scholarly journals Revisiting the Logan plot to account for non-negligible blood volume in brain tissue

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Martin Schain ◽  
Patrik Fazio ◽  
Ladislav Mrzljak ◽  
Nahid Amini ◽  
Nabil Al-Tawil ◽  
...  
Keyword(s):  
2000 ◽  
Vol 93 (2) ◽  
pp. 183-193 ◽  
Author(s):  
Anthony Marmarou ◽  
Panos P. Fatouros ◽  
Pal Barzó ◽  
Gennarina Portella ◽  
Masaaki Yoshihara ◽  
...  

Object. The pathogenesis of traumatic brain swelling remains unclear. The generally held view is that brain swelling is caused primarily by vascular engorgement and that edema plays a relatively minor role in the swelling process. The goal of this study was to examine the roles of cerebral blood volume (CBV) and edema in traumatic brain swelling.Methods. Both brain-tissue water and CBV were measured in 76 head-injured patients, and the relative contribution of edema and blood to total brain swelling was determined. Comparable measures of brain-tissue water were obtained in 30 healthy volunteers and CBV in seven volunteers. Brain edema was measured using magnetic resonance imaging, implementing a new technique for accurate measurement of total tissue water. Measurements of CBV in a subgroup of 31 head-injured patients were based on consecutive measures of cerebral blood flow (CBF) obtained using stable xenon and calculation of mean transit time by dynamic computerized tomography scanning after a rapid bolus injection of iodinated contrast material. The mean (± standard deviation) percentage of swelling due to water was 9.37 ± 8.7%, whereas that due to blood was −0.8 ± 1.32%.Conclusions. The results of this study showed that brain edema is the major fluid component contributing to traumatic brain swelling. Moreover, CBV is reduced in proportion to CBF reduction following severe brain injury.


1992 ◽  
Vol 263 (1) ◽  
pp. H75-H82 ◽  
Author(s):  
M. M. Todd ◽  
J. B. Weeks ◽  
D. S. Warner

The influence of isovolemic hemodilution with 6% hetastarch [hematocrits (Hct) ranging from 43 to 20%] on cerebral blood flow (CBF), cerebral red blood cell and plasma volumes, total cerebral blood volume (CBV), and cerebral Hct was examined in normothermic, normocarbic, halothane-anesthetized Sprague-Dawley rats. CBF was measured via the indicator-fractionation method ([3H]nicotine), red blood cell volume was measured using 99mTc-labeled red blood cells, while plasma volume was measured using [14C]dextran. Brain tissue was fixed in situ by microwave irradiation. All data plots (e.g., CBF vs. Hct) were fitted by linear regression methods. Hemodilution was associated with a progressive increase in forebrain CBF (from a fitted value of 78 ml.100 g-1.min-1 at Hct = 43%, to 171 ml.100 g-1.min-1 at 20%). Cerebral plasma volume also rose, while red blood cell volume decreased. Total CBV (i.e., the sum of red blood cell and plasma volumes) increased in parallel with CBF (from 2.51 ml/100 g at Hct = 43 to 4.94 ml/100 g at Hct = 20%). This increase is larger than can be explained by a simple increase in the diameter of arterial/arteriolar resistance vessels and may be due to either capillary recruitment or to an increase in the volume of postarteriolar structures. Calculated cerebral tissue hematocrit decreased. The magnitude of this decrease was larger than the reduction in arterial Hct; the ratio of cerebral to arterial Hct decreased from 0.780 at an arterial Hct equaling 43% to 0.458 at Hct equaling 20%.(ABSTRACT TRUNCATED AT 250 WORDS)


1987 ◽  
Vol 7 (4) ◽  
pp. 471-479 ◽  
Author(s):  
Alan A. Artru

The study examined the role of cerebral blood volume (CBV), cerebrospinal fluid (CSF) volume, and brain tissue water and electrolytes on CSF pressure during 4 h of hypocapnia in dogs, Group I (n = 6) was examined during hypocapnia (PaCO2 20 mm Hg), with no intracranial mass being present Group II (n = 6) was examined with an intracranial mass present (epidural balloon, CSF pressure 35 cm H2O), but no hypocapnia. In group III (n = 6), an intracranial mass was present, and hypocapnia was used to lower CSF pressure. In group I, hypocapnia initially reduced CBV from 3.4 to 2.4 ml. With continued hypocapnia, CBV reexpanded to 3.4 ml by 4 h. CSF volume changed reciprocally, so that intracranial CSF pressure remained constant. In group II, CBV remained steady (2.7 ml), and CSF volume fell only slightly, so that CSF pressure remained elevated. In group III, hypocapnia initially reduced CBV from 2.8 to 2.2 ml, and CSF pressure fell from 35 to 19 cm H2O. With continued hypocapnia, CBV rose to 2.8 ml by 4 h, but CSF volume fell from 6.1 to 5.0 ml, so that CSF pressure remained low. Net intracranial absorption of CSF did not exceed net intracranial CSF production, suggesting that CSF volume fell because hypocapnia improved access of intracranial CSF to spinal sites of CSF reabsorption. Brain tissue composition was not different among groups. The indicate that hypocapnia lowers elevated CSF pressure initially by lowering CBV. This CSF pressure-lowering effect is sustained (despite reexpansion of CBV) by a further reduction of CSF volume. In this model, brain tissue water or electrolytes did not contribute to changes in CSF pressure.


JAMA ◽  
1966 ◽  
Vol 195 (5) ◽  
pp. 356-361 ◽  
Author(s):  
J. B. McClenahan
Keyword(s):  

1952 ◽  
Vol 21 (4) ◽  
pp. 516-524 ◽  
Author(s):  
Sam Kruger ◽  
Lester Baker ◽  
William D. Mosiman

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