In vitro effects of pH and hemoglobin-oxygen saturation on plasma and erythrocyte K+ levels in blood from trout

1992 ◽  
Vol 72 (4) ◽  
pp. 1291-1296 ◽  
Author(s):  
O. B. Nielsen ◽  
G. Lykkeboe
Keyword(s):  
Hemoglobin Oxygen Saturation ◽  
Blood Samples ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Arterial Blood ◽  
Blood Ph ◽  
Effects Of Ph ◽  
Net Uptake ◽  
In Vitro Effects ◽  
K Concentration

Plasma and erythrocyte K+ were monitored during storage and tonometry of blood samples taken from resting rainbow trout, Oncorhynchus mykiss. During storage of arterial blood samples, plasma K+ concentration increased by 38% in 12 min. During extended tonometry of blood with a pH near 7.9 and full hemoglobin-bound oxygen (HbO2) saturation the erythrocytes showed a net loss of K+. Plasma K+ concentration increased from 2.9 mM to a near steady-state value of 5.6 mM. When tonometered at a pH near 7.2 and a HbO2 saturation at approximately 4% the erythrocytes took up K+, leading to a dramatic reduction in plasma K+ concentration to 0.2 mM. This net uptake was stimulated by isoprenaline and was inhibited by ouabain. It is concluded that net erythrocyte K+ uptake and loss can be induced in trout by changes in blood pH or HbO2 saturation in vitro.

scholarly journals Evaluation of blood electrolyte alterations in cats during elec-tive laparoscopic ovariectomy

2021 ◽  
Vol 26 (2) ◽  
pp. 1-8
Author(s):  
Iulia Melega ◽  
Lucia Victoria Bel ◽  
Cosmina Andreea Dejescu ◽  
Madalina Florina Dragomir ◽  
Bogdan Sevastre ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Venous Blood ◽  
Electrolyte Imbalance ◽  
Anaesthesia Induction ◽  
Blood Samples ◽  
Time Points ◽  
Blood Electrolytes ◽  
Carbon Dioxide Pneumoperitoneum ◽  
Blood Ph ◽  
K Concentration

In a clinical setting, we tested the hypothesis of whether hypercapnia developed during carbon dioxide pneumoperitoneum is associated with changes in blood electrolytes. This prospective study involved ten female cats that underwent elective laparoscopic ovariectomy. Venous blood samples for assessment of electrolytes were collected in the following sequence: T1- before anaesthesia induction, T2 - 10 minutes after anaesthesia induction, T3 - 30 minutes of pneumoperitoneum and T4 - at the end of pneumoperitoneum. Statistical analysis revealed AB disturbances associated with general anaesthesia and pneumoperitoneum, manifested with decreased blood pH, whereas blood PvCO2, PO2 and BE were increased. A constant increase of K+ concentration was recorded in all animals during pneumoperitoneum (P<0.05), whereas iMg registered a significant increase only at T3 (P<0.05). Correlations were recorded between blood pH and Na+, iCa, iMg, as well as between Na+ and Cl¯ at different time points during anaesthesia. No correlations were noted between pH and K+ or PvCO2 and K+. In conclusion, electrolyte imbalance represents a possible complication associated with laparoscopic surgery in healthy cats. However, further studies should investigate the causes involved in K+ concentration elevation.

Cerebrospinal fluid buffering during acute experimental respiratory acidosis

1962 ◽  
Vol 17 (5) ◽  
pp. 812-814 ◽  
Author(s):  
August G. Swanson ◽  
Harold Rosengren
Keyword(s):  
Carbon Dioxide ◽  
Cerebrospinal Fluid ◽  
Respiratory Acidosis ◽  
Buffering Capacity ◽  
Spinal Fluid ◽  
Brain Cells ◽  
Arterial Blood ◽  
Blood Ph

Cerebrospinal fluid (CSF) in vitro has less buffering capacity than blood since it lacks serum protein and cellular hemoglobin buffers. However, during acute respiratory acidosis CSF pH falls less than blood pH, indicating a significant in vivo spinal fluid buffering capacity. The nature of this buffering capacity was studied in anesthetized and artificially ventilated cats. Carbon dioxide tensions of 70–75 mm Hg were induced by 7% CO2 breathing. Simultaneous arterial blood and cisternal CSF samples were drawn at 0, 15, 30, 60, and 120 min. pCO2 and bicarbonate were measured with a radiometer AME-1 pH meter and tonometer, using the Astrup technique. A rapid increase in CSF bicarbonate maintained spinal fluid significantly more alkaline than blood throughout CO2 breathing, even though CSF and blood CO2 tensions were nearly equal. Intravenous bicarbonate did not alter CSF bicarbonate significantly during 2 hr. It is postulated that the buffering capacity of spinal fluid increases as a result of diffusion of preformed bicarbonate from brain cells. Submitted on March 12, 1962

scholarly journals An increased Bohr effect in sickle cell anemia

Blood ◽  
1979 ◽  
Vol 53 (3) ◽  
pp. 472-480 ◽  
Author(s):  
Y Ueda ◽  
RL Nagel ◽  
RM Bookchin
Keyword(s):  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Oxygen Affinity ◽  
Carbon Dioxide Tension ◽  
Red Cells ◽  
Bohr Effect ◽  
Ph Variation ◽  
Blood Ph ◽  
Effects Of Ph

Abstract Recent findings that hemoglobin S gelation and sickling are pH- dependent and also influence oxygen affinity suggested that the red cells containing this hemoglobin variant might show an abnormal Bohr effect. We therefore studied the effects of pH variation on the in vitro oxygen affinity of whole blood from persons with sickle cell anemia (SS) and normal donors (at 37 degrees C and constant carbon dioxide tension of 40 mm Hg). The Bohr effect in SS blood was greatly increased only between blood pH 7.4 and 7.2 (cell pH 7.2 and 7.0, a shift that strongly affects gelation), with delta log p50/deltapH= - 0.92 to -0.99 (normal = -0.42 to -0.46). Thus a drop in SS blood pH below 7.4 in tissue capillaries yields twice the normal decrease in oxygen affinity and a large release of oxygen from red cells, whose risk of sickling is high. Even mild transient acidosis would seem hazardous for patients with sickling disorders.

Role of adrenergic-dependent H+ release from red cells in acidosis induced by hypoxia in trout

1987 ◽  
Vol 252 (2) ◽  
pp. R269-R275 ◽  
Author(s):  
B. Fievet ◽  
R. Motais ◽  
S. Thomas
Keyword(s):  
Blood Lactate ◽  
Beta Blocker ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Second Phase ◽  
Beta Adrenergic ◽  
Blood Ph ◽  
Adrenergic Control ◽  
Net Uptake

The response to severe hypoxia is characterized in trout by a sudden drop in blood pH, which is of metabolic origin, and by an increase in the blood concentration of adrenaline. This acidification is biphasic in nature. The first phase of acidification is not associated with a rise in the blood lactate concentration and no longer occurs after pretreatment of the fish with a beta-blocker agent, propranolol. Thus an acid other than lactic acid is released into the blood at the onset of hypoxia and this release, which is under beta-adrenergic control, is responsible for the first phase of acidification. On the other hand the second phase of acidification is related to an increase in blood lactate and is not modified by a beta-blocker agent. We have also demonstrated that deep hypoxia promotes a rapid increase in red blood cell volume and that this cell enlargement is coincident with a large net uptake of Na+ and Cl-. In the presence of beta-blocking agents the Na+ uptake is blocked and the swelling of the cells is considerably inhibited. The residual swelling is clearly due to the chloride shift induced by both deoxygenation of hemoglobin and change in blood pH. In the light of data obtained in vitro on the effect of catecholamines on trout erythrocytes, it can be considered that the first phase of acidification occurring at the onset of hypoxia, and that is under beta-adrenergic control, is due essentially to the release of H+ by red blood cells in exchange with external sodium mediated by a beta-adrenergic-stimulated Na+-H+ exchanger.(ABSTRACT TRUNCATED AT 250 WORDS)

Normal arterial blood pH, oxygen, and carbon dioxide tensions in unanesthetized dogs

1972 ◽  
Vol 32 (1) ◽  
pp. 152-153 ◽  
Author(s):  
Eric O. Feigl ◽  
Louis G. D'Alecy
Keyword(s):  
Carbon Dioxide ◽  
Rectal Temperature ◽  
Femoral Artery ◽  
Glass Electrode ◽  
Blood Gas ◽  
Blood Samples ◽  
Arterial Blood ◽  
Blood Ph ◽  
Clark Electrode

Femoral artery blood samples from 30 unanesthetized unrestrained nonpanting dogs were analyzed. Average normal pH was 7.42 (sd 0.03), mean Po2 89.5 mm Hg (sd 4.4), and Pco2 36.8 mm Hg (sd 2.4). pH was determined with a glass electrode. Pco2 was measured using a Severinghaus electrode. Po2 was determined with a Clark-type polarographic polypropylene-covered electrode. Measurements were made at 39 C (normal dog rectal temperature). blood gas; Clark electrode; Severinghaus electrode

IN VITRO EFFECTS OF RECOMBINANT TISSUE TYPE PLASMINOGEN ACTIVATOR ON FIBRINOLYTIC AND COAGULATION PARAMETERS AND ITS PREVENTION BY SPECIFIC ANTIBODY, D-PHE-PRO-ARG-CTUCl AND APROTININ

1987 ◽  
Author(s):  
E Seifried ◽  
P Tanswell
Keyword(s):  
Fibrinolytic Therapy ◽  
Tissue Type ◽  
Blood Collection ◽  
Freezing And Thawing ◽  
Blood Samples ◽  
Hemostatic Factors ◽  
In Vitro Effects ◽  
Fibrinolytic Parameters

Monitoring of systemic effects during rt-PA therapy has shown of depletion of fibrinogen-antiplasmin, plasminogen and other hemostatic factors. Because in vitro activation of plasminogen may occur between blood collection and freezing and thawing before assaying we analysed the influence of 0,0.2, 2.0 and 10.0,ug rt-PA/ml citrate blood (final conc.) on hemostatic and fibrinolytic parameters and its inhibition by 3 different inhibitors. Addition of rt-PA to citrated whole blood without an inhibitor induced a concentration-dependent depletion of Fbg, Plgα2-Apl,α2-M, C1 - I, α2-Atrp, a loss of activity of FV, VIII,IX, XIII and alterations of the global coagulation assays. No effect of rt-PA was observed on F II, VII, X, XI, XII, AT III and Protein C. To prevent in vitro fibrinogenolysis 0.1, 0.5 and 1 mg/ml of a polyclonal sheep anti-rt-PA-antibody, 0.3, 1.0 and 10 Aimol/1 PPACK (D-Phe-Pro-Arg-CH2Cl), 75 and 150 KlU/ml aprotinin (final conc.) and saline as a control were added to pooled citrate blood.All samples containing rt-PA and/or inhibitors and/or saline were incubated for 45 min on ice, centrifuged, aliquotted, snap frozen and stored at ™20° C until analysis. Pretreatment of blood samples with anti-rt-PA IgG prevented interferences with all fibrinolytic and most clotting assays in plasma at a dose of 2 ,ug rt-PA/ ml. PPACK was of limited utility in clotting assays, but enabled correct analysis of fibrinolytic assays. Aprotinin was suitable only for a restricted range of both assay types. It is concluded that collection of blood samples on an appropriate antibody may be the most suitable procedure to get correct measurements of in-vivo effects of rt-PA on the hemostatic system in patients undergoing fibrinolytic therapy.

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