Use of specific gravity in the measurement of cerebral edema

178

138

Hydrocephalus is caused by an imbalance in cerebrospinal fluid (CSF) production and absorption, resulting in excess ventricular fluid accumulation and neurologic impairment. Current therapy for hydrocephalus involves surgical diversion of excess ventricular fluid. The water-transporting protein aquaporin-4 (AQP4) is expressed at the brain-CSF and blood-brain barriers. Here, we provide evidence for AQP4-facilitated CSF absorption in hydrocephalus by a transparenchymal pathway into the cerebral vasculature. A mouse model of obstructive hydrocephalus was created by injecting kaolin (2.5 mg/mouse) into the cisterna magna. Intracranial pressure (ICP) was B5 mm Hg and ventricular size < 0.3 mm 3 in control mice. Lateral ventricle volume increased to 3.760.5 and 5.1 60.5 mm 3 in AQP4 null mice at 3 and 5 days after injection, respectively, significantly greater than 2.6 60.3 and 3.560.5 mm 3 in wildtype mice (P < 0.005). The corresponding ICP was 2262 mm Hg at 3 days in AQP4 null mice, significantly greater than 1461 mm Hg in wildtype mice (P < 0.005). Brain parenchymal water content increased by 2% to 3% by 3 days, corresponding to B50 lL of fluid, indicating backflow of CSF from the ventricle into the parenchymal extracellular space. A multicompartment model of hydrocephalus based on experimental data from wildtype mice accurately reproduced the greater severity of hydrocephalus in AQP4 null mice, and predicted a much reduced severity if AQP4 expression/function were increased. Our results indicate a significant role for AQP4-mediated transparenchymal CSF absorption in hydrocephalus and provide a rational basis for evaluation of AQP4 induction as a nonsurgical therapy for hydrocephalus.

“…Data from two to four tissue fragments from both hemispheres were averaged for each mouse. Specific gravities were converted to % brain water as described by Nelson et al (1971).…”

Section: Brain Water Contentmentioning

confidence: 99%

Accelerated Progression of Kaolin-Induced Hydrocephalus in Aquaporin-4-Deficient Mice

Bloch¹,

Auguste

Manley

et al. 2006

178

138

“…The calculation of CBF involves a constant (0.0614) (Meek et al, 1998), which is necessary to convert raw CHbF data generated by the Hamamatsu NIRO 500 from mmol/100 mL min into mL/100 mg min. This conversion incorporates neonatal brain tissue density (1.05) (Nelson et al, 1971) and the molecular weight of Hb (64,500 Da). CDO 2 is the cerebral oxygen delivery, CMRO 2 is the cerebral oxygen consumption.…”

Section: Cerebral Fractional Oxygen Extraction Cerebral Blood Flow mentioning

confidence: 99%

“…The calculation of both CDO 2 and CMRO 2 involves a constant (3.8), which is necessary to convert raw CHbF data generated by the Hamamatsu NIRO 500 from mmol/100 mL min into mmol/100 mg min of oxygen delivered or consumed. This conversion takes into account the ability of each Hb molecule to carry four molecules of oxygen, and incorporates the tissue density of the neonatal brain, which is 1.05 (Nelson et al, 1971). Hb is the arterial haemoglobin concentration, determined by laboratory analysis, measured in g/dL.…”

Section: Cerebral Fractional Oxygen Extraction Cerebral Blood Flow mentioning

confidence: 99%

Cerebral Fractional Oxygen Extraction is Inversely Correlated with Oxygen Delivery in the Sick, Newborn, Preterm Infant

Kissack

Garr

Wardle

et al. 2005

Cerebral blood flow (CBF) is known to be low in newborn infants, but this has not been shown to be damaging. The purpose of this study was to investigate the relationships between cerebral haemoglobin flow, blood flow, oxygen delivery, oxygen consumption, venous saturation, and fractional oxygen extraction (OEF) in newborn, preterm infants. Measurements were made by nearinfrared spectroscopy in 13 very preterm, extremely low birth weight infants (median gestation 25 weeks) during the first 3 days after birth. There was a negative correlation between cerebral oxygen delivery and OEF (n ¼ 13, r ¼ À0.5, P ¼ 0.03), which implies that when there is a reduction in cerebral oxygen delivery in sick preterm infants, increased cerebral oxygen extraction may be responsible for maintaining oxygen availability to the brain. During the first 3 days after birth CBF (n ¼ 13, r ¼ 0.7, P ¼ 0.01), oxygen delivery (n ¼ 13, r ¼ 0.5, P ¼ 0.03), and oxygen consumption (n ¼ 13, r ¼ 0.7, P ¼ 0.004) all increased. This increase in oxygen consumption indicates increased cerebral metabolic activity after birth, which is likely to be a normal adaptation to extrauterine life. The increases in blood flow and oxygen delivery may also be normal adaptations that facilitate this increase in metabolic activity. There was a decrease (P ¼ 0.04) in mean (7s.d.) cerebral OEF between day 1 (0.3770.10) and day 2 (0.2970.09), with no change between day 2 and day 3. Taking into account the negative correlation between OEF and oxygen delivery, this decrease in OEF may be because of increased oxygen delivery during this time.

“…Tissue specific gravity of the two hemispheres was measured on 40-to 50-mg samples taken from the injured zone and from the contralateral hemisphere by linear gra dient columns using a kerosene and bromobenzene mix ture, as described by Nelson et al (1971) and improved by Marmarou et al (1978) …”

Section: Specific Gravity Determinationmentioning

confidence: 99%

Head Injury Induces Increased Prostaglandin Synthesis in Rat Brain

Shohami

Shapira

Sidi

et al. 1987

123

Summary: Head injury was induced in the left hemi sphere of rats, The rats were killed at various time in tervals after trauma (immediately, 15 min, 1 and 18 h, and 4 and 10 days), and the rates of synthesis and release of prostaglandin PGE2, 6-keto-PGF I", and thromboxane TXB2 from cortical slices of both hemispheres were studied. The rate of synthesis of PGE2 after 18 h was six and four times higher than control in the contused and contralateral hemispheres, respectively. By 10 days post trauma, both hemispheres had normal rate of PGE2 re lease. TXB2 and 6-keto-PGFI" synthetases were affected already 15 min after the injury, and a similarly elevated rate of synthesis was found in both hemispheres. The maximal effect was detected after 1 or 18 h with return to