Acid-base and respiratory responses to hypoxia in the grasshopper Schistocerca americana.

1998 ◽  
Vol 201 (20) ◽  
pp. 2843-2855 ◽  
Author(s):  
KJ Greenlee ◽  
JF Harrison

How do quiescent insects maintain constant rates of oxygen consumption at ambient PO2 values as low as 2-5 kPa? To address this question, we examined the response of the American locust Schistocerca americana to hypoxia by measuring the effect of decreasing ambient PO2 on haemolymph acid-base status, tracheal PCO2 and CO2 emission. We also tested the effect of hypoxia on convective ventilation using a new optical technique which measured the changes in abdominal volume during ventilation. Hypoxia caused a progressive increase in haemolymph pH and a decrease in haemolymph PCO2. A Davenport analysis suggests that hypoxia is accompanied by a net transfer of base to the haemolymph, perhaps as a result of intracellular pH regulation. Hypoxia caused a progressive increase in convective ventilation which was mostly attributable to a rise in ventilatory frequency. Carbon dioxide conductance ( micromol h-1 kPa-1) across the spiracles increased more than threefold, while conductance between the haemolymph and primary trachea nearly doubled in 2 kPa O2 relative to room air. The rise in trans-spiracular conductance is completely attributable to the elevations in convective ventilation. The rise in tracheal conductance in response to hypoxia may reflect the removal of fluid from the tracheoles described by Wigglesworth. The low critical PO2 of quiescent insects can be attributed (1) to their relatively low resting metabolic rates, (2) to the possession of tracheal systems adapted for the exchange of gases at much higher rates during activity and (3) to the ability of insects to rapidly modulate tracheal conductance.

1991 ◽  
Vol 156 (1) ◽  
pp. 153-171 ◽  
Author(s):  
YONG TANG ◽  
ROBERT G. BOUTILIER

The intracellular acid-base status of white muscle of freshwater (FW) and seawater (SW) -adapted rainbow trout was examined before and after exhaustive exercise. Exhaustive exercise resulted in a pronounced intracellular acidosis with a greater pH drop in SW (0.82 pH units) than in FW (0.66 pH units) trout; this was accompanied by a marked rise in intracellular lactate levels, with more pronounced increases occurring in SW (54.4 mmoll−1) than in FW (45.7 mmoll−1) trout. Despite the more severe acidosis, recovery was faster in the SW animals, as indicated by a more rapid clearance of metabolic H+ and lactate loads. Compartmental analysis of the distribution of metabolic H+ and lactate loads showed that the more rapid recovery of pH in SW trout could be due to (1) their greater facility for excreting H+ equivalents to the environmental water [e.g. 15.5 % (SW) vs 5.0 % (FW) of the initial H+ load was stored in external water at 250 min post-exercise] and, to a greater extent, (2) the more rapid removal of H+, facilitated via lactate metabolism in situ (white muscle) and/or the Cori cycle (e.g. heart, liver). The slower pH recovery in FW trout may also be due in part to greater production of an ‘unmeasured acid’ [maximum approx. 8.5 mmol kg−1 fish (FW) vs approx. 6 mmol kg−1 fish (SW) at 70–130 min post-exercise] during the recovery period. Furthermore, the analysis revealed that H+-consuming metabolism is quantitatively the most important mechanism for the correction of an endogenously originating acidosis, and that extracellular pH normalization gains priority over intracellular pH regulation during recovery of acid-base status following exhaustive exercise.


2014 ◽  
Vol 5 ◽  
Author(s):  
Vernon A. Ruffin ◽  
Ahlam I. Salameh ◽  
Walter F. Boron ◽  
Mark D. Parker

1984 ◽  
Vol 246 (4) ◽  
pp. R452-R459 ◽  
Author(s):  
J. N. Cameron

In the water-breathing fishes, rising temperatures are accompanied by progressive reduction in pH, reductions in bicarbonate concentration, and slight rises in CO2 partial pressure. The pH-temperature slope of both intra- and extracellular compartments varies considerably, from -0.009 to -0.033/degrees C, with a rather consistent pattern of red muscle greater than white muscle greater than heart. Three different approaches to acid-base analysis, the imidazole-alphastat model, the strong-ion difference analysis, and the delta-bicarbonate approach, were applied to a set of data from the fresh-water channel catfish (Ictalurus punctatus). A principal difficulty encountered in using all three approaches was that assumptions were required regarding the chemical behavior of the intracellular buffers, but the delta-bicarbonate approach has the practical advantage of emphasizing parameters that can be measured directly. Closed-system models are not generally applicable to fish, and the interest for future work lies in deciphering the significance of tissue-to-tissue variations in pH regulation and in elucidating the mechanisms of the strong-ion transfers.


1987 ◽  
Vol 131 (1) ◽  
pp. 89-105
Author(s):  
HANS-OTTO PÖRTNER

The quantitative influence of anaerobic metabolism on acid—base status and on acid-base regulation is investigated in Sipunculus nudus L. Proton generation by metabolism is calculated from theoretical predictions. The quantitative comparison of metabolic protons with non-respiratory protons found in the acid—base status is performed assuming a simplified model of the total animal. Taking the protonequivalent ion exchange between animals and ambient water into account, changes in the anaerobic acid—base status can be explained exclusively by proton generation in metabolism. It is concluded that the classical concept of acid—base physiology is adequate and that the consideration of strong ions is not required for a quantitative treatment of the acid—base status. The hypothesis that a quantitative correlation exists between metabolic and acid—base events is tested by comparing changes in acid—base status and in metabolism in animals exhibiting different metabolic rates. For this purpose, a method is developed for the calculation of intracellular pH from metabolite concentrations and extracellular acid—base parameters. Proton exchange between intra-and extracellular compartments, which is found to depend upon the total amount of accumulated non-respiratory protons, demonstrates that pHi is regulated even during anaerobiosis. The defended pH, value, however, is lower during anaerobiosis than during subsequent recovery. Note: Address for reprint requests


1996 ◽  
Vol 199 (2) ◽  
pp. 379-389 ◽  
Author(s):  
S Gulinson ◽  
J Harrison

We examined the effect of extracellular acid-base status and tracheal gas levels on the ventilation rate of resting Romalea guttata and Schistocerca americana grasshoppers. We manipulated haemolymph pH and [HCO3-] within normal physiological ranges using injections of HCl, NaOH, NaHCO3 and NaCl into the haemocoel. In contrast to terrestrial vertebrates, there was no evidence that extracellular acidification increases ventilation rate in grasshoppers. Elevation of haemolymph bicarbonate levels (by NaHCO3 injection) increased ventilation rate, while depression of haemolymph bicarbonate levels (HCl injection) had no effect. Injection of NaHCO3 also increased tracheal PCO2, suggesting that the effect of the NaHCO3 injection might be mediated by a sensitivity of the ventilatory system to tracheal gases. We tested for effects of tracheal gases on ventilation rate by independently manipulating tracheal PCO2 and PO2 using tracheal perfusions. Ventilation rate was positively correlated with tracheal PCO2 and negatively correlated with tracheal PO2. Increasing tracheal PO2 above normal resting levels or decreasing tracheal PCO2 below normal levels decreased ventilation rate. We conclude that quiescent grasshoppers regulate tracheal PCO2 and PO2 by varying ventilation rate and that both PCO2 and PO2 in the trachea stimulate ventilation in normal, resting grasshoppers.


1992 ◽  
Vol 165 (1) ◽  
pp. 85-96 ◽  
Author(s):  
JON F. HARRISON ◽  
CALVIN J. WONG ◽  
JOHN E. PHILLIPS

Organismal homeostasis requires regulation of extracellular acid-base status; however, the mechanisms by which insects regulate haemolymph pH are poorly known. We evaluated the recovery of desert locusts Schistocerca gregaria Forskal from acute acid loads, initiated by HCl injections into the haemolymph (0.5 pH unit decrease). Haemolymph pH, PCO2 and [HCO3−] recovered in 8–24 h, providing the first unequivocal evidence that insects regulate extracellular pH. There were no changes in the concentrations of the primary haemolymph buffer compounds (protein, inorganic phosphate) during recovery. Within 1 h, the tracheal system effectively eliminated the carbon dioxide derived from bicarbonate buffering. During the remainder of the recovery, haemolymph PCO2 was similar to control values; there was no respiratory compensation for decreased haemolymph pH. Approximately 75 % of the acid equivalents removed from the haemolymph during the recovery process were transferred to the lumens of the crop and midgut. Transfer of acid equivalents to the alimentary lumen provides unfed locusts with a mechanism of haemolymph pH regulation that does not compromise intracellular acid-base status or increase ventilatory water loss. Note: Current address and address for communications: Department of Zoology, Arizona State University, Tempe, AZ 85287–1501, USA.


1981 ◽  
Vol 51 (6) ◽  
pp. 1630-1634 ◽  
Author(s):  
N. C. Gonzalez ◽  
R. L. Clancy

The possible role of a HCO-3/Cl- transmembrane exchange as a mechanism of alkalinization in the myocardial cell was studied in isolated rabbit hearts perfused with Ringer solution. Cl- depletion was produced by replacing Cl- of the perfusate by SO2(-4) or glucuronate. Intracellular pH (pHi) was calculated both in Cl--free and Cl--containing hearts from the distribution of 14C-labeled 5′,5′-dimethyloxazolidine-2,4-dione. Acid-base alterations were produced by changing perfusate HCO-3 concentration and/or CO2 partial pressure (PCO2). Depletion of Cl- resulted in an increase in pHi for any given level of extracellular pH. Increasing PCO2 at constant perfusate HCO-3 resulted in changes in pHi and cell HCO-3 (HCO-3i) that were similar in both Cl--free and Cl--containing hearts. Increasing perfusate HCO-3 at constant PCO2 resulted in increases in pHi and HCO-3i in both Cl--free and Cl--containing preparations. When the increases in HCO-3i secondary to an increase in extracellular HCO-3 were plotted as a function of the initial HCO-3i, a significant negative correlation was observed, suggesting that the elevation of HCO-3i was influenced by the initial HCo-3i and not by the presence or absence of Cl-. It is concluded that even though HCO-3 may enter the myocardial cells in exchange for Cl- during Cl-depletion, lack of Cl- does not alter the ability of the myocardial cell to regulate its pHi. This argues against a HCO-3/Cl- exchange as a mechanism of regulation of myocardial pHi.


1980 ◽  
Vol 84 (1) ◽  
pp. 161-167
Author(s):  
H. D. Hansen ◽  
H. Gesser

There is a large variation in the tolerance of myocardial tissue to cellular acidosis. Assuming the cytoplasmic acid-base status to be mainly a result of intracellular processes, this variation could be produced by variations in the tissue non-bicarbonate buffer value. In the myocardial tissue from nine vertebrate species, the non-bicarbonate buffer value did not correlate either with ability to develop tension under hypercapnic acidiosis or with the indirectly estimated capacity for anaerobic glycolysis. Therefore, differences in myocardial tolerance to acidosis must be explained either by an active pH regulation or by other compensatory mechanisms.


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