction; 2) Since there was no harmful physiologic or histologic cerebral sequela related to vasoconstriction with this first generation HBOC, second generation compounds with less NO scavenging properties may have therapeutic potential for resuscitation of TBI. CPP @ 30 min Hi CO2 - Δ CvO2 sat Lo CO2 - Δ CvO2 pre TBI post TBI pre TBI DCLHb 78±5 -4±4 -11±4 21±3 Saline 56±3 -4±2 -10±3 22±2.

Original languageEnglish
JournalCritical Care Medicine
Volume27
Issue number12 SUPPL.
StatePublished - Dec 1 1999
Externally publishedYes

Fingerprint

Cerebrovascular Circulation
Resuscitation
Hypotension
Hemoglobins
Oxygen
Vasoconstriction
Lactic Acid
Diffuse Axonal Injury
Percussion
Blood Substitutes
Phase III Clinical Trials
Hyperventilation
Subarachnoid Hemorrhage
Traumatic Brain Injury
Swine
diaspirin-cross-linked hemoglobin
Hemorrhage
Wounds and Injuries
Brain

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Resuscitation from traumatic brain injury (TBI) and secondary hypotension with a hemoglobin-based oxygen carrying solution (HBOC). / Gibson, Jeffrey B.; Maxwell, Robert A.; Schweitzer, John B.; Fabian, Timothy C.; Proctor, Kenneth G.

In: Critical Care Medicine, Vol. 27, No. 12 SUPPL., 01.12.1999.

Research output: Contribution to journalArticle

Gibson, Jeffrey B. ; Maxwell, Robert A. ; Schweitzer, John B. ; Fabian, Timothy C. ; Proctor, Kenneth G. / Resuscitation from traumatic brain injury (TBI) and secondary hypotension with a hemoglobin-based oxygen carrying solution (HBOC). In: Critical Care Medicine. 1999 ; Vol. 27, No. 12 SUPPL.
@article{861e1748ce524c568042387f287f672e,
title = "Resuscitation from traumatic brain injury (TBI) and secondary hypotension with a hemoglobin-based oxygen carrying solution (HBOC)",
abstract = "Introduction: We have observed that early transfusion with shed blood vs saline improved cerebral perfusion pressure (CPP) and cerebral venous outflow saturation (CvO2) when hypotension was superimposed on TBI. In patients, it may be difficult to transfuse within the {"}golden hour{"}, which has led to searches for blood substitutes. HBOCs have shown promise in many different models, and are now in phase III clinical trials. However, the potential benefits may be outweighed by vasoconstriction due to NO scavenging. Methods: Anesthetized, ventilated swine (37±1kg) received a fluid-percussion injury and 30{\%} hemorrhage. After 1 hr, resuscitation consisted of 500ml of Baxter's first generation HBOC (DCLHb, n=6) or saline (SAL, n=5), followed by supplemental fluid. To test cerebral vasoreactivity, FiCO 2 = 0.05 and hyperventilation were administered for 10 minutes pre- and post-resuscitation. At 72 hrs, the brains were removed for histopathology. Results: CPP (table) and arterial lactate were significantly higher following DCLHb vs. SAL resuscitation (lactate: 3.3±0.5 vs 1.2±0.2, p<0.05). CvO2changes to the CO2 challenge were similar (table). Histologic findings included subarachnoid hemorrhage, diffuse axonal injury, and infarcts. DCLHb did not aggravate these changes. Conclusions: 1) Initial resuscitation with DCLHb improved CPP but increased systemic lactate, both manifestations of systemic vasoconstriction; 2) Since there was no harmful physiologic or histologic cerebral sequela related to vasoconstriction with this first generation HBOC, second generation compounds with less NO scavenging properties may have therapeutic potential for resuscitation of TBI. CPP @ 30 min Hi CO2 - Δ CvO2 sat Lo CO2 - Δ CvO2 pre TBI post TBI pre TBI DCLHb 78±5 -4±4 -11±4 21±3 Saline 56±3 -4±2 -10±3 22±2.",
author = "Gibson, {Jeffrey B.} and Maxwell, {Robert A.} and Schweitzer, {John B.} and Fabian, {Timothy C.} and Proctor, {Kenneth G}",
year = "1999",
month = "12",
day = "1",
language = "English",
volume = "27",
journal = "Critical Care Medicine",
issn = "0090-3493",
publisher = "Lippincott Williams and Wilkins",
number = "12 SUPPL.",

}

TY - JOUR

T1 - Resuscitation from traumatic brain injury (TBI) and secondary hypotension with a hemoglobin-based oxygen carrying solution (HBOC)

AU - Gibson, Jeffrey B.

AU - Maxwell, Robert A.

AU - Schweitzer, John B.

AU - Fabian, Timothy C.

AU - Proctor, Kenneth G

PY - 1999/12/1

Y1 - 1999/12/1

N2 - Introduction: We have observed that early transfusion with shed blood vs saline improved cerebral perfusion pressure (CPP) and cerebral venous outflow saturation (CvO2) when hypotension was superimposed on TBI. In patients, it may be difficult to transfuse within the "golden hour", which has led to searches for blood substitutes. HBOCs have shown promise in many different models, and are now in phase III clinical trials. However, the potential benefits may be outweighed by vasoconstriction due to NO scavenging. Methods: Anesthetized, ventilated swine (37±1kg) received a fluid-percussion injury and 30% hemorrhage. After 1 hr, resuscitation consisted of 500ml of Baxter's first generation HBOC (DCLHb, n=6) or saline (SAL, n=5), followed by supplemental fluid. To test cerebral vasoreactivity, FiCO 2 = 0.05 and hyperventilation were administered for 10 minutes pre- and post-resuscitation. At 72 hrs, the brains were removed for histopathology. Results: CPP (table) and arterial lactate were significantly higher following DCLHb vs. SAL resuscitation (lactate: 3.3±0.5 vs 1.2±0.2, p<0.05). CvO2changes to the CO2 challenge were similar (table). Histologic findings included subarachnoid hemorrhage, diffuse axonal injury, and infarcts. DCLHb did not aggravate these changes. Conclusions: 1) Initial resuscitation with DCLHb improved CPP but increased systemic lactate, both manifestations of systemic vasoconstriction; 2) Since there was no harmful physiologic or histologic cerebral sequela related to vasoconstriction with this first generation HBOC, second generation compounds with less NO scavenging properties may have therapeutic potential for resuscitation of TBI. CPP @ 30 min Hi CO2 - Δ CvO2 sat Lo CO2 - Δ CvO2 pre TBI post TBI pre TBI DCLHb 78±5 -4±4 -11±4 21±3 Saline 56±3 -4±2 -10±3 22±2.

AB - Introduction: We have observed that early transfusion with shed blood vs saline improved cerebral perfusion pressure (CPP) and cerebral venous outflow saturation (CvO2) when hypotension was superimposed on TBI. In patients, it may be difficult to transfuse within the "golden hour", which has led to searches for blood substitutes. HBOCs have shown promise in many different models, and are now in phase III clinical trials. However, the potential benefits may be outweighed by vasoconstriction due to NO scavenging. Methods: Anesthetized, ventilated swine (37±1kg) received a fluid-percussion injury and 30% hemorrhage. After 1 hr, resuscitation consisted of 500ml of Baxter's first generation HBOC (DCLHb, n=6) or saline (SAL, n=5), followed by supplemental fluid. To test cerebral vasoreactivity, FiCO 2 = 0.05 and hyperventilation were administered for 10 minutes pre- and post-resuscitation. At 72 hrs, the brains were removed for histopathology. Results: CPP (table) and arterial lactate were significantly higher following DCLHb vs. SAL resuscitation (lactate: 3.3±0.5 vs 1.2±0.2, p<0.05). CvO2changes to the CO2 challenge were similar (table). Histologic findings included subarachnoid hemorrhage, diffuse axonal injury, and infarcts. DCLHb did not aggravate these changes. Conclusions: 1) Initial resuscitation with DCLHb improved CPP but increased systemic lactate, both manifestations of systemic vasoconstriction; 2) Since there was no harmful physiologic or histologic cerebral sequela related to vasoconstriction with this first generation HBOC, second generation compounds with less NO scavenging properties may have therapeutic potential for resuscitation of TBI. CPP @ 30 min Hi CO2 - Δ CvO2 sat Lo CO2 - Δ CvO2 pre TBI post TBI pre TBI DCLHb 78±5 -4±4 -11±4 21±3 Saline 56±3 -4±2 -10±3 22±2.

UR - http://www.scopus.com/inward/record.url?scp=33750675230&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33750675230&partnerID=8YFLogxK

M3 - Article

VL - 27

JO - Critical Care Medicine

JF - Critical Care Medicine

SN - 0090-3493

IS - 12 SUPPL.

ER -