scholarly journals Total ischemia in dog hearts, in vitro 2. High energy phosphate depletion and associated defects in energy metabolism, cell volume regulation, and sarcolemmal integrity.

1981 ◽  
Vol 49 (4) ◽  
pp. 901-911 ◽  
Author(s):  
K A Reimer ◽  
R B Jennings ◽  
M L Hill
Keyword(s):  
Energy Metabolism ◽  
Cell Volume ◽  
Volume Regulation ◽  
Cell Volume Regulation ◽  
High Energy ◽  
High Energy Phosphate ◽  
Phosphate Depletion ◽  
Total Ischemia ◽  
Sarcolemmal Integrity

scholarly journals Proximal tubule volume regulation in hypo-osmotic media: intracellular K+, Na+, and Cl-.

1990 ◽  
Vol 1 (2) ◽  
pp. 211-218
Author(s):  
L Rome ◽  
C Lechene ◽  
J J Grantham
Keyword(s):  
Cell Volume ◽  
Volume Regulation ◽  
Cell Volume Regulation ◽  
Rabbit Kidney ◽  
Kidney Cortex ◽  
Volume Regulatory Decrease ◽  
Osmotic Change ◽  
Electrolyte Loss ◽  
The Difference

This study sought to measure the net loss of intracellular K+, Na+, and Cl- that accompanied isosmotic cell volume regulation in hypotonic media and to determine if electrolyte loss depended on the rate at which the extracellular osmolality was reduced. Isolated nonperfused proximal S2 segments from rabbit kidney cortex were studied in vitro. Gradual lowering of osmolality from 295 to 150 mOsm/kg at a rate of 2 mOsm/kg/min did not cause an increase in tubule cell volume until the medium osmolality decreased below 190 mOsm/kg. By contrast, tubules rapidly bathed in low osmolality media exhibited classical osmometric swelling followed by incomplete volume regulatory decrease. Volume regulation associated with gradual and rapid lowering of osmolality was accompanied by the net loss of intracellular K+, Na+, and Cl- (measured by electron probe); however, the temporal pattern of electrolyte loss depended on the rate of osmotic change. With gradual lowering of osmolality, cell K+ content did not decrease significantly until osmolality was lowered below 200 mOsm/kg, whereas Cl- was lost at the 200 mOsm/kg level and below. With rapid lowering of osmolality, cell K+ content was strikingly decreased at the 200 mOsm/kg level, but Cl- did not change appreciably until osmolality was decreased to 150 mOsm/kg. Cell Na+ content decreased in hypo-osmotic media, but the magnitude was relatively small. During volume regulation that accompanied either gradual or rapid lowering of medium osmolality from 295 to 150 mOsm/kg, intracellular osmolal gap, the difference between medium osmolality and the sum of intracellular concentrations of K+, Na+, and Cl- decreased 87 and 58 mOsm/kg, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of hemorrhagic shock on hepatic transmembrane potentials and intracellular electrolytes, in vivo

1981 ◽  
Vol 240 (3) ◽  
pp. R211-R219 ◽  
Author(s):  
M. M. Sayeed ◽  
R. J. Adler ◽  
I. H. Chaudry ◽  
A. E. Baue
Keyword(s):  
Hemorrhagic Shock ◽  
Cell Volume ◽  
Volume Regulation ◽  
Cell Volume Regulation ◽  
Shed Blood ◽  
Average Value ◽  
Transmembrane Potentials ◽  
Relative Membrane Permeability

In this study we investigated in vivo changes in hepatic cellular electrolytes and resting transmembrane potentials (Em) during hemorrhagic shock. Hepatic Na-K transport and cell volume regulation were assessed in vitro. Rats were bled and the ensuing hypotension (40 mmHg) was maintained by returning 25-30% (intermediate-shock, IS) or 55-60% (late-shock, LS) of the shed blood. We resuscitated IS rats by reinfusion of all of the remaining shed blood and Ringer's lactate solution. Hepatic cellular Na and Cl increased and K decreased progressively with shock. Resuscitation of IS rats restored cell K and Cl but not Na to preshock levels. Em decreased from the control average value of -40 (mV) to -31 in IS and -19 in LS. Em was partially restored (-36 mV) after resuscitation. We evaluated changes in relative membrane permeability to Na and K (PNa/PK) with shock by assuming Em either to be a Na-K exchange diffusion potential or due to an unequally coupled movement of Na and K. These evaluations show a lack of effect of shock (IS, with or without resuscitation) on PNa/PK. Our observations are compatible with failure of an electrogenic Na pump in shock. This may be related to loss of hepatic cell volume regulation in shock.

Hemorrhagic shock impairs myocardial cell volume regulation and membrane integrity in dogs

1987 ◽  
Vol 252 (6) ◽  
pp. H1203-H1210
Author(s):  
J. W. Horton
Keyword(s):  
Hemorrhagic Shock ◽  
Cell Volume ◽  
Volume Regulation ◽  
Membrane Integrity ◽  
Cell Volume Regulation ◽  
Calcium Entry ◽  
Tissue Water ◽  
Total Tissue

An in vitro myocardial slice technique was used to quantitate alterations in cell volume regulation and membrane integrity after 2 h of hemorrhagic shock. After in vitro incubation in Krebs-Ringer-phosphate medium containing trace [14C]inulin, values (ml H2O/g dry wt) for control nonshocked myocardial slices were 4.03 +/- 0.11 (SE) for total water, 2.16 +/- 0.07 for inulin impermeable space, and 1.76 +/- 0.15 for inulin diffusible space. Shocked myocardial slices showed impaired response to cold incubation (0 degrees C, 60 min). After 2 h of in vivo shock, total tissue water, inulin diffusible space, and inulin impermeable space increased significantly (+19.2 +/- 2.4, +8.1 +/- 1.9, +34.4 +/- 6.1%, respectively) for subendocardium, whereas changes in subepicardium parameters were minimal. Shock-induced cellular swelling was accompanied by an increased total tissue sodium, but no change in tissue potassium. Calcium entry blockade in vivo (lidoflazine, 20 micrograms X kg-1 X min-1 during the last 60 min of shock) significantly reduced subendocardial total tissue water as compared with shock-untreated dogs. In addition, calcium entry blockade reduced shock-induced increases in inulin impermeable space and inulin diffusible space. In vitro myocardial slice studies confirm alterations in subendocardial membrane integrity after 2 h of in vivo hemorrhagic shock. Shock-induced abnormalities in myocardial cell volume regulation are reduced by calcium entry blockade in vivo.

Control mechanisms in blood fluidity: role of adenosine triphosphate

1963 ◽  
Vol 18 (6) ◽  
pp. 1105-1110 ◽  
Author(s):  
L. O. Pilgeram ◽  
D. A. Loegering
Keyword(s):  
Energy Metabolism ◽  
Adenosine Triphosphate ◽  
High Energy ◽  
Control Mechanisms ◽  
High Energy Phosphate ◽  
Cellular Mechanisms ◽  
Blood Fluidity ◽  
Phosphate Linkage ◽  
Glass Surfaces

A possible role for cellular energy metabolism in the control of the blood clotting mechanism has been shown. High-energy phosphate was found to strongly inhibit the recalcification time of plasma prepared with siliconized or glass surfaces. The nucleotide, adenosine triphosphate, in crystalline form and chromatographically pure, will inhibit or completely prevent coagulation in vitro. Reactivity is based primarily on the high-energy phosphate linkage and secondarily upon the nucleoside, adenosine. The principal site of action for ATP is on an unidentified precursor of thromboplastin. Available evidence indicates an important role for energy metabolism in the cellular mechanisms which effect a control over thromboplastin generation and its possible thrombotic and arteriosclerotic sequelae. cellular control mechanisms; blood fluidity; thrombosis arteriosclerosis; aging Submitted on July 1, 1963

Hypertonic cell volume regulation in mouse thick limbs. I. ADH dependency and nephron heterogeneity

1986 ◽  
Vol 250 (6) ◽  
pp. C907-C919 ◽  
Author(s):  
S. C. Hebert
Keyword(s):  
Cell Volume ◽  
Volume Regulation ◽  
Cell Volume Regulation ◽  
Differential Interference Contrast Microscopy ◽  
Cyclic Monophosphate ◽  
Nacl Absorption ◽  
Nephron Segment ◽  
Interference Contrast Microscopy ◽  
Total Cell Volume

Differential interference contrast microscopy was used in combination with standard electrophysiological techniques in the in vitro perfused mouse medullary (mTALH) and cortical (cTALH) thick ascending limbs of Henle to evaluate the cell volume responses of these nephron segments to sudden increases in peritubular osmolality and to assess the role of antidiuretic hormone (ADH) and net NaCl absorption on hypertonic volume regulation. In the absence of CO2/HCO3- in external media, the cells of the mTALH behaved in a simple osmometric fashion, with an osmotic space equivalent to 70-80% of the total cell volume. However, in CO2/HCO3- -containing media, the cells of the mTALH, but not the cTALH, were able to increase their cell volume to the original volume after shrinkage in peritubular media made hypertonic with either NaCl or mannitol. This volume-regulatory increase response (VRI) in the mTALH was mediated by an increase in intracellular osmoles, and required peritubular ADH, at concentrations that stimulate maximally the rate of net NaCl absorption. This ADH effect on VRI could be mimicked by addition of dibutyryladenosine 3',5'-cyclic monophosphate to the bath in the absence of hormone. However, 10(-4) M luminal furosemide, a concentration that abolishes ADH-dependent NaCl absorption in the mTALH, had no effect on the VRI response. These results indicate that the cells of the mTALH, but not the cTALH, are capable of hypertonic volume regulation, that ADH (via adenosine 3',5'-cyclic monophosphate) is required for expression of the VRI response in the mTALH, and that the effects of ADH on net NaCl absorption and the VRI response in the mTALH are completely dissociable. Thus these results are consistent with a role for ADH in hypertonic VRI in the mammalian mTALH, which may operate to maintain constant cell volume in this nephron segment during antidiuresis.

Correlation between osmoregulation and cell volume regulation

1987 ◽  
Vol 252 (4) ◽  
pp. R768-R773
Author(s):  
M. A. Lang
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Osmotic Pressure ◽  
Cell Volume ◽  
Free Amino Acids ◽  
Volume Regulation ◽  
Free Amino ◽  
Cell Volume Regulation

The euryhaline crab, Callinectes sapidus, behaves both as an osmoregulator when equilibrated in salines in the range of 800 mosM and below and an osmoconformer when equilibrated in salines above 800 mosM. There exists a close correlation between osmoregulation seen in the whole animal in vivo and cell volume regulation studied in vitro. Hyperregulation of the hemolymph osmotic pressure and cell volume regulation both occurred in salines at approximately 800 mosM and below. During long-term equilibration of the crabs to a wide range of saline environments, the total concentration of hemolymph amino acids plus taurine remained below 3 mM. During the first 6 h after an acute osmotic stress to the whole animal, the hemolymph osmotic pressure and Na activity gradually decreased, whereas the free amino acids remained below 3 mM. As the hemolymph osmotic pressure decreased below approximately 850 mosM, the amino acid level began to increase to 17-25 mM. This change was primarily due to increases in glycine, proline, taurine, and alanine. The likely source of the increase in hemolymph free amino acids in vivo is the free amino acid loss from muscle cells observed during cell volume regulation in vitro.

Cell volume regulation in rat thin ascending limb of Henle's loop

1992 ◽  
Vol 263 (3) ◽  
pp. F353-F362
Author(s):  
L. F. Onuchic ◽  
I. R. Arenstein ◽  
A. G. Lopes
Keyword(s):  
Cell Volume ◽  
Volume Regulation ◽  
Osmotic Shock ◽  
Basolateral Membrane ◽  
Cell Volume Regulation ◽  
Tetraacetic Acid ◽  
Volume Regulatory Decrease ◽  
Henle's Loop ◽  
Volume Regulatory Increase

Thin ascending limb cells of Henle's loop from Wistar rats were studied with in vitro microperfusion and video-optical techniques to investigate their ability in regulating cell volume during osmotic shock and to identify mechanisms of ion transport involved in the process. These cells showed a clear volume regulatory decrease (VRD) response in hyposmotic medium, but no volume regulatory increase in hyperosmotic medium. The presence of barium in the bath abolished VRD. Removal of K+ from bath and perfusate also inhibited the VRD response. Reintroduction of K+ in hyposmotic conditions reestablished cell volume regulation. Introduction of anthracene-9-COOH to the basolateral medium blocked cell volume regulatory response. Cl- removal from perfusate and bath solutions also inhibited VRD, probably because of a significant intracellular Cl- depletion. Exposure of cells to ethylene glycol-bis(beta-aminoethyl ether)-N,N,N'N'-tetraacetic acid in perfusate and bath solutions reduced significantly Ca2+ concentration and impaired VRD. Reintroduction of Ca2+ in hyposmotic conditions restored volume regulation. The presence of ouabain in basolateral medium also inhibited VRD. These data suggest that the following mechanisms in the basolateral membrane are involved in VRD response: K+ and Cl- conductive pathways, which might be Ca2+ dependent for activation, and an Na(+)-K(+)-adenosinetriphosphatase.

Cell volume regulation of cerebrovascular endothelium in vitro

1985 ◽  
Vol 123 (1) ◽  
pp. 51-54 ◽  
Author(s):  
O. Kempski ◽  
M. Spatz ◽  
G. Valet ◽  
A. Baethmann
Keyword(s):  
Cell Volume ◽  
Volume Regulation ◽  
Cell Volume Regulation ◽  
Cerebrovascular Endothelium
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