Norbert Heisler

Acid-Base Regulation

Regulation of the acid-base status is an imperative task for maintenance of homeostasis in living animals. Deviations of pH from the predetermined setpoint values may result in reduced metabolic performance as a result of the often pronounced optima in the overall pH/activity relationships of metabolic pathways. The mechanisms involved in acid-base regulation do not differ among and within vertebrate classes, but the extent to which certain processes are, or can be, utilized may be vastly different. Accordingly, buffering, changes in PCO2, and transmembrane and transepithelial acid-base-relevant ion transfer, which are the main regulatory processes in other vertebrates, are also valid mechanisms for elasmobranch fishes (for closer analysis of relative importance and theoretical limitations of these mechanisms in fishes, see Heisler 1986d, e).

Effects of nitrite exposure on blood respiratory properties, acid-base and electrolyte regulation in the carp (Cyprinus carpio)

SummaryAdult carp were subjected to 1 mM environmental nitrite for 48 h and nitrite uptake and changes in blood respiratory properties, extracellular electrolyte composition and acid-base status were examined.A constant influx of nitrite caused an accumulation of NO2− in plasma to 5.4 mM in 48 h. The fraction of methaemoglobin rose with plasma [NO2−] to 83%, and the arterial oxygen content decreased to extremely low values. Arterial

Branchial ion exchange and acid-base regulation after strenuous exercise in rainbow trout (Salmo gairdneri)

P_{{\text{O}}_2 }

Regulation of ventilation and acid-base status in the elasmobranch Scyliorhinus stellaris during hyperoxia-induced hypercapnia

increased as a compensation to this O2-shortage, whereas the O2 saturation of the functional (unoxidized) haemoglobin decreased, revealing a reduction in its O2 affinity.Blood haematocrit decreased as a result of red cell shrinkage, which caused very high red cell haemoglobin (Hb) concentrations. The erythrocytic nucleoside triphosphate (NTP) concentration showed a parallel increase whereby NTP/Hb, as well as the relative contributions of ATP and GTP to NTP, remained unchanged.Plasma [Cl−] declined by 15 mM in 48 h, off-setting the plasma [NO2−] increase, minor changes in plasma [HCO3−] and a considerable increase in plasma [lactate]. Arterial pH and [HCO3−] rose slightly during the first 24 h of nitrite exposure, but returned to control values at 48 h. The rise in plasma [lactate] was not reflected in an extracellular metabolic acidosis. Plasma [K+] increased by 94% in 48 h, revealing an uncompensated extracellular hyperkalemia, whereas plasma [Na+] decreased, and plasma [Ca++] was unchanged. Plasma osmolality remained essentially constant.The NO2− accumulation could be reversed by transfer of the fish to NO2−-free water, but nitrite ‘off-loading’ was slower than the preceding NO2− loading.

Standard metabolic rate, critical oxygen tension, and aerobic scope for spontaneous activity of trout (Salmo gairdneri) and carp (Cyprinus carpio) in acidified water

Abstract o 1. The standard metabolic rate (SMR), and the critical oxygen tension ( P c ) were determined as a function of temperature for carp ( Cyprinus carpio ) and rainbow trout ( Salmo gairdneri ). 2. The SMR increased and Q 10 (increase of SMR per increase in temperature) decreased for both species with increasing temperature. 3. For carp, the values for P c obtained, with the test temperature, were 11 torr, 5°C; 20 torr, 10°C; 21 torr, 15°C; and 20 torr, 25°C. 4. For trout, the P c s were 21 torr, 10°C; 22 torr, 15°C; 27 torr, 20°C. 5. This relative constancy of P c with temperature is not accordance with most earlier studies which showed an increase in the P c with increasing temperature.

6 Acid-Base Regulation in Fishes*

Specimens of rainbow trout (Salmo gairdneri) were electrically stimulated to exhausting activity in a closed water recirculation system and the changes in dorsal aortic plasma pH, PCO2, PO2, O2 content, [Na+], [Cl-], [K+], [Lactate-] and Ht were measured during a 24 h recovery period. Net transfer of H+, Na+, Cl- and ammonia between fish and environment were determined by measurement of the concentration changes in the recirculating water. Strenuous exercise resulted in a severe lactacidosis which was corrected by transient net transfer of H+ ions to the environmental water within 4 h, about 6-8 h before the lactate was metabolically removed. The net transfer of H+ ions was achieved in part by branchial HCO3-/Cl- ion exchanges, but to a larger extent by branchial exchange of H+ and/or NH4+ against Na+. The excretion of ammonia, which was considerably enhanced during the first 4 h after exercise, was at least partially due to non-ionic diffusion across the gill epithelium. The observed elevation in ammonia excretion was probably the result of an exercise-induced increase in nitrogen metabolism rather than of production of ammonia for the purpose of acid-base regulation.

Acid-base regulation in response to environmental hypercapnia in two aquatic salamanders, Siren lacertina and Amphiuma means.

SummaryVentilation, pulmonary O2 uptake, arterial blood gases and pH were measured in fresh water turtles,Chrysemys picta bellii, during voluntary diving and surfacing at temperatures of 10, 20 or 30°C. At each temperature, the animals were also exposed to declining levels of inspired O2 concentration with blood samples taken at various stages of breath holding and during episodes of breathing.The breathing pattern ofChrysemys consists of a series of breaths followed by a breath hold period which usually coincides with a period of submergence. The ventilatory response to hypoxia at all temperatures involved a decrease in the diving time as well as an increase in the tidal volume. The breathing frequency during ventilatory periods decreased slightly during severe hypoxia. The increase of ventilation in response to hypoxia was most pronounced at 30°C; ventilation approximately doubled as arterialPO2 decreased from 60 to 30 Torr and increased more than tenfold as arterialPO2 approached 10 Torr. In comparison, the ventilatory response of animals at lower temperatures occurred at much lower levels of arterialPO2; at 10°C ventilation did not increase relative to normoxic control values until arterialPO2 fell to about 5 Torr.The observed reduction in the ventilatory response to environmental hypoxia at lower temperatures can probably be attributed to the sevenfold reduced pulmonary O2 uptake at 10°C as compared to 30°C in combination with the shift inP50 of the blood oxygen dissociation curves from 29 (30°C) to 5 Torr (10°C). The present data suggest that desaturation of the blood during hypoxia is a leading factor for the increase in ventilation as an attempt to maintain normal O2 uptake.

Regulation of the Acid-Base Status in Fishes

Exposure of the elasmobranch Scyliorhinus stellaris to environmental hyperoxia (PO2 of 500 mm Hg) resulted in a considerable rise of arterial PCO2 from 1.9 mm Hg during normoxia to about 11 mm Hg after 6 days as an expression of the primarily oxygen-oriented regulation of gill ventilation. In contrast to the typical pattern during environmental hypercapnia, however, arterial plasma pH was hardly affected by the considerable hyperoxia-induced hypercapnia. At elevated arterial PO2 values (200-300 mm Hg) gill ventilation was apparently not adjusted exclusively for the oxygen demands of the organism, but was matched to the requirements of acid-base regulation such that the rise in PCO2 could be compensated for by a net gain of bicarbonate-equivalent ions from the environment. This fine adjustment of gill ventilation to the bicarbonate-equivalent uptake rate extended the process of adaptation to about 6 days and resulted in an almost complete pH compensation during the entire process of PCO2 increase. These data suggest that during conditions of reduced oxygen-related respiratory drive the regulation of gill ventilation is primarily dependent upon the acid-base parameters.