Ion-regulation, acid/base-balance, kidney function, and effects of hypoxia in coho salmon, Oncorhynchus kisutch, after long-term acclimation to different salinities

Aquaculture ◽  
2020 ◽  
Vol 528 ◽  
pp. 735571 ◽  
Author(s):  
Christian Damsgaard ◽  
Monica McGrath ◽  
Chris M. Wood ◽  
Jeffrey G. Richards ◽  
Colin J. Brauner
1971 ◽  
Vol 28 (12) ◽  
pp. 1899-1904 ◽  
Author(s):  
Gary Wedemeyer

Changes in gill function, acid–base balance and pituitary activation occurring during standard 200 ppm formalin treatments of juvenile rainbow trout (Salmo gairdneri) and coho salmon (Oncorhynchus kisutch) were compared. Plasma Cl−, Ca++, total CO2, and interrenal vitamin C in the trout declined continuously and in proportion to the exposure time, but the salmon were able to maintain these metabolic parameters at approximately initial levels. Blood pH and alkaline reserve regulation of the salmon was also less affected by formalin treatments, especially during prolonged exposures. The oxygen consumption of both species was depressed, but substantially more so in the trout than could be accounted for by decreased ventilation rates. Little frank hemolysis occurred in either species, but there was a significant bilirubinemia in the trout.


1971 ◽  
Vol 28 (4) ◽  
pp. 606-608 ◽  
Author(s):  
Gary Wedemeyer ◽  
K. Chatterton

Overlapping Gaussian distribution curves were resolved into normal ranges for 1800 clinical test values obtained from caudal arterial blood or plasma of more than 1000 juvenile coho salmon (Oncorhynchus kisutch) held under defined conditions of diet and temperature. Estimated normal blood chemistry ranges were bicarbonate, 9.5–12.6 mEq/liter; blood urea nitrogen (BUN), 0.9–3.4 mg/100 ml; chloride, 122–136 mEq/liter; cholesterol, 88–262 mg/100 ml;pCO2, 2.6–6.1 mm Hg (10 C); glucose, 41–135 mg/100 ml; hematocrit, 32.5–52.5%; hemoglobin, 6.5–9.9 g/100 ml; total protein, 1.4–4.3 g/100 ml; blood pH (10 C), 7.51–7.83. The calculated range of normal acid–base balance vs. water temperature is also presented.


2016 ◽  
Vol 24 (3) ◽  
pp. 116-121
Author(s):  
김지용 ◽  
남상욱 ◽  
김영미 ◽  
이윤진 ◽  
이훈상 ◽  
...  

2000 ◽  
Vol 279 (3) ◽  
pp. F459-F467 ◽  
Author(s):  
Gheun-Ho Kim ◽  
Stephen W. Martin ◽  
Patricia Fernández-Llama ◽  
Shyama Masilamani ◽  
Randall K. Packer ◽  
...  

Increased systemic acid intake is associated with an increase in apical Na/H exchange in the renal proximal tubule mediated by the type 3 Na/H exchanger (NHE3). Because NHE3 mediates both proton secretion and Na absorption, increased NHE3 activity could inappropriately perturb Na balance unless there are compensatory changes in Na handling. In this study, we use semiquantitative immunoblotting of rat kidneys to investigate whether acid loading is associated with compensatory decreases in the abundance of renal tubule Na transporters other than NHE3. Long-term (i.e., 7-day) acid loading with NH4Cl produced large decreases in the abundances of the thiazide-sensitive Na-Cl cotransporter (TSC/NCC) of the distal convoluted tubule and both the β- and γ-subunits of the amiloride-sensitive epithelial Na channel (ENaC) of the collecting duct. In addition, the renal cortical abundance of the proximal type 2 Na-dependent phosphate transporter (NaPi-2) was markedly decreased. In contrast, abundances of the bumetanide-sensitive Na-K-2Cl cotransporter of the thick ascending limb and the α-subunit of ENaC were unchanged. A similar profile of changes was seen with short-term (16-h) acid loading. Long-term (7-day) base loading with NaHCO3resulted in the opposite pattern of response with marked increases in the abundances of the β- and γ-subunits of ENaC and NaPi-2. These adaptations may play critical roles in the maintenance in Na balance when changes in acid-base balance occur.


2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Christian Damsgaard ◽  
Monica McGrath ◽  
Chris M. Wood ◽  
Jeffrey G. Richards ◽  
Colin J. Brauner

2020 ◽  
Vol 9 (5) ◽  
pp. 399-405 ◽  
Author(s):  
Hiroki Nakano ◽  
Toshiyuki Nagai ◽  
Yasuyuki Honda ◽  
Satoshi Honda ◽  
Naotsugu Iwakami ◽  
...  

Background: Acid-base balance can change as a result of pulmonary oedema and low tissue perfusion in acute heart failure patients. However, its long-term prognostic significance remains to be clarified. Methods: We prospectively examined a cohort of 472 consecutive acute heart failure patients who underwent arterial blood gas analysis on admission between January 2013 and May 2016. Acidaemia, alkalaemia and normal range of base excess were defined as pH <7.38, >7.42 and −2 to 2 mEq/L, respectively. The primary outcome was all-cause death. Results: During a median follow-up period of 714 days, 101 patients died. Although there was no difference in mortality among patients with acidaemia, normal pH and alkalaemia ( p = 0.92), patients with high base excess had the highest mortality compared with others. Multivariable Cox proportional hazard models revealed that high base excess was an independent determinant of mortality (hazard ratio 1.83, 95% confidence interval 1.08–3.13 (high versus normal base excess), hazard ratio 0.81, 95% confidence interval 0.47–1.41 (low versus normal base excess)), even after adjustment for significant prognostic covariates. Furthermore, regarding mortality stratified by base excess and carbon dioxide partial pressure (pCO2), patients with high base excess (>2.1 mEq/L) and high pCO2 (>40 mmHg) had the highest mortality compared with others. Conclusions: High base excess, but not low base excess, on admission was associated with long-term mortality in acute heart failure patients, indicating the importance of evaluating acid-base balance on admission by base excess for stratifying the risk of mortality in patients with acute heart failure.


2008 ◽  
Vol 107 (1) ◽  
pp. 264-269 ◽  
Author(s):  
Necmiye Hadimioglu ◽  
Iman Saadawy ◽  
Tayyup Saglam ◽  
Zeki Ertug ◽  
Ayhan Dinckan

1973 ◽  
Vol 30 (2) ◽  
pp. 296-298 ◽  
Author(s):  
Gary A. Wedemeyer ◽  
A. J. Ross

The influence of diet ingredient on the morbidity and biochemical pathogenesis of corynebacterial kidney disease was investigated using juvenile coho salmon (Oncorhynchus kisutch) fed the Abernathy dry ration made up with either corn gluten or cottonseed meal (isoprotein, isocaloric substitution). Evaluation of incidence of infection, pituitary activation and aspects of carbohydrate metabolism, acid-base balance, renal function, and hematopoietic activity showed that the actual disease incidence was about the same for both diets but the nonspecific stress of infection was more severe in fish fed the corn gluten.Discriminant function calculations combining four physiological parameters gave a probability of 0.86 for successfully diagnosing infected fish on the basis of these blood chemistry tests.


2019 ◽  
Vol 1 (1) ◽  
pp. 59-73 ◽  
Author(s):  
Magomedali Magomedaliev ◽  
Daniil Korabelnikov ◽  
Sergey Khoroshilov

Mutual complications of impaired lung and kidney function in severe pneumonia (SP) complicated by acute kidney damage (AKP) are considered. The lungs and kidneys perform some similar functions, such as detoxification and regulation of acid-base balance. Lung damage is complicated by dysfunction or impaired renal function, and vice versa, AKI depressively affects lung function. Initially, all organs and tissues, including the kidneys, suffer from hypoxemic respiratory failure. SP is characterized by increased production of inflammatory mediators, decay products of microorganisms and their toxins and ejection them into the bloodstream. Endothelial vascular insufficiency, disseminated microvascular thrombosis, central hemodynamic disorders develop, and as a result, multiple organ failure develops. With the development of AKI, the elimination of uremic toxins and water is disrupted, hyperhydration is formed with an increase in the volume of extravascular water in the lungs on the background of the already existing broken airborne barrier. Uremic toxins depressively affect the heart muscle on the background of an acute pulmonary heart. There is evidence of a negative effect of mechanical ventilation on kidney function, and, conversely, of an adverse effect of AKI on the need and duration of ventilation. The progression of TP and AKP disrupts the acid - base balance due to excess CO2, impaired H+ ion release, and impaired synthesis of HCO3. The pathophysiological mechanisms underlying these relationships are complex, and their effect on the course of the disease is significant.


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