Regulatory volume response of erythrocytes exposed to a gradual and slow decrease in medium osmolality

 A sudden decrease in external medium osmolality (90 mosmol/kg) causes an immediate swelling of trout erythrocytes, followed by a regulatory volume decrease (RVD) due to activation of both a KCl cotransporter and a taurine transport pathway. Here, we determined how trout red cells respond when they are exposed to a gradual and slow decrease in medium osmolality (80 mosmol/kg at a rate of 0.7 mosmol/kg per min). Erythrocytes were unable to regulate their volume efficiently when swollen gradually and it increased continuously throughout the experimental period (120 min). As long as volume was increased slowly by 15–25%, regulatory pathways remained essentially inactivated, erythrocytes losing no significant amount of intracellular osmotically active solutes. Above this swelling threshold, a response was triggered but the quantity of solutes lost via the regulatory pathways was still not sufficient to counterbalance the continuous entry of water due to the slow and gradual decrease in medium tonicity. Received: 18 January 1999 / Received after revision: 10 February 1999 / Accepted: 11 February 1999     

Adaptive respiratory responses of trout to acute hypoxia. III. Ion movements and pH changes in the red blood cell

In the preceding paper acute hypoxia was shown to elicit within minutes an increase in the blood O2 affinity. From the present data it appears that this rapid change in blood P50 value can be ascribed to an important alkalization of the red blood cell despite a simultaneous decrease in extracellular pH (pHe). The intracellular alkalization is only partially due to beta-adrenergic stimulation of Na/H exchange, deoxygenation of hemoglobin and the rapid decrease of PaCO2 due to hyperventilation being involved in this process via the chloride shift. This high value of intraerythrocytic pH (pHi) is then maintained practically constant throughout the time the fish is kept in hypoxia despite wide changes of external pH. The blocking of pHi accounted for the constant O2 content observed during hypoxia. The uncoupling of pHi from pHe, which occurs at the onset of hypoxia, is still unexplained: for instance, it is not due to inhibition of the anion exchanger responsible for the passive distribution of H+ across the red cell membrane. A general scheme of all the mechanisms involved in the emergency adaptive response to acute hypoxia is presented.     

Continuous peripheral nerve blocks at home for treatment of recurrent complex regional pain syndrome I in children

BACKGROUND: Recurrent complex regional pain syndrome I is not rare in the pediatric population. The authors conducted this study to evaluate the efficacy of continuous peripheral nerve blocks with elastomeric disposable pumps associated with initial Bier blocks for the treatment of recurrent complex regional pain syndrome I in children. METHODS: After parental informed consent, 13 children who did not respond to conventional complex regional pain syndrome treatment were included (mean age, 13 yr; range, 9-16 yr). After general anesthesia, peripheral nerve block was performed using 0.5 ml/kg lidocaine, 1%, with epinephrine and 0.5% ropivacaine injected in the peripheral nerve block catheter. Then, a 20-min Bier block was performed using a tourniquet and 0.2 ml/kg lidocaine, 1%; 3 ml/kg hydroxyethyl starch 130/06; and 5 mg/kg buflomedil injected intravenously. A solution of 0.1 ml . kg . h continuous ropivacaine, 0.2%, was infused through the catheter using an elastomeric pump for 96 h. Need for rescue analgesia, occurrence of side effects, and status of motor and sensory block were recorded at hours 1, 6, 12, 24, 48, 72, and 96. Children and parents completed a satisfaction assessment. All of the children had follow-up visits after 2 months. RESULTS: Postoperative analgesia was excellent. The median pain score was 0 for each period studied. Motor blockade was minimal before 12 h (median, 1) and absent thereafter. One child needed rescue analgesia. All children were able to walk easily after the initial 24-h period (walking score, > 4). Children and parents were all satisfied. Children returned home under parental surveillance beginning in the 24th hour. Neither peripheral nerve block nor Bier block caused side effects. After 2 months, none of the children exhibited any clinical symptom of recurrent complex regional pain syndrome. CONCLUSION: Ambulatory continuous peripheral nerve block associated with an initial Bier block seems to be a significant and novel contribution to treat recurrent pediatric complex regional pain syndrome I. It allows complete pain relief, early mobilization, and rapid return home, representing a psychological advantage for these children.     

Inhibition by amiloride of both adenylate cyclase activity and the Na+/H+ antiporter in fish erythrocytes

In fish erythrocytes isoproterenol stimulates cellular accumulation of cyclic adenosine 3':5'-monophosphate (cyclic AMP) and produces a large increase in sodium permeability which corresponds to the activation of Na+/H+ exchanges and chloride-dependent sodium uptake. The stimulation of sodium transport by isoproterenol was reproduced by adding cyclic AMP or forskolin to the medium and was blocked by propranolol. This increase in sodium permeability was completely inhibited by amiloride at the relatively high levels (0.1-1 mM) of the diuretic required to inhibit the activity of the Na+/H+ exchanger under physiological conditions in various biological systems. It was shown that amiloride inhibited cyclic AMP accumulation. This effect, which was reversible and dose-dependent (ED50 6 X 10(-6) M-maximal effect 0.5 mM), resulted from the inhibition of the catalytic unit of adenylate cyclase. Amiloride also directly inhibited the sodium entry system but the Na transporter was less sensitive than adenylate cyclase to amiloride (ED50 6 X 10(-5) M). It appears from the data presented in this report that the inhibition of sodium permeability observed in fish erythrocytes in the presence of amiloride can result either from the effect of the diuretic on the adenylate cyclase system or from the effect on the sodium transport system, depending on the conditions in which amiloride is used. Thus, caution is required when interpreting amiloride action in terms of inhibition of specific transport processes.