Effects of acute temperature change, in vivo and in vitro, on the acid–base status of blood from yellowfin tuna (Thunnus albacares)

1992 ◽  
Vol 70 (4) ◽  
pp. 654-662 ◽  
Author(s):  
Richard W. Brill ◽  
Peter G. Bushnell ◽  
David R. Jones ◽  
Manabu Shimizu

In most fishes, blood acid–base regulation following a temperature change involves active adjustments of gill ion-exchange rates which take hours or days to complete. Previous studies have shown that isolated blood from skipjack tuna, Katsuwonus pelamis, and albacore, Thunnus alalunga, had rates of pH change with temperature (in the open system) equivalent to those necessary to retain net protein charge in vivo (≈ −0.016 ΔpH∙ °C−1). It was postulated that this is due to protons leaving the hemoglobin combining with plasma bicarbonate [Formula: see text], which is removed as gaseous CO2, and that this ability evolved so that tunas need not adjust gill ion-exchange rates to regulate blood pH appropriately following ambient temperature changes. We reexamined this phenomenon using blood and separated plasma from yellowfin tuna, Thunnus albacares. Unlike previous studies, our CO2 levels (0.5 and 1.5% CO2) span those seen in yellowfin tuna arterial and venous blood. Various bicarbonate concentrations [Formula: see text] were obtained by collecting blood from fully rested as well as vigorously exercised fish. We use our in vitro data to calculate basic physiochemical parameters for yellowfin tuna blood: nonbicarbonate buffering (β), the apparent first dissociation constant of carbonic acid (pKapp), and CO2 solubility (αCO2). We also determined the effects of acute temperature change on arterial pH, [Formula: see text], and partial pressures of O2 and CO2in vivo. The pH shift of yellowfin tuna blood subjected to a closed-system temperature change did not differ from previous studies of other teleosts (≈ −0.016 ΔpH∙ °C−1). The pH shift in blood subjected to open-system temperature change was Pco2 dependent and lower than that in skipjack tuna or albacore blood in vitro, but identical with that seen in yellowfin tuna blood in vivo. However, pH adjustments in vivo were caused by changes in both [Formula: see text] and Pco2. The exact mechanisms responsible for these changes remain to be elucidated.

1992 ◽  
Vol 70 (6) ◽  
pp. 1200-1210 ◽  
Author(s):  
A. P. Farrell ◽  
P. S. Davie ◽  
C. E. Franklin ◽  
J. A. Johansen ◽  
R. W. Brill

An in situ heart preparation perfused with oxygenated saline was used to examine cardiac performance at 25 °C in yellowfin tuna (Thunnus albacares) and skipjack tuna (Katsuwonus pelamis). Heart rates (91–172 bpm in skipjack tuna and 101–157 bpm in yellowfin tuna) were comparable to those measured in vivo, and physiological stroke volumes were possible in yellowfin tuna with subambient filling pressures. In yellowfin tuna, maximum stroke volume and cardiac output were similar to the values obtained in vivo with spinally blocked animals; mean output pressures (up to 145 cmH2O, 1 cmH2O = 0.098 kPa) could exceed in vivo values without a major decrease in the resting cardiac output (homeometric regulation). In contrast, saline-perfused skipjack tuna hearts could not develop physiological output pressures without compromising cardiac output, with cardiac output being only 63% of the in vivo value at an output pressure near the in vivo ventral aortic pressure. The poor performance of the skipjack tuna heart is attributed to limited oxygen diffusion through the thicker walled ventricle. We conclude that the tuna heart is more dependent on its coronary circulation for normal function than the hearts of other fishes examined thus far. The coronary circulation was perfused with saline at various flow rates in isolated hearts from skipjack tuna to develop a pressure–flow relationship for the intact circulation. Coronary resistance reached a minimum of 24 cmH2O∙min∙g ventricular mass/mL at a flow rate of 2 mL/(min∙g ventricular mass) with perfusion pressure about 40 cmH2O. In vivo coronary blood flow was estimated from the pressure–flow relationship as 0.67 mL/(min∙g ventricular mass). Injections of adrenaline, noradrenaline, and phenylephrine into coronary circulation under constant flow conditions increased perfusion pressure, indicating the possibility of α-adrenergic vasoconstriction.


2017 ◽  
Vol 14 (3) ◽  
pp. 313 ◽  
Author(s):  
Budi Nugraha ◽  
Enjah Rahmat

Tulisan ini menyajikan tentang status perikanan huhate di Bitung meliputi deskripsi unit penangkapan, daerah penangkapan, komposisi hasil tangkapan, catch per unit of effort, dan ukuran ikan pertama kali tertangkap. Data dikumpulkan selama tahun 2004 sampai dengan 2005. Hasil penelitian menunjukkan bahwa huhate yang terdapat di Bitung dioperasikan dengan kapal penangkapan yang terbuat dari kayu berukuran 50 sampai dengan 80 GT. Daerah penangkapan di sekitar lokasi rumpon di Laut Sulawesi dan Laut Maluku. Hasil tangkapan yang diperoleh terdiri atas cakalang (Katsuwonus pelamis), madidihang (Thunnus albacares), baby tuna (Thunnus spp.), dan tongkol (Auxis spp.) serta hasil tangkapan sampingan yaitu lemadang (Coryphaena hippurus) dan sunglir (Elagatis bipinnulatus). Hasil analisis catch per unit of effort diperoleh bahwa nilai catch per unit of effort baby tuna (Thunnus spp.) mengalami kenaikan pada bulan Agustus 2004, dan cakalang (Katsuwonus pelamis) mengalami kenaikan pada bulan September 2004. Hasil analisis terhadap ukuran pertama kali cakalang (Katsuwonus pelamis) tertangkap oleh huhate 49,3 FLcm. Ukuran ini lebih panjang dibandingkan ukuran pertama kali cakalang (Katsuwonus pelamis) matang gonad. Sedangkan hasil analisis terhadap ukuran pertama kali madidihang (Thunnus albacares) tertangkap oleh huhate 51,6 FLcm. Ukuran ini lebih pendek dibandingkan ukuran pertama kali madidihang (Thunnus albacares) matang gonad. This paper presents the status of pole and line fishery in Bitung of North Sulawesi, consisting of description of fishing gear, fishing ground, catch composition, catch per unit of effort, and length at first capture. Data were collected during the period of 2004 until 2005. Results show that the pole and line in Bitung operated by wooden vessels of 50 until 80 GT. The fishing grounds were the waters around FADs location in Sulawesi Sea and Maluku Sea. Catch composition consists of skipjack tuna (Katsuwonus pelamis), yellow fin tuna (Thunnus albacares), baby tuna (Thunnus spp.), and frigate tuna (Auxis spp.), while the bycatch consisted of dolphinfish (Coryphaena hippurus) and rainbow runner (Elagatis bipinnulatus). Catch per unit of effort analysis shows that catch per unit of effort value of baby tuna (Thunnus spp.) increased on August 2004, whereas catch per unit of effort value of skipjack tuna (Katsuwonus pelamis) increased on September 2004. The length at first capture of skipjack tuna (Katsuwonus pelamis) was 49,3 FLcm. The catch size was bigger than the length at first maturity for skipjack tuna (Katsuwonus pelamis). The length at first capture of yellowfin tuna (Thunnus albacares) was 51,6 FLcm. This catch size was smaller than the length at first maturity for yellowfin tuna (Thunnus albacares).


1987 ◽  
Vol 252 (2) ◽  
pp. F221-F225 ◽  
Author(s):  
S. Cheema-Dhadli ◽  
R. L. Jungas ◽  
M. L. Halperin

The purpose of this study was to clarify how changes in acid-base balance influence the rate of urea synthesis in vivo. Since ureagenesis was increased by an ammonium infusion into rats, regulation seemed to be a function of the blood ammonium concentration. The rate of urea synthesis was constant at a fixed rate of ammonium infusion and independent of the conjugate base infused, chloride or bicarbonate. The steady-state blood ammonium concentration was higher in the rats that developed metabolic acidosis. Thus it appeared that regulation was not directly mediated by this ammonium concentration per se. The rate of urea synthesis was also independent of the blood pH. Accordingly, the rate of urea synthesis was examined as a function of the plasma NH3 concentration. The rate of ureagenesis was found to be directly proportional to the plasma NH3 concentration. Assuming that plasma NH3 levels reflect those in mitochondria, the NH3 concentration yielding half-maximal rates of urea synthesis (close to 2 microM) was in the same range as Km for the rate-limiting step in ureagenesis, carbamoyl phosphate synthetase (EC 6.3.4.16). These results suggest that, at a constant ammonium concentration, the decreased rate of ureagenesis caused by a pH fall in vitro could reflect an acidosis-induced decline in the concentration of true substrate (NH3) for this pathway.


2012 ◽  
Vol 112 (4) ◽  
pp. 571-579 ◽  
Author(s):  
M. Hilbert ◽  
V. Shushakov ◽  
N. Maassen

Acidification has been reported to provide protective effects on force production in vitro. Thus, in this study, we tested if respiratory acid-base changes influence muscle function and excitability in vivo. Nine subjects performed strenuous, intermittent hand grip exercises (10 cycles of 15 s of work/45 s of rest) under respiratory acidosis by CO2 rebreathing, alkalosis by hyperventilation, or control. The Pco2, pH, K+ concentration ([K+]), and Na+ concentration were measured in venous and arterialized blood. Compound action potentials (M-wave) were elicited to examine the excitability of the sarcolemma. The surface electromyogram (EMG) was recorded to estimate the central drive to the muscle. The lowest venous pH during the exercise period was 7.24 ± 0.03 in controls, 7.31 ± 0.05 with alkalosis, and 7.17 ± 0.04 with acidosis ( P < 0.001). The venous [K+] rose to similar maximum values in all conditions (6.2 ± 0.8 mmol/l). The acidification reduced the decline in contraction speed ( P < 0.001) but decreased the M-wave area to 73.4 ± 19.8% ( P < 0.001) of the initial value. After the first exercise cycle, the M-wave area was smaller with acidosis than with alkalosis, and, after the second cycle, it was smaller with acidosis than with the control condition ( P < 0.001). The duration of the M-wave was not affected. Acidification diminished the reduction in performance, although the M-wave area during exercise was decreased. Respiratory alkalosis stabilized the M-wave area without influencing performance. Thus, we did not find a direct link between performance and alteration of excitability of the sarcolemma due to changes in pH in vivo.


1974 ◽  
Vol 52 (8) ◽  
pp. 706-717 ◽  
Author(s):  
Norman Smith ◽  
David Rubinstein

The exchange of lecithin between rabbit erythrocytes and serum has been investigated. The erythrocyte lecithin was labelled in vivo by administration of Na332PO4, which resulted in the acquisition of [32PJlecithin by the cells primarily by exchange, and in vitro by esterification with [3H]palmitate, [14C]linoleate, or [14C]linolenate. The rate of exchange of erythrocyte [32PJ-phospholipids was independent of specific serum lipoprotein fractions, but was related to the serum phospholipid concentration. Analysis of the erythrocyte inward and outward exchange rates of [32P]lecithin revealed that only 55% of the cellular lecithin pool takes part in the exchange. A similar conclusion can be reached by comparison of the fractional exchange rates of the acyl- and 32P-labelled erythrocyte lecithin, or by comparison of the ratio of acyl to 32P radioactivity of the erythrocyte lecithin with the ratio found in the serum after exchange. These data indicated that the proportion of the acyl-labelled erythrocyte lecithin pool (± S.E.M.) capable of exchange was 53 ± 5%, 64 ± 12%, and 95 ± 6%, when esterified with [14C]linoleate, [3H]palmitate, and [14C]linolenate, respectively. The differences in the proportion of the acyl-labelled erythrocyte lecithin pool undergoing exchange could not be attributed to the preferential exchange of a particular molecular species of lecithin, although the tetraenoic lecithin did exchange to a relatively greater degree. This suggests that cellular lecithin formed by esterification of linolenate is found only in the portion of the pool available for exchange, whereas that formed by esterification of linoleate and probably palmitate is distributed throughout the entire lecithin pool. The fractional exchange rate of [32P]lecithin of isolated erythrocyte membranes was 3 times that of the lecithin of intact cells. However, the difference in fractional exchange rates between [3H]palmityl-lecithin or [14C]linoleyl-lecithin and [32P]lecithin is reversed in the membranes. These observations suggest that a portion of the total cellular lecithin pool becomes available for exchange only upon disruption of the erythrocyte, and may be located in a relatively inaccessible portion of the membrane such as the inner surface.


1990 ◽  
Vol 79 (2) ◽  
pp. 139-147 ◽  
Author(s):  
M. Salleh M. Ardawi ◽  
Yasir S. Jamal

1. The effect of dexamethasone (30 μg day−-1 100 g−-1 body weight) on the regulation of glutamine metabolism was studied in skeletal muscles of rats after 9 days of treatment. 2. Dexamethasone resulted in negative nitrogen balance, and produced increases in the plasma concentrations of alanine (23.4%) and insulin (158%) but a decrease in the plasma concentration of glutamine (28.7%). 3. Dexamethasone treatment increased the rate of glutamine production in muscle, skin and adipose tissue preparations, with muscle production accounting for over 90% of total glutamine produced by the hindlimb. 4. Blood flow and arteriovenous concentration difference measurements across the hindlimb showed an increase in the net exchange rates of glutamine (25.3%) and alanine (90.5%) in dexamethasone-treated rats compared with corresponding controls. 5. Dexamethasone treatment produced significant decreases in the concentrations of skeletal muscle glutamine (51.8%) and 2-oxoglutarate (50.8%). The concentrations of alanine (16.2%), pyruvate (45.9%), ammonia (43.3%) and inosine 5′-phosphate (141.8%) were increased. 6. The maximal activity of glutamine synthetase was increased (21–34%), but there was no change in that of glutaminase, in muscles of dexamethasone-treated rats. 7. It is concluded that glucocorticoid administration enhances the rates of release of both glutamine and alanine from skeletal muscle of rats (both in vitro and in vivo). This may be due to changes in efflux and/or increased intracellular formation of glutamine and alanine.


2007 ◽  
Vol 293 (6) ◽  
pp. R2400-R2411 ◽  
Author(s):  
Alena Brandes ◽  
Oliver Oehlke ◽  
Anne Schümann ◽  
Stefanie Heidrich ◽  
Frank Thévenod ◽  
...  

The cellular distribution of the NH2-terminal electrogenic Na+-HCO3− cotransporter (NBCe1) variants NBCe1-A and NBCe1-B has been investigated in rat kidney and submandibular gland (SMG) under physiological conditions and after systemic acid-base perturbations. Moreover, the in vivo data were complemented in vitro by using an immortalized cell line derived from the S1 segment of the proximal tubule (PT) of normotensive Wistar-Kyoto rats (WKPT-0293 Cl.2). NBCe1-A was basolaterally localized in PT cells, whereas NBCe1-B exhibited intracellular and basolateral distribution. SMG showed transcript and protein expression for NBCe1-A and NBCe1-B. NBCe1-B was basolaterally localized in duct cells; NBCe1-A was found intracellularly in salivary striated ducts and apically in main duct cells. Acute metabolic acidosis significantly increased cells that showed basolateral NBCe1-A in the PT, indicating increased HCO3− reabsorption, and significantly decreased cells that exhibited basolateral NBCe1-B in the salivary ducts, suggesting decreased HCO3− secretion. Chronic acidosis had no effect on NBCe1 distribution in PT but significantly increased the percentage of cells with basolateral NBCe1-A in salivary striated duct cells, suggesting increased HCO3− reabsorption. In contrast, chronic alkalosis caused adaptive redistribution of NBCe1-A and NBCe1-B in renal PT, favoring decreased HCO3− reabsorption. In vitro, WKPT-0293 Cl.2 cells expressed key acid-base transporters. Extracellular alkalosis downregulated NBCe1-A protein. WKPT-0293 Cl.2 cells are therefore a useful model to study renal acid-base regulation in vitro. The results propose redistribution of the transporters as a potential posttranslational regulation modus during acid-base disturbances. Moreover, the data demonstrate that renal PT and salivary duct epithelia respond to acid-base disturbances by an opposite redistribution pattern for NBCe1-A and NBCe1-B, reflecting specialized functions as the HCO3−-reabsorbing and HCO3−-secreting epithelium, respectively.


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