A Method for the Study of Cation Transport in vivo: Effects of Digoxin Administration and of Chronic Renal Failure on the Disposition of An Oral Load of Rubidium Chloride

1984 ◽  
Vol 66 (5) ◽  
pp. 569-574 ◽  
Author(s):  
N. A. Boon ◽  
J. K. Aronson ◽  
K. F. Hallis ◽  
N. J. White ◽  
A. E. G. Raine ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Cation Transport ◽  
The Body ◽  
Control Group ◽  
Loading Dose ◽  
Rubidium Chloride ◽  
Body Tissues

1. In order to study cation transport in vivo we have measured the changes in plasma and intra-erythrocytic rubidium concentrations following an oral load of rubidium chloride. The changes in plasma rubidium concentration are related to the distribution of rubidium to all the body tissues and the changes in intra-erythrocytic rubidium concentrations provide an example of rubidium uptake by one particular tissue. 2. In eight healthy volunteers pretreatment with a loading dose of digoxin (20 μg/kg) enhanced the rise in plasma rubidium concentrations and attenuated the rise in intra-erythrocytic rubidium concentrations after the oral load of rubidium chloride. 3. Ten patients with chronic renal failure, compared with a well-matched control group, were found to have changes similar to, but more marked than, those caused by digoxin, i.e. a much greater rise in plasma rubidium concentrations and a much smaller rise in intra-erythrocytic rubidium concentrations, after the oral load of rubidium chloride. 4. These findings are consistent with widespread reduction in Na+,K+-ATPase activity in subjects who have taken a loading dose of digoxin and patients with chronic renal failure. They are, therefore, consistent with the findings of previous studies in vitro and show that it is possible to demonstrate changes in cation transport in vivo.

Evidence for an Increased Generation of Prostacyclin in the Microvasculature and an Impairment of the Platelet α-Granule Release in Chronic Renal Failure

1988 ◽  
Vol 60 (02) ◽  
pp. 205-208 ◽  
Author(s):  
Paul A Kyrle ◽  
Felix Stockenhuber ◽  
Brigitte Brenner ◽  
Heinz Gössinger ◽  
Christian Korninger ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Blood Clotting ◽  
Normal Subjects ◽  
Chronic Uraemia ◽  
Wall Interaction ◽  
End Stage ◽  
Granule Release

SummaryThe formation of prostacyclin (PGI2) and thromboxane A2 and the release of beta-thromboglobulin (beta-TG) at the site of platelet-vessel wall interaction, i.e. in blood emerging from a standardized injury of the micro vasculature made to determine bleeding time, was studied in patients with end-stage chronic renal failure undergoing regular haemodialysis and in normal subjects. In the uraemic patients, levels of 6-keto-prostaglandin F1α (6-keto-PGF1α) were 1.3-fold to 6.3-fold higher than the corresponding values in the control subjects indicating an increased PGI2 formation in chronic uraemia. Formation of thromboxane B2 (TxB2) at the site of plug formation in vivo and during whole blood clotting in vitro was similar in the uraemic subjects and in the normals excluding a major defect in platelet prostaglandin metabolism in chronic renal failure. Significantly smaller amounts of beta-TG were found in blood obtained from the site of vascular injury as well as after in vitro blood clotting in patients with chronic renal failure indicating an impairment of the a-granule release in chronic uraemia. We therefore conclude that the haemorrhagic diathesis commonly seen in patients with chronic renal failure is - at least partially - due to an acquired defect of the platelet a-granule release and an increased generation of PGI2 in the micro vasculature.

187 EXPLOITATION OF IN VITRO CAPACITATION FOR NANOPARTICLE INCORPORATION WITHIN MAMMALIAN SPERMATOZOA

2016 ◽  
Vol 28 (2) ◽  
pp. 224
Author(s):  
L. Myles ◽  
C. Durfey ◽  
P. Ryan ◽  
S. Willard ◽  
J. Feugang
Keyword(s):  
Plasma Membrane ◽  
Sperm Motility ◽  
Surface Membrane ◽  
Milk Powder ◽  
Noninvasive Evaluation ◽  
Control Group ◽  
Body Tissues ◽  
Sperm Plasma Membrane

Migration and interactions of mammalian gametes occur in deep body tissues after mating, rendering difficult any in situ noninvasive evaluation of their performances with current methods. In our effort to develop an effective and real-time in vivo imaging approach, we have successfully labelled porcine gametes with self-illuminating bioluminescent and red-shifted quantum dot nanoparticles (QD) in our previous studies (Feugang et al. 2012 J. Nanobiotechnol. 10, 45; Feugang et al. 2015, J. Nanobiotechnol. 13, 38). The present effort aimed at investigating whether QD could be incorporated into spermatozoa through induced in vitro capacitation, which increases sperm plasma membrane fluidity. Fresh extended boar semen was placed on top of a Percoll gradient and centrifuged. Purified motile spermatozoa were collected and washed with pre-warmed PBS. Pelleted spermatozoa were resuspended in the modified Tris-buffered medium with BSA fraction-V (1 mg mL–1; modified Tween medium B with milk powder and BSA). Sperm aliquots (108) were supplemented or not (control) with QD only (QD+; 1 nM), QD+caffeine (2 mM), or QD+heparin (10 µg mL–1); with caffeine and heparin being used as routine capacitant agents in fertilization media. All aliquots were incubated at 38.5°C, under 5% CO2 for 0.5, 1, or 3 h. Spermatozoa were then analysed for motility characteristics and imaged for confirmation of QD-sperm interactions (bioluminescence emission) and localization (transmission electron microscope; TEM). Motility data of 5 replicates were analysed with ANOVA-2, and P < 0.05 was set as threshold of significance. Total sperm motility (TSM) significantly improved with the presence of either or both QDs and capacitant agents after 0.5 and 1 h incubations. With exception of the QD+heparin, all other groups had significantly decreased TSM after 3 h of incubation, when compared with TSM at 0.5 and 1 h. Higher proportions of progressive and rapid (≥45 µm s–1) spermatozoa were observed in the presence of both capacitant agents (P < 0.05), and only QD+heparin maintained greater proportions after 3 h. Sperm straight-line velocity significantly increased in the QD+caffeine at 0.5 h and in both QD+caffeine and QD+heparin thereafter. Sperm straightness data were increased by both caffeine and heparin during incubations. Strong bioluminescence signals were observed in spermatozoa incubated with QDs compared to the background signal seen in the control group. The TEM images revealed consistent surface membrane attachment of QDs in all QD+ groups, whereas transmembrane and intra-spermatic localizations were visible in both QD+caffeine and QD+heparin groups. We concluded that supplementations of medium containing QDs with caffeine or heparin allow the crossing of sperm plasma membrane by QD. No toxic effect of QD on sperm motility was observed, which confirmed our previous report using a similar ratio of QDs over spermatozoa. Exploration of efficient incorporation of QD into spermatozoa as a promising approach for noninvasive molecular imaging is still ongoing, as well as further sperm viability assessments. Supported by the NIH grant #5T35OD010432 and USDA-ARS Biophotonics Initiative grant #58–6402–3-0120.

Increased Inward Passive Permeability in Vitro to Sodium in Uraemic Erythrocytes

1996 ◽  
Vol 90 (1) ◽  
pp. 3-8 ◽  
Author(s):  
Dalila B. Corry ◽  
Charma C. Ellis ◽  
Michael L. Tuck
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Cytosolic Calcium ◽  
Na Efflux ◽  
The Mean ◽  
86Rb Influx ◽  
Cell Defect ◽  
External K

1. We have reported a normal sodium (Na) pump, but decreased loop-diuretic-sensitive Na efflux in erythrocytes from patients with chronic renal failure on haemodialysis, suggesting a different mode of co-transport in uraemia. 2. The present work extends these findings and examines in vitro simultaneous unidirectional and radiolabelled Na and K fluxes through the Na/K/Cl co-transport and the Na/K pump in washed erythrocytes from seven subjects with chronic renal failure and seven controls. Erythrocyte cytosolic calcium was also examined. 3. Ouabain-sensitive 86Rb influx was similar in patients and controls (1.76 ± 0.19 versus 1.72 ± 0.13 mmol h−1 litre−1 of erythrocytes) as was ouabain-sensitive 22Na efflux (3.62 ± 0.36 versus 4.04 ± 0.39 mmol h−1 litre−1 of erythrocytes). 4. Bumetanide-sensitive 86Rb and 22Na influx and 22Na efflux were measured at three concentrations (4, 8 and 12 mmol/l) of external K. In chronic renal failure, mean bumetanide-sensitive 22Na efflux was decreased at all external K concentrations compared with controls, and at physiological concentrations (4 mmol/l) external K was lower than controls (0.14 ± 0.01 versus 0.38 ± 0.05 mmol h−1 litre−1 of erythrocytes, P < 0.01). Mean bumetanide-sensitive 86Rb influx was also reduced in chronic renal failure at all external K concentrations, and at 4 mmol/l external K was lower than controls (0.13 ± 0.04 versus 0.34 ± 0.04 mmol h−1 litre−1 of erythrocytes, P < 0.01). Conversely, bumetanide-sensitive 22Na influx was markedly increased at all external K levels in chronic renal failure, and at 4 mmol/l external K values were elevated compared with controls (0.64 ± 0.18 versus 0.34 ± 0.04 mmol h−1 litre−1 of erythrocytes, P < 0.001). The mean cytosolic calcium concentration was higher in erythrocytes in chronic renal failure than controls (134.4 ± 8.6 versus 63.7 ± 5.8 nmol/l, P < 0.001). 5. Thus, in washed erythrocytes incubated in artificial media there is a markedly increased ouabain-insensitive Na influx in subjects with chronic renal failure which might be explained in part by the higher levels of cytosolic calcium. In vivo, this cell defect combined with suppression of the Na/K pump could lead to intracellular Na accumulation and play a role in uraemic complications.

scholarly journals VIABILITAS BAKTERI PROBIOTIK IN-VITRO DAN PENGARUH PEMBERIAN AIR OKSIGEN TERHADAP PERTUMBUHAN BAKTERI PROBIOTIK SECARA IN-VIVO

2007 ◽  
Vol 2 (1) ◽  
pp. 22
Author(s):  
Enok Sobariah ◽  
Ali Khomsan ◽  
Ingrid S. Surono
Keyword(s):  
Body Weight ◽  
Lactic Acid ◽  
Lactic Acid Bacteria ◽  
Day Treatment ◽  
The Body ◽  
Probiotic Bacteria ◽  
Control Group ◽  
Oxygenated Water

<p class="MsoNormal" style="margin: 0cm 12.45pt 6pt 17.85pt; text-align: justify;"><span style="font-size: 10pt;" lang="en-us" xml:lang="en-us">The aim of this study were  to identify the in-vitro tolerance of pro-biotic bacteria to acid and bile salt condition; and  to prove a hypothesis that the supplementation of oxygenated water has a positive effect on the body weight of rat and on viability of pro-biotic bacteria.  The first study was carried out at PAU Laboratory of Bogor Agricultural University, while the second study was conducted at Department of Community Nutrition of Bogor Agricultural University and Microbiology Laboratory of Indonesia Institute of Technology. Forty five rats aged 6 weeks were divided into three groups, i.e., control group without probiotic (a0), Lactobacillus casei Shirota (a1), and Lactobacillus IS-7257 (a2).  Each group (consisting of 5 rats each) has three different treatments, namely, control without oxygenated water (b0), 50 ppm oxygenated water (b2), and 80 ppm oxygenated water (b2). Oxygenated water was administered to the rats twice a day in the morning (3.25 ml) and afternoon (3.00 ml). Observation was carried out on the body  weight of the rats, fecal lactic acid bacteria, coliform, and anaerob bacteria by plate counting, for 4 periods, i.e, prior to the treatment (C0), after three-day treatment (C1), after seven-day treatment (C2), and on the 10<sup>th</sup> day treatment or three days after washed out period. The results indicated that probiotic bacteria are resistant to acid and bile acid condition. Oxygen concentration in water has a significant positive influence on the body weight of rats towards viability of probiotic bacteria (p-level &lt; 0.05).  The supplementation of  oxygenated water 50 ppm significantly increase the population of viable fecal lactic acid bacteria in L. casei Shirota and Lactobacillus IS-7257 groups after 3 and 7 days of treatment.  Lactobacillus IS-7257 gave better response than L. casei Shirota. The supplementation of oxygenated water 80 ppm significantly reduces the fecal coliform in-vivo in both L. casei Shirota and Lactobacillus IS-7257 groups (p-level &lt; 0.05).</span></p>

Role of nitric oxide resistance in erythropoietin-induced hypertension in rats with chronic renal failure

1996 ◽  
Vol 271 (1) ◽  
pp. E113-E122 ◽  
Author(s):  
N. D. Vaziri ◽  
X. J. Zhou ◽  
F. Naqvi ◽  
J. Smith ◽  
F. Oveisi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Magnesium Concentration ◽  
Induced Hypertension ◽  
Group A

We studied the mechanism of erythropoietin (EPO)-induced hypertension (HTN) in rats with chronic renal failure (CRF). After partial nephrectomy, rats were randomized into four groups. Group A received EPO, 150 U/kg, two times weekly for 6 wk to prevent anemia; group B received placebo injections and became anemic; group C received EPO but was kept anemic by dietary iron deficiency; and group D received placebo and regular transfusions to match hematocrit (Hct) in group A. Blood pressure (BP), Hct, platelet cytosolic calcium ([Ca2+]i) and magnesium concentration, and pressor and vasodilatory responses were determined. By design, Hct in groups A and D were comparable and significantly greater (P < 0.01) than in groups B and C. Despite divergent Hct values, the EPO-treated groups A and C showed a significant rise in BP compared with the placebo-treated groups B and D. HTN occurred whether EPO therapy was begun immediately or 4 wk after nephrectomy. EPO therapy augmented the elevation of basal [Ca2+]i and restored the defective thrombin-mediated rise of platelet [Ca2+]i in CRF animals. EPO therapy did not alter caudal artery contraction in response to either 68 mM K(+)-induced depolarization, angiotensin II or alpha 1-agonist, methoxamine in vitro, or the pressor response to angiotensin II in vivo. However, EPO therapy impaired the hypotensive response to nitric oxide (NO) donors, sodium nitroprusside and S-nitroso-N-acetyl-D,L-penicillamine, and reversed the CRF-induced upregulation of guanosine 3',5'-cyclic monophosphate production by thoracic aorta in vitro. Thus EPO-induced HTN in CRF rats is Hct independent and is associated with and perhaps causally related to increased basal and stimulated [Ca2+]i and impaired vasodilatory response to NO.

scholarly journals Renal synthesis of arginine in chronic renal failure: In vivo and in vitro studies in rats with 5/6 nephrectomy

1993 ◽  
Vol 44 (4) ◽  
pp. 676-683 ◽  
Author(s):  
Nadine Bouby ◽  
Christine Hassler ◽  
Philippe Parvy ◽  
Lise Bankir
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
In Vitro Studies

Cation transport abnormalities in vivo in untreated essential hypertension

1986 ◽  
Vol 70 (6) ◽  
pp. 611-616 ◽  
Author(s):  
Nicholas A. Boon ◽  
Jeffrey K. Aronson ◽  
Keith F. Hallis ◽  
David G. Grahame-Smith
Keyword(s):  
Renal Failure ◽  
Essential Hypertension ◽  
Chronic Renal Failure ◽  
Oral Administration ◽  
Matched Control ◽  
Cation Transport ◽  
Short Term ◽  
Sodium Potassium ◽  
Digoxin Therapy

1. In order to study cation transport in vivo we have measured the changes in plasma and intra-erythrocytic rubidium concentrations after the oral administration of rubidium chloride. 2. In this paper we describe our findings in 22 patients with untreated essential hypertension, compared with the findings in 22 carefully matched control subjects. Our findings in patients receiving short-term digoxin therapy and in patients with chronic renal failure are also included for comparison. 3. Whereas the findings in patients receiving digoxin and in patients with chronic renal failure are compatible with a widespread reduction in sodium, potassium-ATPase activity in vivo, the findings in patients with untreated essential hypertension are not. 4. Further analysis of the data and a similar study of the disposition of 42K after the intravenous administration of 42KC1 suggest that in vivo net cation transport is enhanced in the erythrocytes of patients with untreated essential hypertension.

Astatine-211 labelled a small molecule peptide: specific cell killing in vitro and targeted therapy in a nude-mouse model

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Weihao Liu ◽  
Yu Tang ◽  
Huan Ma ◽  
Feize Li ◽  
Yingjiang Hu ◽  
...  
Keyword(s):  
Small Molecule ◽  
Cell Killing ◽  
The Body ◽  
Control Group ◽  
Specific Cell ◽  
Step Method ◽  
Nude Mouse Model ◽  
Tissue Samples

AbstractExtensive interest in the development of α-emitting radionuclides astatine-211 (211At) stems from the potential superiority for the treatment of smaller tumors, disseminated disease, and metastatic disease. VP2, a small molecule fusion peptide, can specifically bind to the VPAC1 receptor which is over-expressed in malignant epithelial tumors. In our recent study, we performed the preparation of 211At labelled VP2 through a one-step method. In this work, we explored the targeted radionuclide therapy with [211At]At-SPC-VP2 in vitro and in vivo. The cytotoxicity and specific cell killing of [211At]At-SPC-VP2 were evaluated using the CCK-8 assay. Compared with the [211At]NaAt, the VPAC1-targeted radionuclide compound [211At]At-SPC-VP2 showed more effective cytotoxicity in vitro. Targeted radioactive therapy trial was carried out in non-small-cell lung cancer (NSCLC) xenograft mice. For the therapy experiment, 4 groups of mice were injected via the tail vein with 370 kBq, 550 kBq, 740 kBq, 3 × ∼246 kBq of [211At]At-SPC-VP2, of which the second and third injections were given 4 and 8 days after the first injection, respectively. As controls, animals were treated with saline or 550 kBq [211At]NaAt. The body weight and tumor size of mice were monitored before the administration and every 2 days thereafter. Cytotoxic radiation of partial tissue samples such as kidneys, liver and stomach of mice were assessed by immunohistochemical examination. The tumor growth was inhibited and significantly improved survival was achieved in mice treated with [211At]At-SPC-VP2, two-fold prolongation of survival compared with the control group, which received normal saline or 550 kBq [211At]NaAt. No renal or hepatic toxicity was observed in the mice receiving [211At]At-SPC-VP2, but gastric pathological sections showed 211At uptake in stomach resulting in later toxicity, highlighting the importance of further enhancing the stability of labelled compounds.

Thyrotrophin-releasing hormone responsiveness and degradation in children with chronic renal failure: effect of time of evolution

1982 ◽  
Vol 99 (4) ◽  
pp. 508-516 ◽  
Author(s):  
C. Marti Henneberg ◽  
J. M. Domenech ◽  
E. Montoya
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Normal Subjects ◽  
Serum Levels ◽  
Significant Negative Correlation ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Degradation Rates

Abstract. In order to study the hypothalamic-pituitarythyroid function in children with chronic renal failure (CRF), the serum levels of l-thyroxine (l-T4), l-triiodothyronine (l-T3), reverse T3 (rT3), thyrotrophin (TSH) and prolactin (Prl) were measured by radioimmunoassay (RIA). Values were compared with those of normal subjects. Low levels of l-T4 were present in CRF patients as compared to controls. l-T3 was also found to be low but less than l-T4, and rT3 was lower in patients with long evolution. No alterations were observed in TSH basal levels, whereas Prl values in patients were high. After thyrotrophin-releasing hormone (TRH) administration, TSH and Prl rose to similar levels in both groups, but high values were maintained throughout (120 min) in CRF. A significant negative correlation was found between the peak rise of the TSH response and the CRF evolution time. The l-T3 response to TRH administration (120 min) was similar in both CRF and controls. The rate of in vivo and in vitro exogenous TRH degradation was decreased in patients with CRF or by their sera, respectively. Our data seem to confirm that the hypothyroid syndrome described in CRF patients is of hypothalamic origin, and the low in vivo and in vitro TRH degradation rates are a consequence of this state.

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