Hypoxic Bradycardia Research Articles

Bimodal regulation of heart rate during hypoxic bradycardia in rainbow trout Oncorhynchus mykiss

Bimodal regulation of heart rate during hypoxic bradycardia in rainbow trout Oncorhynchus mykiss

The role of the vagus nerve in the generation of cardiorespiratory interactions in a neotropical fish, the pacu, Piaractus mesopotamicus

The role of the vagus nerve in determining heart rate (f(H)) and cardiorespiratory interactions was investigated in a neotropical fish, Piaractus mesopotamicus. During progressive hypoxia f(H) initially increased, establishing a 1:1 ratio with ventilation rate (f(R)). Subsequently there was a hypoxic bradycardia. Injection of atropine abolished a normoxic inhibitory tonus on the heart and the f(H) adjustments during progressive hypoxia, confirming that they are imposed by efferent parasympathetic inputs via the vagus nerve. Efferent activity recorded from the cardiac vagus in lightly anesthetized normoxic fish included occasional bursts of activity related to spontaneous changes in ventilation amplitude, which increased the cardiac interval. Restricting the flow of aerated water irrigating the gills resulted in increased respiratory effort and bursts of respiration-related activity in the cardiac vagus that seemed to cause f(H) to couple with f(R). Cell bodies of cardiac vagal pre-ganglionic neurons were located in two distinct groups within the dorsal vagal motor column having an overlapping distribution with respiratory motor-neurons. A small proportion of cardiac vagal pre-ganglionic neurons (2%) was in scattered positions in the ventrolateral medulla. This division of cardiac vagal pre-ganglionic neurons into distinct motor groups may relate to their functional roles in determining cardiorespiratory interactions.

Abolition of reflex bradycardia by cardiac vagotomy has no effect on the regulation of oxygen uptake by Atlantic cod in progressive hypoxia

The functional significance of chemoreflexive hypoxic bradycardia was explored in Atlantic cod Gadus morhua L. (mean mass ∼ 800 g, acclimated to a seawater temperature of 11 °C) by investigating responses to progressive hypoxia following section of the cardiac branches of cranial nerve X. Cardiac denervation had no effect on oxygen uptake rate ( M O 2 ), gill ventilation rate ( f G) or opercular pressure amplitude ( P OP) under normoxic conditions, but caused a significant increase in heart rate ( f H), to 50 ± 1 beats min − 1 by comparison to 40 ± 2 beats min − 1 in sham-operated cod (mean ± s.e.m., n = 9). Sham-operated cod exhibited transient profound bradycardia following oxygen chemoreceptor stimulation by bolus injection of sodium cyanide into the buccal cavity (2 mg in 2 ml seawater), but this cardiac chemoreflex was abolished in denervated cod. Both groups, however, exhibited similar marked transient chemoreflexive hyperventilation following NaCN. When exposed from normoxia ( PO 2 ∼ 18 kPa) to progressive hypoxia at nominal water PO 2's of 8, 6, 5, 4 and 3 kPa, both groups exhibited the same pattern of homeostatic regulation of M O 2 , with no significant difference in their mean critical PO 2 ( P crit) values, which were 7.40 ± 0.81 kPa and 8.73 ± 0.71 kPa, respectively ( n = 9). Both groups exhibited significant bradycardia during progressive hypoxia, although denervated fish always had higher mean f H. The incipient threshold for bradycardia coincided with P crit in sham-operated cod whereas, in denervates, the threshold was below their P crit and bradycardia presumably reflected direct effects of hypoxia on the myocardium. The sham-operated group displayed a significantly more pronounced ventilatory response than denervates in hypoxia, in particular for P OP. In sham-operated cod, peak ventilatory responses occurred in deep hypoxia below P crit whereas, in denervates, more modest peak responses coincided with P crit and, in deep hypoxia, they exhibited a significant decline in f G below their normoxic rate. Only a minority of shams lost equilibrium in hypoxia whereas a majority of denervates did, some of which failed to recover. The results indicate that chemoreflexive bradycardia plays no role in the homeostatic regulation of oxygen uptake by cod in hypoxia, but does contribute to maintenance of overall functional integrity below P crit.

Why hypoxic bradycardia in fishes?

Why hypoxic bradycardia in fishes?

The effect of hypoxic bradycardia on the oxygen consumption by the European eel (Anguilla anguilla)

The effect of hypoxic bradycardia on the oxygen consumption by the European eel (Anguilla anguilla)

Tribute to P. L. Lutz: a message from the heart – why hypoxic bradycardia in fishes?

The sensing and processing of hypoxic signals, the responses to these signals and the modulation of these responses by other physical and physiological factors are an immense topic filled with numerous novel and exciting discoveries. Nestled among these discoveries, and in contrast to mammals, is the unusual cardiac response of many fish to environmental hypoxia - a reflex slowing of heart rate. The afferent and efferent arms of this reflex have been characterised, but the benefits of the hypoxic bradycardia remain enigmatic since equivocal results have emerged from experiments examining the benefit to oxygen transfer across the gills. The main thesis developed here is that hypoxic bradycardia could afford a number of direct benefits to the fish heart, largely because the oxygen supply to the spongy myocardium is precarious (i.e. it is determined primarily by the partial pressure of oxygen in venous blood, Pv(O(2))) and, secondarily, because the fish heart has an unusual ability to produce large increases in cardiac stroke volume (V(SH)) that allow cardiac output to be maintained during hypoxic bradycardia. Among the putative benefits of hypoxic bradycardia is an increase in the diastolic residence time of blood in the lumen of the heart, which offers an advantage of increased time for diffusion, and improved cardiac contractility through the negative force-frequency effect. The increase in V(SH) will stretch the cardiac chambers, potentially reducing the diffusion distance for oxygen. Hypoxic bradycardia could also reduce cardiac oxygen demand by reducing cardiac dP/dt and cardiac power output, something that could be masked at cold temperature because of a reduced myocardial work load. While the presence of a coronary circulation in certain fishes decreases the reliance of the heart on Pv(O(2)), hypoxic bradycardia could still benefit oxygen delivery via an extended diastolic period during which peak coronary blood flow occurs. The notable absence of hypoxic bradycardia among fishes that breathe air during aquatic hypoxia and thereby raise their Pv(O(2)), opens the possibility that that the evolutionary loss of hypoxic bradycardia may have coincided with some forms of air breathing in fishes. Experiments are needed to test some of these possibilities. Ultimately, any potential benefit of hypoxic bradycardia must be placed in the proper context of myocardial oxygen supply and demand, and must consider the ability of the fish heart to support its routine cardiac power output through glycolysis.

A TRIBUTE TO PETER LUTZ

![Figure][1] One defining feature of Peter Lutz's career was that he was fascinated by a wide range of animals and how they coped with environmental extremes, particularly hypoxia and anoxia. When he passed away in February 2005, his friends and colleagues wanted to celebrate his career and

The role of the M2 muscarinic receptor in the development of hypoxic bradycardia in zebrafish (Danio rerio) larvae

The role of the M2 muscarinic receptor in the development of hypoxic bradycardia in zebrafish (Danio rerio) larvae

Cardiovascular changes after naloxone administration in propofol-sedated piglets during opioid overdose

Naloxone is an opioid receptor antagonist. Even when used in modest doses, it has been associated with serious cardiopulmonary side-effects. In this experimental porcine study, we examined the cardiac effects of naloxone during an opioid overdose. Cardiac parameters, changes in the left ventricular compliance and the magnitude of catecholamine release were evaluated in eight spontaneously breathing piglets under propofol sedation. Cardiac parameters were recorded every 30 s and transthoracic echocardiography was used for the continuous assessment of cardiac performance. Respiratory arrest was induced by morphine (8 mg/kg). Ten minutes after morphine administration, naloxone (80 microg/kg) was injected intravenously. Every 5 min, arterial blood gases were measured and, every 10 min, a sample for the analysis of plasma catecholamines was drawn. There were no statistically significant changes in left ventricular ejection fraction and no signs of pulmonary hypertension. There was a statistically significant increase in the mean arterial pressure immediately after naloxone administration and in norepinephrine concentration before naloxone administration. After naloxone administration, the plasma catecholamine levels decreased in all but one animal. Two animals developed cardiac arrest (pulseless electrical activity and ventricular fibrillation) shortly after receiving naloxone. Although they were both administered naloxone prematurely due to hypoxic bradycardia, naloxone could have contributed to the development of ventricular fibrillation. Naloxone did not cause changes in ejection fraction or mean pulmonary artery pressure in hypoxic and hypercarbic conditions. After naloxone administration, the plasma catecholamine levels returned to baseline in all but one animal, and two animals developed cardiac arrest.

The role of branchial and orobranchial O2 chemoreceptors in the control of aquatic surface respiration in the neotropical fish tambaqui(Colossoma macropomum): progressive responses to prolonged hypoxia

The present study examined the role of branchial and orobranchial O(2) chemoreceptors in the cardiorespiratory responses, aquatic surface respiration (ASR), and the development of inferior lip swelling in tambaqui during prolonged (6 h) exposure to hypoxia. Intact fish (control) and three groups of denervated fish (bilateral denervation of cranial nerves IX+X (to the gills), of cranial nerves V+VII (to the orobranchial cavity) or of cranial nerves V alone), were exposed to severe hypoxia (Pw(O)2=10 mmHg) for 360 min. Respiratory frequency (fr) and heart rate (fh) were recorded simultaneously with ASR. Intact (control) fish increased fr, ventilation amplitude (V(AMP)) and developed hypoxic bradycardia in the first 60 min of hypoxia. The bradycardia, however, abated progressively and had returned to normoxic levels by the last hour of exposure to hypoxia. The changes in respiratory frequency and the hypoxic bradycardia were eliminated by denervation of cranial nerves IX and X but were not affected by denervation of cranial nerves V or V+VII. The V(AMP) was not abolished by the various denervation protocols. The fh in fish with denervation of cranial nerves V or V+VII, however, did not recover to control values as in intact fish. After 360 min of exposure to hypoxia only the intact and IX+X denervated fish performed ASR. Denervation of cranial nerve V abolished the ASR behavior. However, all (control and denervated (IX+X, V and V+VII) fish developed inferior lip swelling. These results indicate that ASR is triggered by O(2) chemoreceptors innervated by cranial nerve V but that other mechanisms, such as a direct effect of hypoxia on the lip tissue, trigger lip swelling.

Reflex Cardioventilatory Responses to Hypoxia in the Flathead Gray Mullet (Mugil cephalus) and Their Behavioral Modulation by Perceived Threat of Predation and Water Turbidity

In hypoxia, gray mullet surface to ventilate well-oxygenated water in contact with air, an adaptive response known as aquatic surface respiration (ASR). Reflex control of ASR and its behavioral modulation by perceived threat of aerial predation and turbid water were studied on mullet in a partly sheltered aquarium with free surface access. Injections of sodium cyanide (NaCN) into either the bloodstream (internal) or ventilatory water stream (external) revealed that ASR, hypoxic bradycardia, and branchial hyperventilation were stimulated by chemoreceptors sensitive to both systemic and water O2 levels. Sight of a model avian predator elicited bradycardia and hypoventilation, a fear response that inhibited reflex hyperventilation following external NaCN. The time lag to initiation of ASR following NaCN increased, but response intensity (number of events, time at the surface) was unchanged. Mullet, however, modified their behavior to surface under shelter or near the aquarium edges. Turbid water abolished the fear response and effects of the predator on gill ventilation and timing of ASR following external NaCN, presumably because of reduced visibility. However, in turbidity, mullet consistently performed ASR under shelter or near the aquarium edges. These adaptive modulations of ASR behavior would allow mullet to retain advantages of the chemoreflex when threatened by avian predators or when unable to perceive potential threats in turbidity.

Adenosinergic and cholinergic control mechanisms during hypoxia in the epaulette shark (Hemiscyllium ocellatum), with emphasis on branchial circulation

Coral reef platforms may become hypoxic at night during low tide. One animal in that habitat, the epaulette shark (Hemiscyllium ocellatum), survives hours of severe hypoxia and at least one hour of anoxia. Here, we examine the branchial effects of severe hypoxia (<0.3 mg oxygen l(-1) for 20 min in anaesthetized epaulette shark), by measuring ventral and dorsal aortic blood pressure (P(VA) and P(DA)), heart rate (fh), and observing gill microcirculation using epi-illumination microscopy. Hypoxia induced a flow of blood in two parallel blood vessels, termed longitudinal vessels, in the outer borders of the free tip of the gill filament. Hypoxia also induced significant falls in fh, P(VA) and P(DA), and a biphasic change in ventilation frequency (increase followed by decrease). Adenosine injection (1 micromol kg(-1)) also initiated blood flow in the longitudinal vessels, in addition to significant drops in P(VA), P(DA) and fh, and a biphasic response in ventilation frequency (decrease followed by increase) indicating that adenosine influences ventilation. Aminophylline (10 mg kg(-1)), an A(1) and A(2) adenosine receptor antagonist, blocked the effects of adenosine injection, and also significantly reduced blood flow in the longitudinal vessels during hypoxia. In the second part of the study, we examined the cholinergic influence on the cardiovascular circulation during severe hypoxia (<0.3 mg l(-1)) using antagonists against muscarinic (atropine 2 mg kg(-1)) and nicotinic (tubocurarine 5 mg kg(-1)) receptors. Injection of acetylcholine (ACh; 1 micromol kg(-1)) into the ventral aorta caused a marked fall in fh, a large increase in P(VA), but small changes in P(DA) (suggesting increased R(gill)). Atropine was able to inhibit the branchial vascular responses to ACh but not the hypoxic bradycardia, suggesting the presence of muscarinic receptors on the heart and gill vasculature, and that the hypoxia induced bradycardia is of non-cholinergic origin. The results suggest that adenosine mediates increases in the arterio-venous circulation in the gill during hypoxia. This may serve to increase blood supply to heart and gill tissue.

Effects of chronic hypoxia on inward rectifier K(+) current ( I(K1)) in ventricular myocytes of crucian carp (Carassius carassius) heart.

Some ectothermic vertebrates show unusually good tolerance to oxygen shortage and it is therefore assumed that they might, as a defense mechanism, decrease number or activity of ion channels in order to reduce membrane leakage and thereby ATP-dependent ion pumping in hypoxia. Although several studies have provided indirect evidence in favor of this 'channel arrest' hypothesis, only few experiments have examined activity of ion channels directly from animals exposed to chronic hypoxia or anoxia in vivo. Here we compare the inwardly rectifying K(+) current (I(K1)), a major leak and repolarizing K(+) pathway of the heart, in cardiac myocytes of normoxic and hypoxic crucian carp, using the whole-cell and cell-attached single-channel patch-clamp methods. Whole-cell conductance of I(K1) was 0.5 +/- 0.04 nS/pF in normoxic fish and did not change during the 4 weeks hypoxic (O2 < 0.4 mg/l; 2.68 mmHg) period, meanwhile the activity of Na(+)/K(+)ATPase decreased 33%. Single-channel conductance of the I(K1) was 20.5 +/- 0.8 pS in control fish and 21.4 +/- 1.1 pS in hypoxic fish, and the open probability of the channel was 0.80 +/- 0.03 and 0.74 +/- 0.04 ( P > 0.05) in control and hypoxic fish, respectively. Open and closed times also had identical distributions in normoxic and hypoxic animals. These results suggest that the density and activity of the inward rectifier K(+) channel is not modified by chronic hypoxia in ventricular myocytes of the crucian carp heart. It is concluded that instead of channel arrest, the hypoxic fish cardiac myocytes obtain energy savings through 'action potential arrest' due to hypoxic bradycardia.

Cardiovascular regulation during hypoxia in embryos of the domestic chicken Gallus gallus.

Renewed interest in the use of the embryonic chicken as a model of perinatal cardiovascular regulation has inspired new questions about the control mechanisms that respond to acute perturbations, such as hypoxia. The objectives of this study were to determine the cardiovascular responses, the regulatory mechanisms involved in those cardiovascular responses, and whether those mechanisms involved the central nervous system (CNS) of embryonic chickens. Heart rate (f(H)) and blood pressure were measured in chicken embryos of different incubation ages during exposure to different levels of hypoxia (15, 10, and 5% O(2)). At all levels of hypoxia and at all developmental ages, a depression of f(H) and arterial pressure was observed, with the exception of day 20 embryos in 15 and 10% O(2). The intensity of the embryonic f(H) and blood pressure responses were directly related to the level of hypoxia used. Muscarinic and alpha-adrenergic receptor stimulation limited the hypoxic hypotension on days 15-19 and 15-21, respectively, as indicated after blockade with atropine and phentolamine. During the final 3 days of incubation, the intensity of the hypoxic hypotension was magnified due to alpha-vasodilation caused by beta-adrenergic and muscarinic receptor stimulation. In 19- to 21-day-old embryos, the f(H) response to hypoxia was limited by alpha-adrenergic receptor stimulation as indicated by the accentuated bradycardia after blockade with phentolamine. Furthermore, on day 21, atropine limited the hypoxic bradycardia, indicating that muscarinic receptors also play a role in the f(H) response at this age. In addition, the muscarinic actions on the heart and the adrenergic effects on the vasculature appeared to occur through a hypoxic-induced direct release from chromaffin tissue and autonomic nerve terminals. Thus, in embryonic chickens, the only cardiovascular response to hypoxia that involves the CNS was the cholinergic regulation of arterial pressure after day 15 of incubation. Therefore, although embryonic chickens and fetal sheep, the standard models of perinatal cardiovascular physiology, respond to hypoxia with a similar redistribution of cardiac output, the underlying mechanisms differ between these species.

Decrease in Oxygen Saturation with Pulse Oximetry Caused by Postintubation Croup in Pediatric Patients

Background: Postintubation croup (PC) is the rapid development of upper-airway obstruction as evidenced by hoarseness, stridor and/or chest retraction. This complication can lead to arterial desatura- tion and hypoxic bradycardia and these results may be serious, especially in pediatric patients. This study was undertaken to find the relationship between the oxygen desaturation and the duration of anesthesia. At the same time we tried to determine the incidence and etiologic factors of this complication. Methods: For this study, 400 children who received general anesthesia were studied. We investigated the several contnbuting factors in PC, such as age, anesthesia duration, and trauma during intubation. And the arterial oxygen saturation was measured by pulse oximetry. Results: The incidence of PC in children was 2 percent, Fifty percent of the patients with PC were 1-4 years old. There was no significant difference between sexes. 62.6% of the children received general anesthesia over 1 hour. There was no significance detected between the degree of oxygen desaturation and the anesthesia duration. Conclusions: We confirmed that the anesthesia duration (>1 hour) and age (1-4 years old) were important etiologic factors of PC. But the degree of oxygen desaturation was not correlated with the duration of anesthesia. (Korean J Anesthesiol 2001; 41: 297-301)

O2 consumption and heart rate in developing zebrafish (Danio rerio): influence of temperature and ambient O2.

Body mass, length, oxygen consumption (MO2) and heart rate (fH) were measured in "embryos" (prior to hatching), "larvae" (days 10-20), "juveniles" (days 30-70 in 10-day intervals), and "adults" (day 100) of the zebrafish Danio rerio. Fish were chronically reared at either 25, 28, or 31 degreesC and then acutely exposed to hypoxia at different developmental stages. We hypothesized that at any given rearing and measurement temperature, D. rerio would maintain MO2 at lower ambient PO2 [i.e., have a lower critical partial pressure (Pcrit)] as development progressed and that at any given developmental stage individuals reared and measured at higher temperatures would show a more pronounced hypoxic bradycardia. MO2 in normoxic fish at 28 degreesC peaked at approximately 40 micromol. g-1. h-1 at day 10, thereafter falling to 4-5 micromol. g-1. h-1 at day 100. The Q10 for MO2 was 4-5 in embryos, falling to 2-3 from day 10 to day 60 and rising again to 4-5 at day 100. Pcrit at 28 degreesC was approximately 80 mmHg in embryos but decreased sharply to 20 mmHg at 100 days, supporting the hypothesis that more mature fish would be better able to oxygen regulate to lower ambient PO2 levels. Pcrit increased sharply with measurement temperature. Heart rate (fH) at 28 degreesC increased from about 125 beats/min in embryos to a peak of approximately 175 beats/min at days 10-30 and then fell to approximately 130 beats/min by day 100. Unlike for MO2, the Q10 for fH was more constant at 1.2-2.5 throughout development. Hypoxic exposure at any temperature had no effect on fH until approximately day 30, after which time a hypoxic bradycardia was evident. As evident for MO2, the bradycardia in older larvae was more profound at higher temperatures. On the assumption that bradycardia is indicative of hypoxic stress, the increasing prevalence of a hypoxic bradycardia in older, warmer individuals supports the hypothesis that increasing hypoxic susceptibility with development would be exacerbated by increasing temperature. Collectively, these data indicate that the ability to regulate MO2 and fH in response to the compounding demands of increased temperature and/or decreased oxygen availability first develops after approximately 20 days in D. rerio and, thereafter, the ability to maintain MO2 in the face of ambient hypoxia progressively builds through to adulthood. Additionally, the temperature responses of metabolism and heart rate differ substantially at different phases of development, suggesting a loose coupling between the respiratory and cardiovascular systems, at least early in development.

The influence of aquatic surface respiration (ASR) on cardio-respiratory function of the serrasalmid fish Piaractus mesopotamicus

When exposed to severely hypoxic water, many teleosts skim the better oxygenated surface layer (aquatic surface respiration, ASR). Information is scarce concerning the thresholds triggering ASR and its cardio-respiratory consequences. To assess the ambient conditions leading to ASR and to evaluate its effects on cardio-respiratory function, we exposed specimens of Piaractus mesopotamicus to gradual hypoxia (water oxygen tension ranging from 120 to 10 torr) with or, alternatively, without access to the surface. Concurrently, ASR, cardiac and respiratory frequencies, O 2 uptake and gill ventilation were monitored. With surface access, ASR developed below the critical tension for O 2 uptake (34 torr) by normal gill ventilation. Moreover, the time spent in ASR increased with prolonged hypoxic exposure to a maximum of 95% of total time. Without surface access, the species exhibited hypoxic bradycardia, that had not occurred in the group with fully developed ASR. Even without ASR, P. mesopotamicus recovered readily from hypoxic exposure, showing that this species possesses a number of mechanisms to cope with environmental hypoxia.

Cardio-respiratory function of swimming blue crab Callinectes danae Smith, during normoxia and graded hypoxia

Swimming blue crabs Callinectes danae Smith were studied as to the respiratory (oxygen uptake, MO 2 and scaphognathite beat frequency, f sc ) and cardiac (ECG and heart beat frequency, f H ) responses to normoxia (154 mmHg) and graded hypoxia (130, 100, 70, 50, 30 and 20 mmHg). C. Danae kept constant MO 2 from normoxia until the critical oxygen tension (PcO 2) of 97 mmHg was reached, below which it declined markedly. Scaphognathite beat frequency ( f sc ) remained constant at all PwO 2 values studied. Cardiac frequency decreased gradually below 70 mmHg down to the more severe hypoxic levels. The same tendency was recorded for the ECG amplitude, suggesting a causal relationship between cardiac dysfunction and hypoxic bradycardia. Simple scaphognathite reversals remained constant independent of the PwO 2 reductions but significant increases in the frequencies of reversals associated with cardiac arrest were recorded below the PcO 2. When compared with earlier studied exclusively water breathing crabs, C. danae demonstrated high PcO 2 and limited cardio-respiratory adjustments in response to hypoxia.

Intrapartum fetal atrial bigeminy — Diagnostic and therapeutic role of the fetal scalp stimulation test

Concern for fetal hypoxia often leads to cesarean delivery when persistent fetal bradycardia is identified. A fetus with premature atrial contractions had a prolonged second-stage heart rate of 80 beats/min. Intrapartum echocardiography and electronic fetal heart rate monitoring distinguished bradycardia caused by blocked atrial bigeminy from hypoxic bradycardia. The fetal scalp stimulation test documented normal acid-base balance and normalized the ventricular rate, avoiding cesarean delivery. (A M J O BSTET G YNECOL 1996;174:1649-50.)

Aspects of cardioventilatory control in the adriatic sturgeon ( Acipenser naccarii)

Cardioventilatory responses to hypoxia, the O 2 chemoreceptor stimulant sodium cyanide (NaCN), and intra-arterial injection of atropine, noradrenaline and DL-propranolol were investigated in the adriatic sturgeon. Hypoxia elicited a bradycardia and hyperventilation. 1 mg NaCN added to water entering the buccal cavity stimulated a transient bradycardia but intra-arterial infusion of 150 μg NaCN did not, indicating that hypoxic bradycardia is controlled by chemoreceptors sensitive only to water O 2 levels. NaCN stimulated hyperventilation both when added to the water and when infused intra-arterially, indicating that hypoxic hyperventilation is controlled by chemoreceptors sensitive to both internal and external milieux. Atropine abolished the hypoxic bradycardia and returned heart rate to normoxic values indicating that this species has no inhibitory vagal tone in normoxia. Noradrenaline stimulated ventilation, an effect abolished by DL-propranolol. Propranolol blocked ventilatory responses to intra-arterial infusion of NaCN whereas responses to NaCN added to the water remained unaffected, indicating that propranolol may inhibit internally-oriented O 2-chemoreceptor activity or that ventilatory responses to intra-arterial NaCN are stimulated by a release of circulating catecholamines. Cardioventilatory control systems in sturgeon are similar to those of other actinopterygians but also show some characteristics of the system described for elasmobranchs.