The Effects of PaCO2Reduction on Regional Cerebral Blood Flow in the Acute Phase of Brain Injury

1977 ◽  
Vol 21 (5) ◽  
pp. 359-367 ◽  
Author(s):  
Georg E. Cold ◽  
Finn Taagehøj Jensen ◽  
Richard Malmros
2012 ◽  
Vol 27 (5) ◽  
pp. 526.e7-526.e12 ◽  
Author(s):  
Michael T. Scalfani ◽  
Rajat Dhar ◽  
Allyson R. Zazulia ◽  
Tom O. Videen ◽  
Michael N. Diringer

1987 ◽  
Vol 67 (2) ◽  
pp. 278-283 ◽  
Author(s):  
Laura R. Ment ◽  
William B. Stewart ◽  
Charles C. Duncan ◽  
Bruce R. Pitt ◽  
Judith Cole

✓ Asphyxia is the most common cause of severe brain injury in very young children, and frequently results in lesions of the periventricular white matter in addition to other neuropathological changes. This study examines the effects of asphyxia on regional cerebral blood flow (rCBF) and the role of prostaglandins (PG's) in its control in the newborn beagle pup. Pups were anesthetized, tracheotomized, paralyzed, artificially ventilated, and randomly assigned to two groups: asphyxial insult produced by discontinuing ventilatory support, and no insult. Experiments for carbon-14-iodoantipyrine autoradiographic determination of rCBF and regional cerebral PG determination were performed on separate groups of pups. These studies demonstrated a significant increase in cortical gray PGE2 levels at a time when rCBF was significantly impaired in response to severe asphyxial insult. No such increase was noted in the periventricular white matter zones.


2016 ◽  
Vol 37 (5) ◽  
pp. 1670-1686 ◽  
Author(s):  
Baptiste Balança ◽  
Anne Meiller ◽  
Laurent Bezin ◽  
Jens P. Dreier ◽  
Stéphane Marinesco ◽  
...  

Spreading depolarizations are waves of near-complete breakdown of neuronal transmembrane ion gradients, free energy starving, and mass depolarization. Spreading depolarizations in electrically inactive tissue are associated with poor outcome in patients with traumatic brain injury. Here, we studied changes in regional cerebral blood flow and brain oxygen (PbtO2), glucose ([Glc]b), and lactate ([Lac]b) concentrations in rats, using minimally invasive real-time sensors. Rats underwent either spreading depolarizations chemically triggered by KCl in naïve cortex in absence of traumatic brain injury or spontaneous spreading depolarizations in the traumatic penumbra after traumatic brain injury, or a cluster of spreading depolarizations triggered chemically by KCl in a remote window from which spreading depolarizations invaded penumbral tissue. Spreading depolarizations in noninjured cortex induced a hypermetabolic response characterized by a decline in [Glc]b and monophasic increases in regional cerebral blood flow, PbtO2, and [Lac]b, indicating transient hyperglycolysis. Following traumatic brain injury, spontaneous spreading depolarizations occurred, causing further decline in [Glc]b and reducing the increase in regional cerebral blood flow and biphasic responses of PbtO2 and [Lac]b, followed by prolonged decline. Recovery of PbtO2 and [Lac]b was significantly delayed in traumatized animals. Prespreading depolarization [Glc]b levels determined the metabolic response to clusters. The results suggest a compromised hypermetabolic response to spreading depolarizations and slower return to physiological conditions following traumatic brain injury-induced spreading depolarizations.


1994 ◽  
Vol 11 (1) ◽  
pp. 83-95 ◽  
Author(s):  
KOICHI OKIYAMA ◽  
TED S. ROSENKRANTZ ◽  
DOUGLAS H. SMITH ◽  
THOMAS A. GENNARELLI ◽  
TRACY K. McINTOSH

2013 ◽  
pp. 103-109
Author(s):  
Kazuyuki Miyamoto ◽  
Hirokazu Ohtaki ◽  
Kenji Dohi ◽  
Tomomi Tsumuraya ◽  
Hiroyasu Nakano ◽  
...  

1991 ◽  
Vol 11 (4) ◽  
pp. 655-660 ◽  
Author(s):  
Iwao Yamakami ◽  
Tracy K. McIntosh

To elucidate the temporal changes in regional cerebral blood flow (rCBF) after experimental traumatic brain injury, serial rCBF measurements were made during a 24-h period following fluid-percussion (F-P) traumatic brain injury in the rat. Brain injury of 2.2 atm was induced over the left parietal cortex and serial measurements of rCBF were performed using the radiolabeled microsphere method. rCBF values were obtained prior to injury and at 15 and 30 min and 1, 2, 4, and 24 h postinjury. At 15 min postinjury, there was a profound, widespread reduction in rCBF in all brain regions studied (p < 0.05). At 30 min and 1 h postinjury, all brain regions except pons-medulla and cerebellum showed significantly reduced rCBF compared to the preinjury values (p < 0.05). By 2 h postinjury, however, a significant focal reduction of rCBF was observed only in the cerebral tissue surrounding the trauma site (p < 0.05); rCBF in the remaining brain regions had recovered to the preinjury levels. By 4 h postinjury, rCBF had returned to normal in all brain regions studied. This recovery of rCBF was still evident at 24 h postinjury. The present study demonstrates that, following the experimental traumatic brain injury in the rat, (a) an initial global suppression of rCBF occurs up to 1 h postinjury; (b) at the trauma site, a more persistent focal reduction of rCBF occurs; and (c) these alterations in rCBF after trauma dissolve by 4 h postinjury. The result was discussed in the context of the neurological, electroencephalographic, magnetic resonance spectroscopic, and pathological findings observed in our lateral F-P brain injury rat model.


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