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Body fluids and electrolytes
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Transcellular fluid is contained within specialised cavities of the body, e.g., pleural, synovial, pericardial fluids and digestive secretions, which are separated from the interstitial compartment by cell membranes of specialised tissue. This fluid is similar to interstitial fluid and is often considered to be part of the interstitial volume. At any given time, transcellular fluid is approximately one litre in volume. Figure 4.1 shows how fluids are distributed in the body.
Gastrointestinal Tract as a Major Route of Pharmaceutical Administration
Published in Shayne C. Gad, Toxicology of the Gastrointestinal Tract, 2018
Body water is distributed primarily into the following major body compartments while the total body water as a percentage of body weight varies from 50% to 70% in women and men, respectively. Extracellular fluid comprises the blood plasma and contains approximately 4.5% of the body weight, while interstitial fluid is ∼16% while lymph ∼1.2%. Interstitial fluid (30%–40%) is the sum of the fluid contents of all cells in the body. Transcellular fluid (∼2.5) includes cerebrospinal, intraocular, peritoneal, pleural, and synovial fluids as well as digestive secretions. Fat is ∼20% (Rang et al., 2016). Within each of the aqueous compartments, substances usually exist both in free solution and in bound form. Substances are transported via the circulatory system partially unbound and partly bound as noted previously. Proteins such as albumin chemically “lock” a substance which renders it pharmacologically inactive while the unbound portion of the substance is considered to be the free fraction and is the pharmacologically active portion of the substance. Plasma protein binding significantly influences both the distribution and the relationship between the pharmacological activity and the substance concentration in the plasma (Waterhouse and Farmery, 2012). As the number of available binding sites approaches saturation at higher substance concentration levels, other substances may be displaced. This displacement activity is a critical function in chemical interactions.
Body Water
Published in Flavia Meyer, Zbigniew Szygula, Boguslaw Wilk, Fluid Balance, Hydration, and Athletic Performance, 2016
Craig Horswill, Jeremy Fransen
TBW is compartmentalized into extracellular fluid (ECF) space and intracellular fluid (ICF) space. The ECF is further divided into the blood plasma found in the vascular space, and the interstitial fluid, which baths the cells but is outside of the vascular space. One other general ECF compartment that can be identified but will not be discussed further in this chapter is the transcellular space. This includes fluids in the cerebrospinal space, intraocular space, synovial space, and peritoneal and pericar-dial spaces. The total combined transcellular fluid amounts to approximately 1–2 L.
Neurotoxic effects of nephrotoxic compound diethylene glycol
Published in Clinical Toxicology, 2021
Courtney N. Jamison, Robert D. Dayton, Brian Latimer, Mary P. McKinney, Hannah G. Mitchell, Kenneth E. McMartin
In rats that developed AKI from DEG administration, we observed an increase in total CSF protein, similar to what was observed in human cases in Panama where 17 out of the 19 CSF samples had elevated protein levels [3]. An increase in protein in the CSF, suggestive of a demyelination occurring in the nervous system, is similar in appearance to conditions such as acute inflammatory demyelinating polyradiculoneuropathy or Guillain-Barré syndrome, both of which were included in the differential diagnosis during the 2006 Panama case study [3]. DGA has also been detected in the CSF of 7 out of 8 patient samples that developed neurotoxic effects from DEG-poisoning in the Panama outbreak [4]. This observation, along with the accumulation of DGA in the brain of DEG-treated rats in this study, suggest that an accumulation of the presumed toxic metabolite may play a role in the pathological and functional neurological changes that have been elucidated in this study. The primary proposed mechanism of these neurologic effects, based on nerve conduction studies by Sosa and coworkers, is a severe axonal sensorimotor neuropathy [3]. These symptoms are also comparable with other xenobiotic-induced peripheral neuropathies [3,35]. Some other suggested mechanisms of DEG neurotoxicity include transcellular fluid shifts, membrane destabilization through phospholipid or ion channel effects, acid–base derangements, or osmotic metabolite accumulation within cells [21], as well as alteration of neurofilament transport or axonal swelling from demyelination [11]. Like in the kidney, DGA was also concentrated by an unknown mechanism into the brain. The presence of brain DGA correlated with the increased CSF protein and the decreased motor function. The scope of this study could not demonstrate the order in which nephrotoxicity and neurotoxicity occur, because rats were tested for neurotoxicity only at the end of the study or after the indications of renal dysfunction were present. Studies in which rats were examined at timed intervals for the presence of nephrotoxicity and neurotoxicity would be necessary to determine if one preceded the other. Nevertheless, these studies did observe that neurotoxicity was only present in rats that also had AKI suggesting a linkage.