Cerebral perfusion pressure directed therapy following traumatic brain injury and hypotension in swine.
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(cv)O(2)), cerebro-vascular carbon dioxide reactivity (DeltaS(cv)O(2)), and brain structural damage (beta-amyloid precursor protein [betaAPP] 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 S(cv)O(2) (p < 0.05 at 180, 210, 240, 270, and 300 min post-TBI). At baseline, 5% CO(2) evoked a 16 +/- 4% increase in S(cv)O(2), 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 betaAPP 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 CO(2) reactivity. Brain edema was lower, but lung edema was greater, suggesting a higher propensity for pulmonary complications.
Department of Surgery, Medical College of Virginia, Virginia Commonwealth University, 1200 E. Broad Street, West Hospital, 15th Floor East, PO Box 980454, Richmond, VA 23298, USA. akmalhot@hsc.vcu.edu
Ajai K
AK
Malhotra
John B
JB
Schweitzer
Jerry L
JL
Fox
Timothy C
TC
Fabian
Kenneth G
KG
Proctor
D000818:Animals; D001930:Brain Injuries / Q000188:drug therapy* / Q000503:physiopathology / Q000628:therapy; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D007022:Hypotension / Q000188:drug therapy* / Q000503:physiopathology / Q000628:therapy; D007427:Intracranial Pressure / Q000187:drug effects / Q000502:physiology*; D010656:Phenylephrine / Q000494:pharmacology / Q000627:therapeutic use*; D013552:Swine
D010656:Phenylephrine