104 Metabolic, electrolyte and acid-base parameters in blood and fluids of the reproductive tracts during in vivo maturation of bovine oocytes

2022 ◽  
Vol 34 (2) ◽  
pp. 289
Author(s):  
O. Gungor ◽  
S. Salman ◽  
S. Ranjitkar ◽  
D. Zhang ◽  
X. Tian
2021 ◽  
Author(s):  
Omer F. Gungor ◽  
Saleh Salman ◽  
Saurav Ranjitkar ◽  
Delong Zhang ◽  
Xiuchun (Cindy) Tian

Abstract Follicular fluid is the microenvironment that supports oocyte maturation and competence. Using Abbott iSTAT1™ and NanoDrop, we determined the dynamics of acid-base, electrolyte, metabolites, and total protein in venous blood, fluids of the dominant follicle (FF), oviduct (OF), and uterus (UF) during the window of oocyte maturation. Holstein heifers (n=36) were synchronized with PGF2α on Days -11 and 0, CIDR during Days -6 to 1, and GnRH given on Day 2 after 2nd PG. Samples were collected at 24h, 48h, 60h, 72h, and 78h after 2nd PG. Most electrolytes analyzed, Cl-, K+, and Ca2+ were significantly affected in blood and FF (P<0.05) by CIDR removal. Similarly, Cl- and Na+ also significantly changed in OF and UF across time. Glucose, lactate, and creatinine significantly changed across time points in FF compared to blood. Moreover, pO2, pCO2, TCO2, and pH significantly changed across time in FF. Most parameters were not significantly correlated between blood and FF across time points except for glucose, Cl- and creatinine. Furthermore, pO2 in FF was nearly 3X higher than blood, suggesting low O2 during in vitro maturation is inappropriate. In conclusion, components of the follicular fluid undergo major changes during the window of oocyte maturation.


1990 ◽  
Vol 258 (1) ◽  
pp. F69-F74 ◽  
Author(s):  
R. T. Kunau ◽  
K. A. Walker

The present studies examined the effect of three-fourths nephrectomy on the rate of acidification, i.e., total CO2 (tCO2) absorption (JtCO2) in the superficial distal tubule of the rat. Total glomerular filtration rate following three-fourths nephrectomy was 1.29 +/- 0.06 vs. 3.29 +/- 0.08 ml/min in sham controls, P less than 0.001. Systemic acid-base parameters were the same in both groups, but urine pH was lower in nephrectomized rats. In vivo microperfusion with identical isohydric solutions revealed that the JtCO2, fluid absorption (Jv), lumen-negative transepithelial potential difference (VT) were all significantly greater in the distal tubule of remnant kidneys. As the relative increase in Jv exceeded JtCO2, the perfusate tCO2 concentration increased markedly in remnant kidney distal tubules from 30.3 +/- 0.59 to 39.9 +/- 1.73 mM. To determine if the increase in tCO2 concentration accounted for the difference in JtCO2, a second control group was studied using a perfusate tCO2 concentration of 39.6 +/- 0.79 mM. Distal tubular JtCO2, Jv, and VT were significantly less in this control group than in the remnant kidney group. In separate studies, 10(-4) M amiloride was added to the perfusate used in remnant kidneys and controls studied with the elevated perfusate tCO2 concentration. The addition of 10(-4) M amiloride to the perfusate reduced VT and JtCO2. At identical values for VT, JtCO2 was higher in the distal tubule of remnant kidneys than in controls. We conclude the following. 1) The rate of acidification is increased in the distal tubule of remnant kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)


2009 ◽  
Vol 87 (6) ◽  
pp. 471-478 ◽  
Author(s):  
Norma Alva ◽  
Teresa Carbonell ◽  
Jesús Palomeque

Although clinical hypothermia is used for reducing postischemic damage, injurious effects have also been reported. To determine whether hypoxia and oxidative stress are induced by systemic deep hypothermia, we used an in vivo rat model keeping the arterial Pco2constant. Animals were divided into 4 groups: sham, 2 h deep hypothermia (21 °C), 1 h posthypothermia (rewarmed to 37 °C after 2 h deep hypothermia), and 3 h normothermia. Blood gases, portal vein blood flow, arterial pressure, and heart rate were monitored throughout the experiment. Liver enzyme antioxidant activity was also examined. The hemodynamic parameters decreased drastically during hypothermia, but were fully restored after rewarming. No changes in hepatic antioxidant activity (catalase, glutathione peroxidase, and superoxide dismutase) were observed. The redox level in liver (GSH/GSSG ratio) was preserved in hypothermia but decreased when animals were rewarmed. ALT did not increase and no evidence of tissue hypoxia was detected in liver regarding the restricted flow during hypothermia. With the described protocol, deep hypothermia is regarded as an experimental safe model.


2010 ◽  
Vol 299 (1) ◽  
pp. G255-G264 ◽  
Author(s):  
Elise S. Demitrack ◽  
Manoocher Soleimani ◽  
Marshall H. Montrose

Gastric surface pH (pHo) transiently increases in response to focal epithelial damage. The sources of that increase, either from paracellular leakage of interstitial fluid or transcellular acid/base fluxes, have not been determined. Using in vivo microscopy approaches we measured pHowith Cl-NERF, tissue permeability with intravenous fluorescent-dextrans to label interstitial fluid (paracellular leakage), and gastric epithelial intracellular pH (pHi) with SNARF-5F (cellular acid/base fluxes). In response to two-photon photodamage, we found that cell-impermeant dyes entered damaged cells from luminal or tissue compartments, suggesting a possible slow transcellular, but not paracellular, route for increased permeability after damage. Regarding cytosolic acid/base status, we found that damaged cells acidified (6.63 ± 0.03) after photodamage, compared with healthy surface cells both near (7.12 ± 0.06) and far (7.07 ± 0.04) from damage ( P < 0.05). This damaged cell acidification was further attenuated with 20 μM intravenous EIPA (6.34 ± 0.05, P < 0.05) but unchanged by addition of 0.5 mM luminal H2DIDS (6.64 ± 0.08, P > 0.05). Raising luminal pH did not realkalinize damaged cells, suggesting that the mechanism of acidification is not attributable to leakiness to luminal protons. Inhibition of apical HCO3−secretion with 0.5 mM luminal H2DIDS or genetic deletion of the solute-like carrier 26A9 (SLC26A9) Cl−/HCO3−exchanger blocked the pHoincrease normally observed in control animals but did not compromise repair of damaged tissue. Addition of exogenous PGE2significantly increased pHoin wild-type, but not SLC26A9 knockout, animals, suggesting that prostaglandin-stimulated HCO3−secretion is fully mediated by SLC26A9. We conclude that cellular HCO3−secretion, likely through SLC26A9, is the dominant mechanism whereby surface pH transiently increases in response to photodamage.


1984 ◽  
Vol 246 (4) ◽  
pp. R441-R451 ◽  
Author(s):  
N. Heisler

The contributions of transmembrane and transepithelial ion transfer processes and of nonbicarbonate buffering to the in vivo acid-base regulation have been evaluated. Model calculations were performed utilizing experimental data on transepithelial transfer of ions relevant for the acid-base regulation, the intracellular buffering properties of fish tissues, and the behavior of intracellular and extracellular pH and bicarbonate concentration with changes of temperature. The results of these studies indicate that the changes in the pK values of physiological nonbicarbonate buffers with changes in temperature support the adjustment of pH to lower values with rising temperature; however, transmembrane and transepithelial ion transfer mechanisms determine the acid-base regulation of intracellular and extracellular compartments.


Author(s):  
J.R. Lugon ◽  
G.R.M. Pereira ◽  
J.P. Strogoff-de-Matos ◽  
A.J. Peixoto

2008 ◽  
Vol 39 (1) ◽  
pp. 6-12 ◽  
Author(s):  
Conor Kilgallon ◽  
Tom Bailey ◽  
Barbara Arca-Ruibal ◽  
Martha Misheff ◽  
Declan O'Donovan

1965 ◽  
Vol 37 (7) ◽  
pp. 466-479 ◽  
Author(s):  
J. NORMAN ◽  
J.R. LEDSOME ◽  
R.J. LINDED
Keyword(s):  

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