7 Afferent Inputs Associated with Cardioventilatory Control in Fish

AB, and then decreased after it. However, modulation of inhibitory cholinergic tone was responsible for the major proportion of HRV, including the precise beat-to-beat modulation of f H around each AB. Pharmacological blockade of all variations in f H associated with air breathing in deep hypoxia did not, however, have a significant effect upon f AB or the regulation of M tO 2. Thus, the functional significance of the profound HRV during air breathing remains a mystery.

Section: Discussionmentioning

confidence: 99%

The autonomic control and functional significance of the changes in heart rate associated with air breathing in the jeju,Hoplerythrinus unitaeniatus

McKenzie

Campbell

Taylor

et al. 2007

“…Increasingly, however, the weight of evidence from experiments designed to distinguish directly between internal and external stimuli suggests that reflex cardiorespiratory responses to hypercarbia are mediated by externally oriented chemoreceptors. In this regard, the situation for CO 2 /pH sensing differs from that for O 2 , in that a population of internally oriented O 2 chemoreceptors exists; these receptors are distributed over all gill arches and linked specifically to ventilatory reflexes (Burleson et al, 1992;Burleson, 1995).…”

Section: (N) Cardiorespiratory Responses To Hypercarbia In Tambaquimentioning

confidence: 99%

Cardiorespiratory responses to hypercarbia in tambaquiColossoma macropomum: chemoreceptor orientation and specificity

Gilmour

Milsom

Rantin

et al. 2005

SUMMARY Experiments were carried out to test the hypothesis that ventilatory and cardiovascular responses to hypercarbia (elevated water PCO2) in the tambaqui Colossoma macropomum are stimulated by externally oriented receptors that are sensitive to water CO2 tension as opposed to water pH. Cardiorespiratory responses to acute hypercarbia were evaluated in both the absence and presence of internal hypercarbia (elevated blood PCO2), achieved by treating fish with the carbonic anhydrase inhibitor acetazolamide. Exposure to acute hypercarbia (15 min at each level, final water CO2 tensions of 7.2,15.5 and 26.3 mmHg) elicited significant increases in ventilation frequency(at 26.3 mmHg, a 42% increase over the normocarbic value) and amplitude(128%), together with a fall in heart rate (35%) and an increase in cardiac stroke volume (62%). Rapid washout of CO2 from the water reversed these effects, and the timing of the changes in cardiorespiratory variables corresponded more closely to the fall in water PCO2(PwCO2) than to that in blood PCO2(PaCO2). Similar responses to acute hypercarbia (15 min,final PwCO2 of 13.6 mmHg) were observed in acetazolamide-treated (30 mg kg-1) tambaqui. Acetazolamide treatment itself, however, increased PaCO2 (from 4.81±0.58 to 13.83±0.91 mmHg, mean ± s.e.m.; N=8) in the absence of significant change in ventilation, heart rate or cardiac stroke volume. The lack of response to changes in blood PCO2 and/or pH were confirmed by comparing responses to the bolus injection of hypercarbic saline(5% or 10% CO2; 2 ml kg-1) into the caudal vein with those to the injection of CO2-enriched water (1%, 3%, 5% or 10%CO2; 50 ml kg-1) into the buccal cavity. Whereas injections of hypercarbic saline were ineffective in eliciting cardiorespiratory responses, changes in ventilation and cardiovascular parameters accompanied injection of CO2-laden water into the mouth. Similar injections of CO2-free water acidified to the corresponding pH of the hypercarbic water (pH 6.3, 5.6, 5.3 or 4.9, respectively) generally did not stimulate cardiorespiratory responses. These results are in agreement with the hypothesis that in tambaqui, externally oriented chemoreceptors that are predominantly activated by increases in water PCO2,rather than by accompanying decreases in water pH, are linked to the initiation of cardiorespiratory responses to hypercarbia.

“…Essentially, hyperventilation allows the arterial blood partial pressure of oxygen (Pa O2 ), and hence O 2 content, to be maintained at higher levels than would otherwise be possible. The increased ventilation in response to hypoxia arises from the stimulation of externally and/or internally oriented O 2 chemoreceptors, which respond to changes in O 2 partial pressure in the inspired water or the arterial blood, respectively (Saunders and Sutterlin, 1971;Milsom and Brill, 1986;Burleson and Smatresk, 1990) (reviewed by Burleson et al, 1992;Perry et al, 2009b). The neuroepithelial cell (NEC) of the gill filament has long been suspected as the O 2 chemoreceptor of the fish gill (DunelErb et al, 1982;Bailly et al, 1992), based on its structural similarity to the O 2 sensing glomus cell of the mammalian carotid body or pulmonary neuroepithelial bodies (Bailly et al, 1992), and some indirect evidence of its activation during severe hypoxia in trout (Dunel-Erb et al, 1982).…”

Section: Introductionmentioning

confidence: 99%

The control of breathing in goldfish (Carassius auratus) experiencing thermally induced gill remodelling

Tzaneva

Perry

2010

SUMMARY At temperatures below 15°C the gill lamellae of goldfish (Carassius auratus) are largely covered by an interlamellar cell mass (ILCM) which decreases the functional surface area of the gill. The presence of the ILCM in goldfish acclimated to cold water conceivably could lead to a covering of the neuroepithelial cells (NECs), which are believed to be important for sensing ambient O2 and CO2 levels. In this study we tested the hypothesis that goldfish with covered lamellae (and presumably fewer NECs exposed to the water) exhibit a decreased capacity to hyperventilate in response to hypoxic stimuli. Measurements of ventilation amplitude and frequency were performed during exposure to acute hypoxia (PwO2=30 mmHg) or following injections of the O2 chemoreceptor stimulant NaCN into the buccal cavity or caudal vein of fish acclimated to 25°C (uncovered lamellae) or 7°C (covered lamellae) to stimulate predominantly the externally or internally oriented NECs, respectively. The results demonstrated no significant differences in the response to hypoxia, with each group exhibiting similar percentage increases in ventilation amplitude (90–91%) and frequency (34–43%). Similarly, with the exception of a rightward shift of the ventilation frequency dose–response in the fish acclimated to 7°C, there were no significant differences between the two groups of fish in the ED50 values. These findings suggest that goldfish with covered lamellae retain the capacity to sense external hypoxic stimuli. Using immunohistochemistry to identify serotonin-enriched NECs, it was demonstrated that the presence of the ILCM results in the NECs being redistributed towards the distal regions of the lamellae. In 25°C-acclimated fish, the NECs were distributed evenly along the length of the lamellae with 53±3% of them in the distal half, whereas in fish acclimated to 7°C, 83±5% of the NECs were confined to the distal half. Using the neuronal marker antibody ZN-12, it was demonstrated that the NECs at the distal edges of the lamellae are innervated by nerve fibres. Thus, it is hypothesised that the capacity to sense external hypoxic stimuli in goldfish acclimated to cold water is maintained despite the increasing coverage of the gill epithelial surfaces because of a redistribution of innervated NECs to the exposed distal regions of the lamellae.