Untersuchungen zur Regulation des Säuren-Basen- und Elektrolythaushaltes beim Karpfen (Cyprinus carpio L.) bei Normoxie, Hyperkapnie und erhöhten Wasserkonzentrationen von Ammoniak / Ammonium anhand arterieller Blutwerte

Abstract

1. The described investigations were performed under precisely standardized experimental conditions, with respect to housing and environmental conditions of the animals.

2. A modified technique of catheterisation was used under continous rinsing of the catheter to maintain patency of the lumen.

The animals were bled in regular intervalls. In order to keep erythrocyte counts constant we used the method of reinfusion of ca 85% of the particulate blood components. This method assured relative constant levels of the hematocrit and hemoglobin values throughout the experiments. This method has proven to be efficient to prevent dramatically reduced values of hematocrit and hemoglobin.

There was a slight shift in blood parameters under normoxic and normocapnic conditions. These changes were correlated with changing environmental conditions in the water, which was influenced by the excretion of metabolic products of the animals. These findings were not influenced by the experimental setup.

The experimental conditions have proven to be suitable to maintain low stress levels (prehypercapnic and control conditions) with respect to catecholamine levels in plasma, which remained at constant concentrations in the low normal range.

3. Hypercapnia-induced respiratory and metabolic acidosis induced compensatory mechanisms, which have a regulatory effect on the acid-base balance, as well as on systemic oxygen supply.

This leads to increased levels of the hematocrit and hemoglobin concentration in arterial blood, as well as an increased volume of the erythrocyte (MCHC reduction). This feature is correlated with changes in the ion-exchange conditions of the erythrocyte membrane.

4. The hypercapnia-induced mixed acidosis is inducing changes in the concentration of several plasma electrolytes, comparable to a HCl-induced metabolic acidosis (Ultsch et al., 1981).

Claiborne and Haisler (1984; 1986) described ion-exchange conditions between carp and the environmental water during and after hypercapnic conditions. These investigations correlated only partially with our results with respect to plasma concentrations of the ions. Sodium and chloride ions on the plasma were greatly reduced in spite of stimulated uptake from the environment of Na+ during hypercapnia, and Cl- in the post-hypercapnic phase.

5. These are the first results about adrenalin- and noradrenalin kinetics in arterial blood in carps under normoxic and hypercapnic conditions of the environment. The concentrations (adrenalin and noradrenalin) were determined without extraneous manipulation of the carps.

Increased concentrations of catecholamines in arterial blood (mainly noradrenalin) are induced by hypercapnic-hypoxemic conditions which were maintained over 36 hours, were slowly approaching pre-hypercapnic values during this time period.

In contrast to the findings of Fuchs and Albers (1988), we did not observe increased concentrations of adrenalin with concurrent hypoxemia.

Improvement of the gas-exchange can be influenced by cardiovascular, ventilatory and metabolic effects of increased noradrenalin concentrations, as well as activation of the beta-adrenergic Na+ / H+ exchanger of the erythrocyte membrane.

The constant low concentrations of adrenalin did most likely not affect the above described exchange conditions.

6. During the hypercapnic intervall of 36 hours, there is little compensation of the bicarbonat controlled (influenced) pHa concentration .These results are in concordance with Claiborne and Heisler (1984; 1986).

Twelve hours after reestablishment of normocapnic conditions, most blood parameters approached pre-hypercapnic values.

The lowest plasma concentrations of sodium- and chloride ions were determined at the end of the experiment.

7. Total ammonium plasma concentrations are increasing during hypercapnia.

Increased concentrations of ammonium in environmental water, lead to increased plasma ammonium concentrations in arterial blood as long as a concentration gradient is maintained.

The above described results are probably caused by diminished release of ammonium from the gill epithelia under hypercapnic conditions.

The experimentally chosen ammoniumchloride concentration of 20 mgl-1 has no evident influence of the acid-base balance (pHa, paCO2, [HCO3-]a, BE) in the hypercapnic phase. This concentration is however possibly responsible for the pronounced reduction of the plasma bi-carbonate concentration in experimental group 2. This phenomena is possibly explained by increased substrate availability in exchange for Cl-/HCO3-.

In spite of dramatically increased ammonium concentration in environmental water in experimental group 2, there was a more rapid reduction of the plasma ammonium levels during the post-hypercapnic phase, compared to experimental group 1.

In summary there is evidence that the investigated ammoniumchloride concentration in environmental water, seems to be beneficial for regulatory mechanisms of the acid-base and electrolyte balance during the posthypercapnic phase.