Intracellular Volume Registration

2009 ◽  
Author(s):  
Shin Yoshizawa ◽  
Satoko Takemoto ◽  
Miwa Takahashi ◽  
Makoto Muroi ◽  
Sayaka Kazami ◽  
...  
Keyword(s):  
Volume Registration ◽  
Intracellular Volume

Isobaric volume registration in the assessment of detrusor instability

1983 ◽  
Vol 2 (3) ◽  
pp. 205-212 ◽  
Author(s):  
Magnus Fall ◽  
Björn-Erik Erlandson
Keyword(s):  
Detrusor Instability ◽  
Volume Registration

Disorders of Antidiuretic Hormone Secretion

1992 ◽  
Vol 3 (2) ◽  
pp. 370-378 ◽  
Author(s):  
Joyce Batcheller
Keyword(s):  
Diabetes Insipidus ◽  
Antidiuretic Hormone ◽  
Critically Ill ◽  
Blood Volume ◽  
Urine Output ◽  
Hormone Secretion ◽  
Team Approach ◽  
Antidiuretic Hormone Secretion ◽  
Intracellular Volume ◽  
Age And Sex

Depending upon the age and sex of a human, water constitutes 55% to 80% of the body’s weight and provides a milieu vital for survival. Water imbalance is common among the critically ill. Excessive increases or decreases in body water can be lethal. There are numerous pathologic and iatrogenic causes for water imbalance, the most troublesome being disorders of antidiuretic hormone (ADH) secretion. Antidiuretic hormone plays a pivotal role in conserving water by increasing reabsorption of water by the kidney. Without the influence of ADH (as is seen in diabetes insipidus), a person would be required to ingest between 5 and 15 L of water daily to match urinary losses. Conversely, excessive ADH secretion would reduce urine output in adults to as little as 500 mL per day, dangerously diluting blood volume and expanding intracellular volume. This is what causes the symptoms of the syndrome of inappropriate ADH (SIADH). The care of patients who are critically ill and have disorders of ADH secretion can be challenging. The challenge lies in the recognition and treatment of the disorder. A collaborative team approach helps patients achieve and maintain the delicate balance of body fluids

Na-K-Cl cotransport regulates intracellular volume and monolayer permeability of trabecular meshwork cells

1995 ◽  
Vol 268 (4) ◽  
pp. C1067-C1074 ◽  
Author(s):  
M. E. O'Donnell ◽  
J. D. Brandt ◽  
F. R. Curry
Keyword(s):  
Trabecular Meshwork ◽  
Ethacrynic Acid ◽  
Vascular Endothelial Cells ◽  
Critical Role ◽  
Cell Types ◽  
Cell Monolayers ◽  
Aqueous Humor Outflow ◽  
Trabecular Meshwork Cells ◽  
Intracellular Volume ◽  
Underlying Mechanisms

The trabecular meshwork (TM) of the eye plays a critical role in modulating intraocular pressure (IOP) through regulation of aqueous humor outflow, although the underlying mechanisms remain unknown. Ethacrynic acid, an agent known to inhibit Na-K-Cl cotransport of a number of cell types, recently has been reported to increase aqueous outflow and lower IOP through an unknown effect on the TM. In vascular endothelial cells and a variety of other cell types, the Na-K-Cl cotransporter functions to regulate intracellular volume. The present study was conducted to evaluate TM cells for the presence of Na-K-Cl cotransport activity and to test the hypothesis that modulation of cotransport activity alters intracellular volume and, consequently, permeability of the TM. We demonstrate here that bovine and human TM cells exhibit robust Na-K-Cl cotransport activity that is inhibited by bumetanide and by ethacrynic acid. Our studies also show that TM cell Na-K-Cl cotransport is modulated by a variety of hormones and neurotransmitters. Inhibition of the cotransporter either by bumetanide, ethacrynic acid, or inhibitory hormones reduces TM intracellular volume, whereas stimulatory hormones increase cell volume. In addition, shrinkage of the cells by hypertonic media stimulates cotransport activity and initiates a subsequent regulatory volume increase. Permeability of TM cell monolayers, assessed as transmonolayer flux of [14C]sucrose, is increased by hypertonicity-induced cell shrinkage and by bumetanide. These findings suggest that Na-K-Cl cotransport of TM cells is of central importance to regulation of intracellular volume and TM permeability. Defects of Na-K-Cl cotransport may underlie the pathophysiology of glaucoma.

scholarly journals Cross-Modal Attention for MRI and Ultrasound Volume Registration

2021 ◽  
pp. 66-75
Author(s):  
Xinrui Song ◽  
Hengtao Guo ◽  
Xuanang Xu ◽  
Hanqing Chao ◽  
Sheng Xu ◽  
...  
Keyword(s):  
Volume Registration

scholarly journals Moderate-to-severe ischemic conditions increase activity and phosphorylation of the cerebral microvascular endothelial cell Na+-K+-Cl− cotransporter

2005 ◽  
Vol 289 (6) ◽  
pp. C1492-C1501 ◽  
Author(s):  
Shahin Foroutan ◽  
Julien Brillault ◽  
Biff Forbush ◽  
Martha E. O’Donnell
Keyword(s):  
Atpase Activity ◽  
Brain Edema ◽  
Artery Occlusion ◽  
Luciferase Assay ◽  
Microvascular Endothelial Cell ◽  
Atp Content ◽  
Edema Formation ◽  
Hypoxic Conditions ◽  
Intracellular Volume ◽  
Microvascular Endothelial

Brain edema that forms during the early stages of stroke involves increased transport of Na+ and Cl− across an intact blood-brain barrier (BBB). Our previous studies have shown that a luminal BBB Na+-K+-Cl− cotransporter is stimulated by conditions present during ischemia and that inhibition of the cotransporter by intravenous bumetanide greatly reduces edema formation in the rat middle cerebral artery occlusion model of stroke. The present study focused on investigating the effects of hypoxia, which develops rapidly in the brain during ischemia, on the activity and expression of the BBB Na+-K+-Cl− cotransporter, as well as on Na+-K+-ATPase activity, cell ATP content, and intracellular volume. Cerebral microvascular endothelial cells (CMECs) were assessed for Na+-K+-Cl− cotransporter and Na+-K+-ATPase activities as bumetanide-sensitive and ouabain-sensitive 86Rb influxes, respectively. ATP content was assessed by luciferase assay and intracellular volume by [3H]-3-O-methyl-d-glucose and [14C]-sucrose equilibration. We found that 30-min exposure of CMECs to hypoxia ranging from 7.5% to 0.5% O2 (vs. 19% normoxic O2) significantly increased cotransporter activity as did 7.5% or 2% O2 for up to 2 h. This was not associated with reduction in Na+-K+-ATPase activity or ATP content. CMEC intracellular volume increased only after 4 to 5 h of hypoxia. Furthermore, glucose and pyruvate deprivation increased cotransporter activity under both normoxic and hypoxic conditions. Finally, we found that hypoxia increased phosphorylation but not abundance of the cotransporter protein. These findings support the hypothesis that hypoxia stimulation of the BBB Na+-K+-Cl− cotransporter contributes to ischemia-induced brain edema formation.

Histological Studies on the Genus Fucus

1968 ◽  
Vol 3 (1) ◽  
pp. 1-16
Author(s):  
MARGARET E. MCCULLY
Keyword(s):  
Inorganic Carbon ◽  
Alginic Acid ◽  
Light And Electron Microscopy ◽  
Epidermal Cells ◽  
Membrane Interface ◽  
Histological Studies ◽  
Basal Nuclei ◽  
Golgi System ◽  
Intracellular Volume

The fine structure of the epidermal cells of the vegetative Fucus thallus has been examined in material fixed with acrolein. These cells are highly polarized, with basal nuclei and chloroplasts, a hypertrophied perinuclear Golgi system, and a much convoluted wall/plasma membrane interface. Much of the intracellular volume is occupied by single membrane-bounded vesicles containing alginic acid, fucoidin and polyphenols. The chloroplasts were examined by light and electron microscopy and shown to contain structured inclusions not previously described in Fucus plastids. It is suggested on the basis of their morphology that the epidermal cells may be specialized for the absorption of inorganic carbon and sulphate from the outside of the plant and for the secretion of alginic acid, fucoidin and polyphenols. The possible role of these cells in the prevention of desiccation and in osmoregulation is discussed.

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