Abstract
There is a paucity of studies, clinical and experimental, attesting to the benefit of cerebral perfusion pressure (CPP) directed pressor therapy following traumatic brain injury (TBI). The current study evaluates this therapy in a swine model of TBI and hypotension. Forty-five anesthetized and ventilated swine received TBI followed by a 45% blood volume bleed. After 1 h, all animals were resuscitated with 0.9% sodium chloride equal to three times the shed blood volume. The experimental group (PHE) received phenylephrine to maintain CPP > 80 mm Hg; the control group (SAL) did not. Outcomes in the first phase (n = 33) of the study were as follows: cerebro-venous oxygen saturation (S cvO2), cerebro-vascular carbon dioxide reactivity (δScvO2), and brain structural damage (β-amyloid precursor protein [βAPP] immunoreactivity). In the second phase (n = 12) of the study, extravascular blood free water (EVBFW) was measured in the brain and lung. After resuscitation, intracranial and mean arterial pressures were >15 and >80 mm Hg, respectively, in both groups. CPP declined to 64 ± 5 mm Hg in the SAL group, despite fluid supplements. CPP was maintained at >80 mm Hg with pressors in the PHE group. PHE animals maintained better ScvO2 (p < 0.05 at 180, 210, 240, 270, and 300 min post-TBI). At baseline, 5% CO2 evoked a 16 ± 4% increase in ScvO2, indicating cerebral vasodilatation and luxury perfusion. By 240 min, this response was absent in SAL animals and preserved in PHE animals (p < 0.05). Brain EVBFW was higher in SAL animals; however, lung EVBFW was higher in PHE animals. There was no difference in βAPP immunoreactivity between the SAL and PHE groups (p > 0.05). In this swine model of TBI and hypotension, CPP directed pressor therapy improved brain oxygenation and maintained cerebro-vascular CO2 reactivity. Brain edema was lower, but lung edema was greater, suggesting a higher propensity for pulmonary complications.
| Original language | English |
|---|---|
| Pages (from-to) | 827-839 |
| Number of pages | 13 |
| Journal | Journal of Neurotrauma |
| Volume | 20 |
| Issue number | 9 |
| State | Published - Sep 1 2003 |
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Keywords
- Beta-amyloid precursor protein
- Brain edema
- Brain injury
- Cerebral oxygenation
- Cerebral perfusion pressure
- Cerebro-vascular CO reactivity
- Pressor
ASJC Scopus subject areas
- Clinical Neurology
- Neuroscience(all)
Cite this
Cerebral perfusion pressure directed therapy following traumatic brain injury and hypotension in swine. / Malhotra, Ajai K.; Schweitzer, John B.; Fox, Jerry L.; Fabian, Timothy C.; Proctor, Kenneth G.
In: Journal of Neurotrauma, Vol. 20, No. 9, 01.09.2003, p. 827-839.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Cerebral perfusion pressure directed therapy following traumatic brain injury and hypotension in swine
AU - Malhotra, Ajai K.
AU - Schweitzer, John B.
AU - Fox, Jerry L.
AU - Fabian, Timothy C.
AU - Proctor, Kenneth G
PY - 2003/9/1
Y1 - 2003/9/1
N2 - There is a paucity of studies, clinical and experimental, attesting to the benefit of cerebral perfusion pressure (CPP) directed pressor therapy following traumatic brain injury (TBI). The current study evaluates this therapy in a swine model of TBI and hypotension. Forty-five anesthetized and ventilated swine received TBI followed by a 45% blood volume bleed. After 1 h, all animals were resuscitated with 0.9% sodium chloride equal to three times the shed blood volume. The experimental group (PHE) received phenylephrine to maintain CPP > 80 mm Hg; the control group (SAL) did not. Outcomes in the first phase (n = 33) of the study were as follows: cerebro-venous oxygen saturation (S cvO2), cerebro-vascular carbon dioxide reactivity (δScvO2), and brain structural damage (β-amyloid precursor protein [βAPP] immunoreactivity). In the second phase (n = 12) of the study, extravascular blood free water (EVBFW) was measured in the brain and lung. After resuscitation, intracranial and mean arterial pressures were >15 and >80 mm Hg, respectively, in both groups. CPP declined to 64 ± 5 mm Hg in the SAL group, despite fluid supplements. CPP was maintained at >80 mm Hg with pressors in the PHE group. PHE animals maintained better ScvO2 (p < 0.05 at 180, 210, 240, 270, and 300 min post-TBI). At baseline, 5% CO2 evoked a 16 ± 4% increase in ScvO2, indicating cerebral vasodilatation and luxury perfusion. By 240 min, this response was absent in SAL animals and preserved in PHE animals (p < 0.05). Brain EVBFW was higher in SAL animals; however, lung EVBFW was higher in PHE animals. There was no difference in βAPP immunoreactivity between the SAL and PHE groups (p > 0.05). In this swine model of TBI and hypotension, CPP directed pressor therapy improved brain oxygenation and maintained cerebro-vascular CO2 reactivity. Brain edema was lower, but lung edema was greater, suggesting a higher propensity for pulmonary complications.
AB - There is a paucity of studies, clinical and experimental, attesting to the benefit of cerebral perfusion pressure (CPP) directed pressor therapy following traumatic brain injury (TBI). The current study evaluates this therapy in a swine model of TBI and hypotension. Forty-five anesthetized and ventilated swine received TBI followed by a 45% blood volume bleed. After 1 h, all animals were resuscitated with 0.9% sodium chloride equal to three times the shed blood volume. The experimental group (PHE) received phenylephrine to maintain CPP > 80 mm Hg; the control group (SAL) did not. Outcomes in the first phase (n = 33) of the study were as follows: cerebro-venous oxygen saturation (S cvO2), cerebro-vascular carbon dioxide reactivity (δScvO2), and brain structural damage (β-amyloid precursor protein [βAPP] immunoreactivity). In the second phase (n = 12) of the study, extravascular blood free water (EVBFW) was measured in the brain and lung. After resuscitation, intracranial and mean arterial pressures were >15 and >80 mm Hg, respectively, in both groups. CPP declined to 64 ± 5 mm Hg in the SAL group, despite fluid supplements. CPP was maintained at >80 mm Hg with pressors in the PHE group. PHE animals maintained better ScvO2 (p < 0.05 at 180, 210, 240, 270, and 300 min post-TBI). At baseline, 5% CO2 evoked a 16 ± 4% increase in ScvO2, indicating cerebral vasodilatation and luxury perfusion. By 240 min, this response was absent in SAL animals and preserved in PHE animals (p < 0.05). Brain EVBFW was higher in SAL animals; however, lung EVBFW was higher in PHE animals. There was no difference in βAPP immunoreactivity between the SAL and PHE groups (p > 0.05). In this swine model of TBI and hypotension, CPP directed pressor therapy improved brain oxygenation and maintained cerebro-vascular CO2 reactivity. Brain edema was lower, but lung edema was greater, suggesting a higher propensity for pulmonary complications.
KW - Beta-amyloid precursor protein
KW - Brain edema
KW - Brain injury
KW - Cerebral oxygenation
KW - Cerebral perfusion pressure
KW - Cerebro-vascular CO reactivity
KW - Pressor
UR - http://www.scopus.com/inward/record.url?scp=0141566710&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0141566710&partnerID=8YFLogxK
M3 - Article
C2 - 14577861
AN - SCOPUS:0141566710
VL - 20
SP - 827
EP - 839
JO - Journal of Neurotrauma
JF - Journal of Neurotrauma
SN - 0897-7151
IS - 9
ER -