EFFECTS OF OVARIAN HORMONES ON THE CONTENT AND DISTRIBUTION OF CATION IN INTACT AND EXTRACTED RABBIT AND CAT UTERUS

1957 ◽  
Vol 35 (12) ◽  
pp. 1205-1223 ◽  
Author(s):  
Edwin E. Daniel ◽  
Betty N. Daniel

The uteri of rabbits and cats have been analyzed for sodium, potassium, and chloride, usually after various preliminary treatments with estrogen and progesterone. These tissues contain less potassium (50–80 meq./kg.) than striate muscle and more sodium (75–118 meq./kg.) than other highly cellular tissues. It appears that this cation composition can be attributed in part to a relatively large extracellular fluid volume (EFV).Various methods have been used to estimate the EFV in these tissues. The radiosulphate space (in vitro) does not appear to be reliable as a measure of extracellular space. The chloride space varies, but exceeds 400 ml./kg. in all cases, and in some approaches 700 ml./kg. Inulin space (in vitro) is about 60% of the chloride space, which in turn is usually smaller than the sodium space. The chloride space appears to provide the best approximation to the EFV since its volume of distribution rarely exceeds the sodium space, and since chloride (but not sodium) can be removed completely on leaching in isotonic sucrose.Calculated cellular potassium concentrations are as high as or higher (150–210 meq./l.) than in striate muscle. Apparently the low total tissue potassium concentration is a consequence of the large EFV.Appreciable quantities of sodium (20–50 meq./l.) reside outside of the chloride space in most cases, presumably in cellular water. Furthermore, a residue of sodium remains in uterine tissue after leaching in isotonic sucrose or choline chloride. With appropriate leaching procedures, an initial rapid depletion of tissue sodium is followed by a period of relatively slow loss, indicating derivation of sodium from at least two separate tissue spaces. Equilibration in isotonic potassium chloride causes nearly complete equilibration of potassium and chloride throughout tissue water, but does not remove residual sodium, suggesting chemical binding rather than Donnan distribution as the mechanism of sodium retention.The effects of estrogen and progesterone on the concentrations of cations in uterine cells are shown to be relatively small. Estrogen causes expansion of the cellular compartment relative to the extracellular space in both rabbit and cat and decreases the concentration of cation (per liter of tissue water and per liter of intracellular fluid). Progesterone treatment, given after estrogen, interfered with the ready entrance of chloride into the cellular space of rabbit uterus exposed to isotonic choline chloride. Cat uterus was not so affected, there being very little penetration of chloride even after estrogen alone.

1957 ◽  
Vol 35 (1) ◽  
pp. 1205-1223 ◽  
Author(s):  
Edwin E. Daniel ◽  
Betty N. Daniel

The uteri of rabbits and cats have been analyzed for sodium, potassium, and chloride, usually after various preliminary treatments with estrogen and progesterone. These tissues contain less potassium (50–80 meq./kg.) than striate muscle and more sodium (75–118 meq./kg.) than other highly cellular tissues. It appears that this cation composition can be attributed in part to a relatively large extracellular fluid volume (EFV).Various methods have been used to estimate the EFV in these tissues. The radiosulphate space (in vitro) does not appear to be reliable as a measure of extracellular space. The chloride space varies, but exceeds 400 ml./kg. in all cases, and in some approaches 700 ml./kg. Inulin space (in vitro) is about 60% of the chloride space, which in turn is usually smaller than the sodium space. The chloride space appears to provide the best approximation to the EFV since its volume of distribution rarely exceeds the sodium space, and since chloride (but not sodium) can be removed completely on leaching in isotonic sucrose.Calculated cellular potassium concentrations are as high as or higher (150–210 meq./l.) than in striate muscle. Apparently the low total tissue potassium concentration is a consequence of the large EFV.Appreciable quantities of sodium (20–50 meq./l.) reside outside of the chloride space in most cases, presumably in cellular water. Furthermore, a residue of sodium remains in uterine tissue after leaching in isotonic sucrose or choline chloride. With appropriate leaching procedures, an initial rapid depletion of tissue sodium is followed by a period of relatively slow loss, indicating derivation of sodium from at least two separate tissue spaces. Equilibration in isotonic potassium chloride causes nearly complete equilibration of potassium and chloride throughout tissue water, but does not remove residual sodium, suggesting chemical binding rather than Donnan distribution as the mechanism of sodium retention.The effects of estrogen and progesterone on the concentrations of cations in uterine cells are shown to be relatively small. Estrogen causes expansion of the cellular compartment relative to the extracellular space in both rabbit and cat and decreases the concentration of cation (per liter of tissue water and per liter of intracellular fluid). Progesterone treatment, given after estrogen, interfered with the ready entrance of chloride into the cellular space of rabbit uterus exposed to isotonic choline chloride. Cat uterus was not so affected, there being very little penetration of chloride even after estrogen alone.


1973 ◽  
Vol 51 (1) ◽  
pp. 22-28
Author(s):  
Joël de la Noüe ◽  
André Gagnon

In order to calculate the intracellular concentration of accumulated L-alanine, the extracellular space (inulin-14C) of frog intestine was measured. To check the validity of the technique, frog liver and gastrocnemius were used too. By scraping proximal portions of intestine, the inulin space was found to be similar (around 20% of total tissue water) in both the muscle layer and the mucosa. The mucosal epithelium is an imperfect barrier to inulin while the serosa is very permeable. These results suggest that the interstitial solute concentration is best approximated by equating it to that of the serosal solution. The in vitro inulin space, compared to the in vivo one, increases with time, as does the cellular hydration. The data obtained from measurements of extracellular space and from L-alanine uptake show that the intracellular amino acid is in a free state.


1961 ◽  
Vol 16 (1) ◽  
pp. 95-102 ◽  
Author(s):  
I. M. Taylor ◽  
W. D. Huffines ◽  
D. T. Young

An apparatus and technique for perfusion of rats' hearts is described. At 27°C hearts beat spontaneously, and the preparation is stable for periods in excess of 12 hours as judged by heart rate, EKG configuration, force of contraction, pH of perfusion medium and intracellular potassium. Carbon-14 labeled sucrose has been compared with chloride as a measure of tissue extracellular space and has been found unsatisfactory because volume of distribution for carbon-14 is larger than for chloride in most experiments. Carbon-14 labeled inulin-carboxylic acid (ICA), in contrast, appears to be a satisfactory marker for extracellular space. Distribution of ICA is complete in 1 hour. Values for intracellular electrolytes and water, derived assuming extracellularity of ICA, are: water, 2.56 α 0.14 gm/gm dry tissue; Na+ 24.36 α 14.12 mEq/kg cell water or 6.18 α 3.53 mEq/100 gm dry tissue; Cl- 23.16 α 6.70 mEq/kg cell water or 5.96 α 1.93 mEq/100 gm dry tissue; and K+ 144.69 α 7.31 mEq/kg cell water or 36.99 α 1.55 mEq/100 gm dry tissue. Chloride is not a satisfactory measure of extracellular space in the isolated perfused rat heart. Submitted on July 20, 1960


1965 ◽  
Vol 20 (5) ◽  
pp. 885-889 ◽  
Author(s):  
E. B. Brown ◽  
Richard L. Clancy

In vivo CO2 blood buffer curves determined on blood drawn from dogs breathing 100% O2, 15% CO2 in O2, and 25–30% CO2 in O2 have a distinctly lower slope than in vitro curves obtained by equilibrating blood from the same animal with 5, 15, and 30% CO2 in O2. The lower slope of the in vivo curve is due to the greater volume of distribution of bicarbonate in vivo. With hyperventilation of 10–15 min duration the in vivo curve is regularly depressed so that its slope is essentially the same as the in vitro curve. This depression is probably due to an increase in blood lactic acid. The increase in total bicarbonate in the extracellular fluid, resulting from an increase in CO2 tension, is more than can be accounted for by the increase in blood. This suggests that some source of buffer, other than blood, is available to the interstitial fluid. Note: (With the Technical Assistance of Patricia Elledge and Rita Herman) bicarbonate Submitted on October 28, 1964


1998 ◽  
Vol 42 (9) ◽  
pp. 2174-2177 ◽  
Author(s):  
Natalia Borg ◽  
Lars Ståhle

ABSTRACT Microdialysis was applied to sample the unbound drug concentration in the extracellular fluid in brain and muscle of rats given zalcitabine (2′,3′-dideoxycytidine; n = 4) or BEA005 (2′,3′-dideoxy-3′-hydroxymethylcytidine; n = 4) (50 mg/kg of body weight given subcutaneously). Zalcitabine and BEA005 were analyzed by high-pressure liquid chromatography with UV detection. The maximum concentration of zalcitabine in the dialysate (C max) was 31.4 ± 5.1 μM (mean ± standard error of the mean) for the brain and 238.3 ± 48.1 μM for muscle. The time to C max was found to be from 30 to 45 min for the brain and from 15 to 30 min for muscle. Zalcitabine was eliminated from the brain and muscle with half-lives 1.28 ± 0.64 and 0.85 ± 0.13 h, respectively. The ratio of the area under the concentration-time curve (AUC) (from 0 to 180 min) for the brain and the AUC for muscle (AUC ratio) was 0.191 ± 0.037. The concentrations of BEA005 attained in the brain and muscle were lower than those of zalcitabine, withC maxs of 5.7 ± 1.4 μM in the brain and 61.3 ± 12.0 μM in the muscle. The peak concentration in the brain was attained 50 to 70 min after injection, and that in muscle was achieved 30 to 50 min after injection. The half-lives of BEA005 in the brain and muscle were 5.51 ± 1.45 and 0.64 ± 0.06 h, respectively. The AUC ratio (from 0 to 180 min) between brain and muscle was 0.162 ± 0.026. The log octanol/water partition coefficients were found to be −1.19 ± 0.04 and −1.47 ± 0.01 for zalcitabine and BEA005, respectively. The degrees of plasma protein binding of zalcitabine (11% ± 4%) and BEA005 (18% ± 2%) were measured by microdialysis in vitro. The differences between zalcitabine and BEA005 with respect to the AUC ratio (P = 0.481), half-life in muscle (P = 0.279), and level of protein binding (P = 0.174) were not statistically significant. The differences were statistically significant in the case of the half-life in the brain (P = 0.032), clearance (P = 0.046), volume of distribution (P = 0.027) in muscle, and octanol/water partition coefficient (P = 0.019).


1972 ◽  
Vol 50 (7) ◽  
pp. 730-733 ◽  
Author(s):  
B. J. Hodgson ◽  
A. M. Kidwai ◽  
E. E. Daniel

140La3+ was taken up and tightly bound by rat myometrium. Its calculated volume of distribution was much greater than tissue water, and it was associated after cell fractionation with cellular particulates. The highest amounts were found in mitochondria. These results invalidate assumptions that La3+ is confined to the extracellular space and limited in its action to the cell surface.


1972 ◽  
Vol 42 (5) ◽  
pp. 647-649
Author(s):  
J. Patrick ◽  
P. J. Hilton

1. The extracellular space of an in vitro system of human leucocytes in an artificial extracellular fluid has been measured with Na235SO4, 131I-labelled human serum albumin and 125I-labelled polyvinylpyrrolidone of high molecular weight. 2. There was no significant difference between the space measured with Na235SO4 and 125I-labelled polyvinylpyrrolidone. The space measured with 131I-labelled human serum albumin was significantly larger than that measured with 125I-labelled polyvinylpyrrolidone. 3. High-molecular-weight 125I-labelled polyvinylpyrrolidone appears to be a useful extracellular marker for this in vitro system.


1996 ◽  
Vol 270 (1) ◽  
pp. F1-F8 ◽  
Author(s):  
P. F. Moon ◽  
M. A. Hollyfield-Gilbert ◽  
T. L. Myers ◽  
T. Uchida ◽  
G. C. Kramer

Postresuscitation organ failure may be associated with detrimental changes in body fluid compartments. We measured how shock and resuscitation acutely alters the interstitial, cellular, and plasma compartments in different organs. Nephrectomized, anesthetized rats were bled to 50 mmHg mean arterial pressure for 1 h, followed by 60 min of resuscitation to restore blood pressure using 0.9% normal saline (NS,n = 10), 7.5% hypertonic saline (HS,n = 8), 10% hyperoncotic albumin (HA, n = 8), or 7.5% hypertonic saline and 10% hyperoncotic albumin (HSA, n = 7). A 2-h 51Cr-EDTA distribution space estimated extracellular fluid volume (ECFV), and a 5-min 125I-labeled albumin distribution space measured plasma volume (PV). Total tissue water (TW) was measured from wet and dry weights; interstitial fluid volume (ISFV) and cell water were calculated. NS resuscitation required 7 times more fluid (50.9 +/- 7.7 vs. 8.6 +/- 0.7 for HA, 5.9 +/- 0.4 for HS, and 3.9 +/- 0.5 ml/kg for HSA), but there were no differences between solutions in whole animal PV, ECFV, or ISFV. Fluid shifts within tissues depended on resuscitation solution and type of tissue. TW was significantly reduced by hypertonic saline groups in heart, muscle, and liver (P < 0.05). ISFV was significantly reduced by HA groups in the skin. In all tissues, mean cell water in groups receiving HS was smaller; this was significant for heart, lung, muscle, and skin. In conclusion, 1) HS solutions mobilize fluid from cells while expanding both PV and ISFV, and 2) TW and cellular water increase with both isotonic crystalloids and hyperoncotic colloids in many tissues.


Blood ◽  
1982 ◽  
Vol 60 (3) ◽  
pp. 618-622 ◽  
Author(s):  
PP Bradley ◽  
RD Christensen ◽  
G Rothstein

We explored the effect of in vitro phagocytosis and in vivo inflammation on the MPO content of functioning neutrophils and on the ability of these cells to export active MPO into the extracellular environment. After ingestion of staphylococci, neutrophils retained 52% of their MPO and released 8% into the medium in active form; the remaining 40% of their MPO could no longer be detected. During bacterial infection induced by intradermally injecting staphylococci, neutrophils harvested from minced infected lesions contained 52% of the MPO of circulating neutrophils that had not reached the lesions. Extracellular fluid from the lesions contained active MPO secreted by the neutrophils, and concentrations of 10–45 U/ml were detected. These data demonstrate that functioning neutrophils can lose approximately half of their MPO. In vitro, 4%-8% of neutrophilic MPO appears in the extracellular space and 40% is inactivated. In vivo, the MPO content of inflammatory neutrophils also decreases, and MPO appears in the extracellular fluid in active form where it is available to participate in a variety of physiologic processes.


Blood ◽  
1982 ◽  
Vol 60 (3) ◽  
pp. 618-622 ◽  
Author(s):  
PP Bradley ◽  
RD Christensen ◽  
G Rothstein

Abstract We explored the effect of in vitro phagocytosis and in vivo inflammation on the MPO content of functioning neutrophils and on the ability of these cells to export active MPO into the extracellular environment. After ingestion of staphylococci, neutrophils retained 52% of their MPO and released 8% into the medium in active form; the remaining 40% of their MPO could no longer be detected. During bacterial infection induced by intradermally injecting staphylococci, neutrophils harvested from minced infected lesions contained 52% of the MPO of circulating neutrophils that had not reached the lesions. Extracellular fluid from the lesions contained active MPO secreted by the neutrophils, and concentrations of 10–45 U/ml were detected. These data demonstrate that functioning neutrophils can lose approximately half of their MPO. In vitro, 4%-8% of neutrophilic MPO appears in the extracellular space and 40% is inactivated. In vivo, the MPO content of inflammatory neutrophils also decreases, and MPO appears in the extracellular fluid in active form where it is available to participate in a variety of physiologic processes.


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