Influence of Mannitol and Furosemide, Alone and in Combination, on Brain Water Content after Fluid Percussion Injury

2006 ◽  
Vol 105 (6) ◽  
pp. 1176-1181 ◽  
Author(s):  
Michael M. Todd ◽  
Johann Cutkomp ◽  
Johnny E. Brian
Keyword(s):  
Water Content ◽  
Plasma Osmolality ◽  
Control Group ◽  
Brain Water Content ◽  
Fluid Percussion ◽  
Fluid Percussion Injury ◽  
Injured Brain ◽  
The Impact ◽  
Reduced Water ◽  
Brain Water

Background Furosemide and mannitol are used to reduce intracranial pressure, but the impact of furosemide on edema of injured brain is unclear. The authors examined the effects of furosemide and mannitol, alone and in combination, on brain water content in brain-injured rats. Methods Anesthetized rats were subjected to a 2.2-atm left hemispheric fluid percussion injury. Two and three-quarters hours later, animals received 0.5, 1, 4, or 8 g/kg mannitol; 8 mg/kg furosemide; a combination of 4 g/kg mannitol plus 4 mg/kg furosemide; or 8 g/kg mannitol plus 8 mg/kg furosemide. One hour later (4 h after injury), plasma osmolality was measured, and hemispheric water content was determined by drying. Other animals were subjected to injury without drug treatment (impact only) or did not undergo injury (control). Pairwise group comparisons regarding the effects of mannitol and furosemide were restricted to only four groups: impact only, 8 g/kg mannitol, 8 mg/kg furosemide, and 8 g/kg mannitol plus 8 mg/kg furosemide. Results The water content of both hemispheres in the impact-only group was greater than in the control group (left greater than right). Mannitol, 8 g/kg, increased osmolality from 306 +/- 4 to 351 +/- 6 mOsm/kg (mean +/- SD) and reduced water content in the left hemisphere from 80.06 +/- 0.84% (impact only) to 78.24 +/- 0.73%. Furosemide, 8 mg/kg, had no effect on osmolality or water content. Brain water in animals treated with 8 g/kg mannitol plus 8 mg/kg furosemide did not differ from that seen with 8 g/kg mannitol alone. Conclusions Mannitol increased plasma osmolality and reduced water content of the injured and contralateral hemispheres, whereas the authors observed no effect of furosemide when given either alone or in combination with mannitol.

The Influence of Mannitol and Furosemide on Brain Water Content Following Fluid Percussion Injury

2002 ◽  
Vol 96 (Sup 2) ◽  
pp. A737
Author(s):  
Michael M. Todd ◽  
Johnny E. Brian ◽  
Joanne Cutcomp ◽  
JoAnn Schwarting ◽  
Phillip G. Schmid
Keyword(s):  
Water Content ◽  
Brain Water Content ◽  
Fluid Percussion ◽  
Fluid Percussion Injury ◽  
Brain Water

Abstract P790: Landiolol Attenuates Global Cerebral Edema Following Experimental Cardiac Arrest in Mice

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Tomoyuki Iwai ◽  
Shin Nakayama
Keyword(s):  
Cardiac Arrest ◽  
Water Content ◽  
Cerebral Edema ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
P Value ◽  
Brain Water Content ◽  
Arterial Blood ◽  
The Brain ◽  
Brain Water

Introduction: Cerebral edema following cardiac arrest and cardiopulmonary resuscitation (CA/CPR) is associated with unfavorable neurologic outcome. The Na + -K + -2Cl - water cotransporter NKCC1 is suspected to be a critical mediator of edema formation after ischemia. It is reported that β1 adrenoreceptor antagonists protect neurons following brain ischemia in rodents. β1 adrenoreceptor antagonists inhibit the Na + -K + -ATPase, which can inhibit driving force of NKCC1 that theoretically reduces cerebral edema following ischemia-reperfusion injury. In this study, we examined whether landiolol, a selective β1 adrenoreceptor antagonist, attenuates cerebral edema following CA/CPR. Methods: Isoflurane-anesthetized adult male mice (C57BL/6J, 25-30g) were randomized into landiolol group or control group. After 7-min CA followed by CPR, landiolol (0.5ml, 830μg/ml) was administered by continuous infusion intravenously for 4 hours. Animals in control group were given normal saline (0.5ml) in the same manner. Twenty-four hours after CA/CPR, the brain was removed to assess brain water content using wet-to-dry method. The primary outcome was measurement of the brain water content. Heart rate and arterial blood pressure were recorded. Measured parameters were analyzed by one-way ANOVA with post hoc Tukey-Kramer test using SPSS® statistics 25. Differences were considered statistically significant at a P value < 0.05. Results: Brain water contents was increased in control group mice after CA/CPR (n=10) compared with those in sham operated mice (n=5) (79.5±0.85% vs 78.3±0.14%, P=0.003). Compared with control group, landiolol treatment significantly reduced brain water content in mice subjected to CA/CPR (n=12) (78.9±0.51% vs 79.5±0.85%, P=0.04). Conclusion: Landiolol attenuated brain edema following CA/CPR. These results may suggest selective β1-blocker could be alternative treatment for neuroprotection in patients who suffered CA/CPR.

Plasma Osmolality and Brain Water Content in a Rat Glioma Model

Neurosurgery ◽  
1994 ◽  
Vol 34 (3) ◽  
pp. 505???511 ◽  
Author(s):  
Thomas D. Hansen ◽  
David S. Warner ◽  
Vincent C. Traynelis ◽  
Michael M. Todd
Keyword(s):  
Water Content ◽  
Plasma Osmolality ◽  
Brain Water Content ◽  
Rat Glioma ◽  
Glioma Model ◽  
Brain Water

scholarly journals Placental ischemia-induced increases in brain water content and cerebrovascular permeability: role of TNF-α

2015 ◽  
Vol 309 (11) ◽  
pp. R1425-R1431 ◽  
Author(s):  
Junie P. Warrington ◽  
Heather A. Drummond ◽  
Joey P. Granger ◽  
Michael J. Ryan
Keyword(s):  
Water Content ◽  
Brain Water Content ◽  
Pregnant Rats ◽  
Increased Risk ◽  
Tnf Α ◽  
Bbb Permeability ◽  
The Impact ◽  
Placental Ischemia ◽  
Brain Water

Cerebrovascular complications and increased risk of encephalopathies are characteristic of preeclampsia and contribute to 40% of preeclampsia/eclampsia-related deaths. Circulating tumor necrosis factor-α (TNF-α) is elevated in preeclamptic women, and infusion of TNF-α into pregnant rats mimics characteristics of preeclampsia. While this suggests that TNF-α has a mechanistic role to promote preeclampsia, the impact of TNF-α on the cerebral vasculature during pregnancy remains unclear. We tested the hypothesis that TNF-α contributes to cerebrovascular abnormalities during placental ischemia by first infusing TNF-α in pregnant rats (200 ng/day ip, from gestational day 14 to 19) at levels to mimic those reported in preeclamptic women. TNF-α increased mean arterial pressure (MAP, P < 0.05) and brain water content in the anterior cerebrum ( P < 0.05); however, TNF-α infusion had no effect on blood-brain barrier (BBB) permeability in the anterior cerebrum or posterior cerebrum. We then assessed the role of endogenous TNF-α in mediating these abnormalities in a model of placental ischemia induced by reducing uterine perfusion pressure followed by treatment with the soluble TNF-α receptor (etanercept, 0.8 mg/kg sc) on gestational day 18. Etanercept reduced placental ischemia-mediated increases in MAP, anterior brain water content ( P < 0.05), and BBB permeability (202 ± 44% in placental ischemic rats to 101 ± 28% of normal pregnant rats). Our results indicate that TNF-α mechanistically contributes to cerebral edema by increasing BBB permeability and is an underlying factor in the development of cerebrovascular abnormalities associated with preeclampsia complicated by placental ischemia.

Effect of Mannitol and Furosemide on Plasma Osmolality and Brain Water

2002 ◽  
Vol 96 (2) ◽  
pp. 416-421 ◽  
Author(s):  
Kokila Thenuwara ◽  
Michael M. Todd ◽  
Johnny E. Brian
Keyword(s):  
Water Content ◽  
Plasma Osmolality ◽  
Dry Weight ◽  
Potential Interaction ◽  
Interactive Effects ◽  
Brain Water Content ◽  
Mechanically Ventilated ◽  
Physiologic Parameters ◽  
Normal Rat ◽  
Brain Water

Background Mannitol and furosemide are used to reduce increased intracranial pressure (ICP) and to reduce brain bulk during neurosurgery. One mechanism by which these changes might occur is via a reduction in brain water content. Although mannitol and furosemide are commonly used in combination, there has been no formal evaluation of the interactive effects of these two drugs on brain water. The effect of mannitol and furosemide alone and in combination on water content of normal rat brain was examined. Methods The lungs of rats anesthetized with halothane were mechanically ventilated to maintain normal physiologic parameters. After baseline measurement of plasma osmolality, mannitol (1, 4, or 8 g/kg), furosemide (2, 4, or 8 mg/kg), or a combination of furosemide (8 mg/kg) and mannitol (1, 4, or 8 g/kg) was administered intravenously over approximately 15 min. One hour later, plasma osmolality was measured, the animals were killed, and brain water content was determined by wet and dry weight measurements. Results Mannitol produced a dose-dependent increase in plasma osmolality and reduction of brain water content. There was a linear relation between plasma osmolality and brain water content. Furosemide alone did not affect plasma osmolality or brain water at any dose. The combination of furosemide with mannitol resulted in a greater increase in plasma osmolality than seen with mannitol alone and a greater decrease in brain water at 4 and 8 g/kg of mannitol. Conclusions The doses of mannitol and furosemide utilized were much larger than clinically applicable doses and were selected to maximize the ability to detect effect on brain water. The combination of mannitol and furosemide resulted in greater reduction of brain water content than did mannitol alone. Furosemide enhanced the effect of mannitol on plasma osmolality, resulting in a greater reduction of brain water content. Potential interaction (if any) of smaller, clinically used doses of mannitol and furosemide cannot be surmised from the current study.

Plasma Osmolality and Brain Water Content in a Rat Glioma Model

Neurosurgery ◽  
1994 ◽  
Vol 34 (3) ◽  
pp. 505-511 ◽  
Author(s):  
Thomas D. Hansen ◽  
David S. Warner ◽  
Vincent C. Traynelis ◽  
Michael M. Todd
Keyword(s):  
Water Content ◽  
Plasma Osmolality ◽  
Brain Water Content ◽  
Rat Glioma ◽  
Glioma Model ◽  
Brain Water

scholarly journals Efficacy of Danhong injection on serum concentration of TNF-α, IL-6 and NF-κB in rats with intracerebral hemorrhage

2018 ◽  
Vol 13 (1) ◽  
pp. 77-81
Author(s):  
Chen Peng ◽  
Shibo Duan ◽  
Lou Gang
Keyword(s):  
Intracerebral Hemorrhage ◽  
Water Content ◽  
Control Group ◽  
Brain Water Content ◽  
Model Group ◽  
Danhong Injection ◽  
Tnf Α ◽  
The Brain ◽  
Brain Water ◽  
Time Point

AbstractObjectiveTo investigate the efficacy of Danhong injection on the serum concentration of tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6) and nuclear factor kappa-light-chain-enhancer of activated B (NF-κB) in rats with intracerebral hemorrhage (ICH) and evaluate its therapeutic effects on inflammation and cerebral edema.MethodsSixty male Wistar rats were randomly divided into control, model and Danhong groups with 25 rats in each group. Intracerebral injection of autologous arterial blood was performed on model and Danhong groups in order to establish intracerebral hemorrhage model. Rats in the control group were given the same operation procedure without blood injection. After successfully establishing the intracerebral hemorrhage model, the rats were given Danhong (2ml/kg/d) through intraperitoneal injection. Rats in the control and model groups were given the same amount of normal saline respectively. The brain water content (BWC) and serum level of TNF-α, IL-6 and NF-κB were measured in all groups at the time points of day 1, 3, 5, 7 and 9.ResultsThe neurological deficit score (NDS) were not statistical different in days 1, 3 and 5 between the model and Danhong group (P>0.05); However, on day 7 and 9 after modeling, the NDS in the Danhong group was significant lower than that of the Model group (P<0.05). The brain water content in the model and Danhong groups were significantly elevated compared to control group (P<0.05). The brain water content was significant elevated after modeling in the model and Danhong groups on day 3 and gradually decreased over the next 6 days.The brain water content was significantly higher in the model group for days 3 to 9 compared to the Danhong group (P<0.05). Compared to the model group, the serum NF-κb was significantly lower in the Danhong group for the time point of day 3 and 5 (P<0.05); However, compared to the model group, the serum TNF-α and IL-6 levels in the Danhong group were significantly lower for each time point (P<0.05). Conclusion Danhong injection can reduce cerebral edema in rats with cerebral hemorrhage, and protect the brain nerve function. These effects may be related to its function of regulating serum TNF-α, NF-κB and IL-6 expression.

Experimental Carbon Dioxide Laser Brain Lesions and Intracranial Dynamics: Part 2

Neurosurgery ◽  
1985 ◽  
Vol 16 (4) ◽  
pp. 454-457
Author(s):  
Ernesto G. Tiznado ◽  
Hector E. James ◽  
Susan Moore
Keyword(s):  
Carbon Dioxide ◽  
White Matter ◽  
Water Content ◽  
Gray Matter ◽  
Carbon Dioxide Laser ◽  
Brain Lesions ◽  
Brain Water Content ◽  
The Impact ◽  
The Brain ◽  
Brain Water

Abstract Experimental brain lesions were created over the left parietooccipital cortex of the albino rabbit through the intact dura mater with high radiating carbon dioxide laser energy (40-W impact, 0.5-second duration, for a total time of 4 seconds on a 12.5-mm surface). The brain water content was studied 2, 6, and 24 hours after the insult. Another two groups of animals received acute therapy with either dexamethasone (1 mg/kg) or furosemide (1 mg/kg). In all groups, Evans blue extravasation uniformly extended from the impact crater into the surrounding white matter. The brain water content in the gray matter was elevated from the control value by 2 hours after impact (P &lt; 0.005) and remained elevated at 6 and 24 hours. The white matter brain water content did not increase until 6 hours after impact and remained elevated in the 24-hour group (P &lt; 0.005). After dexamethasone treatment, there was a significant decrease of water in the gray matter (P &lt; 0.01), but not in the white matter. With furosemide therapy, there was no reduction of gray or white matter brain water.

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