Brain Is Made Up Of How Much Water

Transl Stroke Res. Writer manuscript; available in PMC 2013 Jun i.

Published in final edited form as:

PMCID: PMC3413327

NIHMSID: NIHMS376847

Brain water content. A misunderstood measurement?

Richard F Keep

¹Departments of Neurosurgery, University of Michigan, Ann Arbor, Michigan

^twoR5018, BSRB, University of Michigan, Ann Arbor, Michigan 48109-2200

Ya Hua

¹Departments of Neurosurgery, Academy of Michigan, Ann Arbor, Michigan

Guohua Xi

ⁱDepartments of Neurosurgery, University of Michigan, Ann Arbor, Michigan

Abstract

Brain edema is a major contributor to poor outcome following ischemic and hemorrhagic stroke. In animal models, edema has historically been quantified as a alter in % encephalon water content (water content/moisture weight). As described in this advice, this number tin be misleading, equally 'pocket-size' changes in % brain h2o content actually reflect much bigger changes in brain swelling. Using either h2o content, expressed as g/g dry out weight, or a measure of encephalon swelling, ameliorate reflect the bear upon of edema later stroke and encephalon injury.

Keywords: Brain edema, swelling, h2o content, cerebral hemorrhage, cerebral ischemia

Cerebral edema is a major contributor to poor upshot in many neurological conditions (e.k. hemorrhagic stroke, ischemic stroke, traumatic encephalon injury and encephalon tumors). Historically, in beast disease models, edema has been quantified by comparison the water content of the afflicted tissue with normal brain. The water content has been expressed equally % brain water, determined from the difference in moisture and dry weights (i.e. the water weight) divided by the moisture weight (1–3). As described beneath, this is unfortunate as it tin can atomic number 82 to a misinterpretation of the impact of 'small' changes in % brain h2o.

To examine this event, different examples of brain injury are used from the literature and three parameters are calculated by the equations.

%Water content = 100^∗(wet weight - dry out weight)/wet weight

Equation 1

Water content = (moisture weight - dry out weight)/dry weight

Equation 2

%Tissue swelling = 100^∗(final wet weight - initial wet weight)/initial wet weight

Equation 3

To demonstrate these terms, data from Betz et al. (four) is used. Rats underwent six hours of permanent middle cognitive artery occlusion (MCAO) and and so tissue was sampled from the ipsilateral (ischemic) and contralateral cortex. For a 100 mg sample of the ipsilateral cortex, the dry weight was 17.6 mg and the water weight was 82.4 mg. For the contralateral cortex, the aforementioned moisture weight of sample had a dry weight of 21.4 mg and a water weight of 78.6 mg. From Equation 1, the ipsi- and contralateral cortex samples had % water contents of 82.4 and 78.half dozen%, respectively, a deviation of 3.eight%. However, using Equation 2, the water content in the ipsilateral cortex is iv.68 g water/yard dry weight, while that for the ipsilateral cortex is three.67 yard h2o/one thousand dry weight. Assuming that the dry tissue weight doesn't change during the course of six hours of MCAO, this means that there is a 27.5% increase in h2o content. Using the contralateral cortical sample water content, and the final ipsilateral dry weight, it is possible to summate an initial wet weight for the ipsilateral sample (3.67+1)*17.six = 82.two mg and, thus, using Equation 3 the tissue swelling as 21.six%. This example shows that a adequately small change in % h2o content really reflects large changes in tissue h2o and tissue swelling.

Table one gives 5 examples from the literature to encompass different neurological conditions. Wagner et al. (5) reported that for perihematomal white thing in the squealer the % h2o content was 86%, compared to 73% in the contralateral hemisphere. In terms of water content (chiliad/chiliad dry weight), this represents a 127% change, while tissue swelling was 93%. These results show the magnitude of the changes in water content and swelling that can outcome from brain edema. It should besides be noted that the relationship between % water content and either h2o content (g/grand dry weight) or brain swelling is non linear. This is emphasized in Effigy 1 which plots changes in % water content with the other two parameters for a hypothetical tissue, with an initial 77% water content. A change in % water content of 1% results (to 78%) in a 6 and 4.5% increase in water content (g/g dry weight) and brain swelling, respectively, but a 10% increase in % water content (to 87%) results in a 100 and 77% change in these two parameters.

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Graph showing the relationship between % h2o content and either per centum changes in water content (g/1000 dry weight) or swelling. The % water content of a hypothetical slice of brain tissue is increased in ane% increment from a baseline of 77%. For each increment, the per centum change in water content (chiliad/g dry weight) is calculated as is the caste of swelling of the tissue.

Table 1

% Encephalon water content, water content (g/g dry out weight) and % brain swelling in five studies on brain injury from the literature (meet equations 1–iii for how these were calculated). Delight note that the % changes in the latter two parameters with injury were 4 to 7-fold greater than that for % brain water content. ICH = Intracerebral hemorrhage, TBI = traumatic brain injury.

Model	% Brain water content			Water content (g/thousand dry out weight)			Brain swelling
Model	Not- injured	Injured	% change	Non- injured	Injured	% change	% change
Rat global ischemia (7)	77.16%	78.two%	1.3%	iii.38	3.59	6.2%	four.8%
Rat focal ischemia (4)	78.6%	82.iv%	4.8%	three.67	iv.68	27.5%	21.6%
Rat ICH (Reference)	78.0%	81.9%	five.0%	3.54	4.52	27.6%	21.5%
Rat TBI (eight)	78.vi%	84.2%	7.i%	3.67	5.33	45.1%	35.4
Sus scrofa ICH -white matter (5)	73%	86%	17.8%	2.70	6.xiv	127%	93%

Gerriets et al. made measurements of % h2o content (wet/dry out weight method) and hemispheric swelling (using magnetic resonance imaging) in the same rats 24 hours later on permanent MCAO (6). They reported % water contents of 80.08 and 75.89% in the ipsi- and contralateral hemispheres, respectively, an increase of 4.19%. This was accompanied by an xviii.34% swelling of the ipsilateral hemisphere equally assessed by MRI. These direct measurements also indicate that relatively 'small' changes in % water content actually reflect large alter in tissue swelling.

The bear upon of brain edema may be local, through change in spatial relationships between cells and local blood flow, or global, due to changes intracranial force per unit area, blood flow and potential herniation. In this regards, Table one lists four rat studies, one of which is from a model of global ischemia with reperfusion (seven) and the other iii are from more focal injuries (MCAO, intracerebral hemorrhage and traumatic brain injury with more local tissue sampling; (4, 8, ix)). The global ischemia study reported an increase in % brain water content from 77.16 to 78.2%, a smaller increase than reported for the three focal models. It should exist noted, notwithstanding, that these small-scale global increases may have a profound effect on intracranial pressure level (and potential herniation). Brain swelling can initially be compensated by CSF (and blood) deportation. However, the CSF just accounts for ~15% of cranial volume (intracranial CSF volume of ~200 ml (x) and encephalon weight of 1350 yard) and, every bit depicted in Figure 1, an increase in brain water content from 77 to fourscore% would cause xv% brain swelling, exhausting any possible displacement.

As a measurement, % brain h2o content has the disadvantage that edema (an increase in water) affects both the numerator and the denominator, the water mass and the moisture weight. It is, unfortunately, ingrained in the scientific customs. It is, therefore, important to realize that relatively pocket-sized changes in % brain water content can really reflect large changes in the absolute water content of the brain and encephalon swelling. These may potentially cause major local disruption of construction and/or global effects on intracranial pressure and claret flow.

Acknowledgments

This piece of work was supported by the National Institutes of Health grants NS034709 (RFK), NS039866 (GX), NS057539 (YH) and a grant from the American Centre Association, 0840016N. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH or the AHA.

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