Mediation of serotonin-induced hyperventilation via 5-HT3-receptor in European eel Anguilla anguilla.

The effects of serotonin (5-hydroxytryptamine) on ventilation were investigated by continuous measurements of intrabuccal pressure in unrestrained eel. Intravenous administration of 5-hydroxytryptamine (30 micrograms.kg-1) caused a large increase in ventilatory frequency (+ 100%) and amplitude (+ 140%). The 5-hydroxytryptamine-induced hyperventilation was blocked by the 5-HT3-receptor antagonists metoclopramide (1.0 mg.kg-1) or MDL72222 (1.0 mg.kg-1), and was insensitive to the 5-HT1/2-receptor antagonist methysergide (3.0 mg.kg-1) and to the 5-HT4-receptor antagonist DAU 6285 CL (3.0 mg.kg-1). The hyperventilatory response to 5-hydroxytryptamine could be mimicked by the 5-HT3 receptor agonist 1-phenylbiguanide (300 micrograms.kg-1). These results strongly implicate the 5-HT3-receptor as the mediator of the 5-hydroxytryptamine-induced hyperventilation in eel.

Effects of serotonin on the cardio-circulatory system of the European eel (Anguilla anguilla) in vivo.

The effects of serotonin on continuously recorded cardiac parameters (heart rate, cardiac output, cardiac stroke volume), ventral and dorsal aortic blood pressures, branchial and systemic vascular resistances were investigated in the European eel in vivo. Intravenous administration of serotonin (30 micrograms.kg-1) caused a marked bradycardia (45%) and a simultaneous decrease in cardiac output (50%), ventral (35%) and dorsal (50%) aortic blood pressures. Branchial resistance was markedly increased (60%) and systemic resistance decreased (30%). Cardiac stroke volume remained unchanged. The effects of serotonin on cardiac parameters were suppressed either by methysergide or a bilateral section of the cardiac vagus. Bradycardia could then be regarded as the consequence of a vagal mechanism triggered by serotonin action on central methysergide-sensitive serotonergic receptors. No inotropic effect of serotonin was observed. This lack of myocardiac contractility modification is discussed. The serotonin-mediated branchial vasoconstriction was attenuated by vagotomy, whereas the residual increase in branchial resistance (40%) was suppressed by methysergide. The serotonin-mediated branchial vasoconstriction could be the consequence of both a passive mechanism (compliance) caused by the decrease in cardiac output and an active mechanism involving methysergide-sensitive serotonergic receptors of the branchial vasculature. A possible involvement of this vasomotor effect in gill oxygen uptake is discussed. The serotonin-induced systemic vasodilation was insensitive either to cardiac vagotomy or to 5-HT1/2, 5-HT3 and 5-HT4 receptor antagonists, suggesting the involvement of a local mechanism which remains to be assessed.

Ventilatory and circulatory adjustments in the European eel (Anguilla anguilla L.) exposed to short term hypoxia.

Respiratory and circulatory (measured and calculated) variables were obtained at the same time in resting eels, during normoxia and after 1 h exposure to environmental hypoxia (water PO2 of 40 torr). In normoxia, values of respiratory and circulatory variables appeared less than those reported for most other fish. These differences could be partly explained by a lower level of standard metabolism and a greater uptake of O2 through the skin. Hypoxia caused a marked decrease in heart rate (40%), cardiac output (37%), ventral and dorsal arterial blood pressures (22% and 32%), associated with a constriction of prebranchial veno-venous shunt, and an increase in branchial vascular resistance (30%). Atropine treatment during hypoxia reduced, but did not abolish, bradycardia, and branchial vascular resistance remained unchanged. The lack of increase in cardiac stroke volume as well as the slowing of the heart in atropine-treated eel, could be regarded as metabolic effects of sustained hypoxia. The increase in branchial resistance and constriction of prebranchial veno-venous shunt could be regarded as a direct myogenic effect of hypoxia. Hypoxic exposure resulted in an increase in ventilatory water flow Vg (more than twofold), a decrease in gill O2 uptake (50%) and oxygen partial pressure in arterial (PaO2 80%) and mixed venous blood (PvO2 78%), and in increase in the transfer factor for O2 of the gills, TO2, (+66%). The ventilatory convection requirement increased (fivefold) while extraction (EwO2%) and effectiveness (Eff%) of gill oxygen transfer were maintained in spite of hyperventilation. Hypoxic hyperventilation reduced partial pressure of CO2 (PaCO2 from 3.4 to 0.7 torr) and markedly raised pH (pHa from 7.98 to 8.33) in arterial blood, thus causing a typical respiratory alkalosis, which resulted in increased O2 affinity and capacity of eel haemoglobin.

A study of barosensitivity in the European eel (Anguilla anguilla, L.): effects of arterial pressure changes on heart rate and ventilation.

A study of the effects of arterial pressure changes on heart rate and ventilation was carried out on the eel (Anguilla anguilla L.). The anatomical characteristics of this fish enabled extracorporeal circulation in both the ventral and dorsal aorta to be set up. The pressure was changed mechanically, either by clamping external circulations or, in some cases, by modifying the frequency of a pulsatory pump placed in series with the heart, thus ensuring constant blood flows in the ventral aorta. The maximal pressure decreases obtained by clamping the external ventral aorta circulation (70%-80%) failed to induce significant changes in either heart rate or ventilation. An increase of arterial pressure up to about 50% of the control values did not induce bradycardia and ventilatory response. In the range of 50%-100% increase, a weak decrease of heart rate and slight hyperventilation were observed. Such a ventilatory response was contrary to the hypoventilation classically reported in mammals when systemic arterial pressure was increased, but similar to the hyperventilation observed when blood pressure was increased in the pulmonary arteries. The results emphasized functional analogies in regulation, originating from the circulatory bed, between the two highly compliant circulatory systems: fish circulation and pulmonary circulation of mammals.

Cutaneous and gill O2 uptake in the European eel (Anguilla anguilla L.) in relation to ambient PO2, 10-400 Torr.

The partition of O2 uptake between gills and skin was examined in the freshwater eel (Anguilla anguilla L.) at ambient PO2 ranging from hyperoxia (PO2 = 400 Torr) to severe hypoxia (PO2 = 10 Torr), using a technique of open-flow respirometry. All the expired water was collected, and the ventilatory flow and the mixed expired water PO2 were directly measured. The ventilatory water flow decreased moderately in hyperoxia, increased markedly between normoxia and 40 Torr, and below 40 Torr, hyperventilation was gradually reduced. Between PO2 400 and 70 Torr, the total O2 uptake was constant and the skin O2 uptake was lower than gill O2 uptake (32% of total uptake in normoxia). Between 70 and 10 Torr, the skin contribution to the total O2 uptake progressively increased, and was higher than gill O2 uptake in severe hypoxia. A possible facilitation of cutaneous O2 uptake in hypoxia is discussed from estimates of the O2 diffusing capacity of the skin.

Physiological evidence for the occurrence of pathways shunting blood away from the secondary lamellae of eel gills.

1. Several cardiovascular and respiratory measurements have been performed in eels before and after intravenous injections of adrenaline. These experiments have allowed a comparison to be made of values for the cardiac output determined directly (Q) and using the Fick principle (QF) on individual fish under these two conditions. 2. Under control conditions it was shown that QF/Q = 0.72, indicating that about 30% of the mixed venous blood afferent to the gills is returned directly to the heart and bypasses the lamellar circulation via veno-venous anastomoses between the afferent filament arteries and the central venous space of the gill filaments. 3. Adrenaline, which during winter only has its action due to stimulation of alpha-adrenoreceptors, induced a hypoventilation but no changes in cardiac output in spite of a bradycardia. The oxygen content of the mixed venous blood was markedly increased whereas Ca,O2 remained unchanged as did the percentage utilization of oxygen from the water as it passed over the gills. The efferent blood flow from the gills after injection of adrenaline was almost equal to the total cardiac output. It is suggested that such a circulatory change was due to adrenaline-mediated constriction of veno-venous anastomoses in the gills of the eel.