The Effects of Branchial Denervation and Pseudobranch Ablation on Cardioventilatory Control in an Air-Breathing Fish

1991 ◽  
Vol 161 (1) ◽  
pp. 347-365 ◽  
Author(s):  
DAVID J. McKENZIE ◽  
MARK L. BURLESON ◽  
DAVID J. RANDALL
Keyword(s):  
Cardiovascular Responses ◽  
Sodium Cyanide ◽  
Air Breathing ◽  
Ventilatory Responses ◽  
Reflex Bradycardia ◽  
Afferent Information ◽  
Gill Ventilation ◽  
Air Ventilation ◽  
Amia Calva

Present address and address for reprint requests: Istituto di Scienze Farmacologiche, via Balzaretti 9, Università di Milano, Milano 20133, Italy. The role of sensory afferent information from the gills of Amia calva in cardiovascular and ventilatory control was investigated by bilateral branchial denervation and pseudobranch ablation. Aquatic hypoxia or 1 mg of sodium cyanide (NaCN) in the water flowing over the gills stimulated bradycardia, and gill and air ventilation in sham-operated fish. Sodium cyanide, noradrenaline (NA) and adrenaline (A) infusion into the dorsal aorta increased gill ventilation, and NA and A infusion also stimulated tachycardia and an increase in blood pressure. Following denervation and pseudobranch ablation, O2 consumption (V·OO2), airbreathing frequency (fAB) and arterial O2 tension (PaOO2) declined, and circulating NA levels increased, as compared with sham-operated fish. Cardiovascular and air-breathing responses to hypoxia were abolished and gill ventilatory responses attenuated. All ventilatory and cardiovascular responses to NaCN were abolished and gill ventilatory responses to NA and A were attenuated in animals following denervation and pseudobranch ablation. These results demonstrate that O2-sensitive chemoreceptors in the gills and pseudobranch control reflex bradycardia and air-breathing responses in Amia, but that gill ventilatory responses to hypoxia, NA and A are partially mediated by extrabranchial mechanisms. Plasma NA levels increased during hypoxia in shamoperated and denervated animals, indicating that circulating NA may have mediated gill ventilatory responses in denervated animals.

An Examination of Central Chemosensitivity in an Air-Breathing Fish (Amia Calva)

1991 ◽  
Vol 155 (1) ◽  
pp. 165-174 ◽  
Author(s):  
M. S. HEDRICK ◽  
M. L. BURLESON ◽  
D. R. JONES ◽  
W. K. MILSOM
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cerebral Ventricles ◽  
Air Breathing ◽  
Central Chemosensitivity ◽  
Central Chemoreceptors ◽  
Gill Ventilation ◽  
Amia Calva ◽  
Affect Heart Rate

The role of central chemosensitivity in the control of ventilation in fishes was investigated directly by perfusing a mock extradural fluid (EDF) through the cranial space in the medullary region of conscious air-breathing fish, Amia calva. Perfusions with Sudan Black dye showed that the mock EDF communicated with the cerebrospinal fluid (CSF) and entered the cerebral ventricles. Altering the PO2, PCO2 and/or pH of the mock EDF had no effect on gill- or air-breathing rates, heart rate or blood pressure during exposure to normoxic water. Aquatic hypoxia, however, stimulated gill ventilation and elevated blood pressure, but did not affect heart rate; altering the gas tensions and/or pH of mock EDF still had no effect on recorded variables. Sodium cyanide (NaCN) added to the mock EDF caused struggling at concentrations above 500 μgml−1, but did not uniformly stimulate ventilation. These results suggest that central chemoreceptors, which mediate cardiovascular or ventilatory reflexes, are absent in Amia.

scholarly journals Role of nitric oxide-containing factors in the ventilatory and cardiovascular responses elicited by hypoxic challenge in isoflurane-anesthetized rats

2014 ◽  
Vol 116 (11) ◽  
pp. 1371-1381 ◽  
Author(s):  
James P. Mendoza ◽  
Rachael J. Passafaro ◽  
Santhosh M. Baby ◽  
Alex P. Young ◽  
James N. Bates ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Cardiovascular Responses ◽  
Vital Role ◽  
Initial Increase ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Before And After

Exposure to hypoxia elicits changes in mean arterial blood pressure (MAP), heart rate, and frequency of breathing (fr). The objective of this study was to determine the role of nitric oxide (NO) in the cardiovascular and ventilatory responses elicited by brief exposures to hypoxia in isoflurane-anesthetized rats. The rats were instrumented to record MAP, heart rate, and fr and then exposed to 90 s episodes of hypoxia (10% O2, 90% N2) before and after injection of vehicle, the NO synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME), or the inactive enantiomer d-NAME (both at 50 μmol/kg iv). Each episode of hypoxia elicited a decrease in MAP, bidirectional changes in heart rate (initial increase and then a decrease), and an increase in fr. These responses were similar before and after injection of vehicle or d-NAME. In contrast, the hypoxia-induced decreases in MAP were attenuated after administration of l-NAME. The initial increases in heart rate during hypoxia were amplified whereas the subsequent decreases in heart rate were attenuated in l-NAME-treated rats. Finally, the hypoxia-induced increases in fr were virtually identical before and after administration of l-NAME. These findings suggest that NO factors play a vital role in the expression of the cardiovascular but not the ventilatory responses elicited by brief episodes of hypoxia in isoflurane-anesthetized rats. Based on existing evidence that NO factors play a vital role in carotid body and central responses to hypoxia in conscious rats, our findings raise the novel possibility that isoflurane blunts this NO-dependent signaling.

scholarly journals Control of gill ventilation and air-breathing in the bowfin amia calva

1999 ◽  
Vol 202 (1) ◽  
pp. 87-94
Author(s):  
M.S. Hedrick ◽  
D.R. Jones
Keyword(s):  
Bladder Volume ◽  
Control Fish ◽  
Type I ◽  
Type Ii ◽  
Afferent Pathways ◽  
Air Breathing ◽  
Gas Bladder ◽  
Stretch Receptors ◽  
Gill Ventilation ◽  
Amia Calva

The purpose of this study was to investigate the roles of branchial and gas bladder reflex pathways in the control of gill ventilation and air-breathing in the bowfin Amia calva. We have previously determined that bowfin use two distinct air-breathing mechanisms to ventilate the gas bladder: type I air breaths are characterized by exhalation followed by inhalation, are stimulated by aquatic or aerial hypoxia and appear to regulate O2 gas exchange; type II air breaths are characterized by inhalation alone and possibly regulate gas bladder volume and buoyancy. In the present study, we test the hypotheses (1) that gill ventilation and type I air breaths are controlled by O2-sensitive chemoreceptors located in the branchial region, and (2) that type II air breaths are controlled by gas bladder mechanosensitive stretch receptors. Hypothesis 1 was tested by examining the effects of partial or complete branchial denervation of cranial nerves IX and X to the gill arches on gill ventilation frequency (fg) and the proportion of type I air breaths during normoxia and hypoxia; hypothesis II was tested by gas bladder inflation and deflation. Following complete bilateral branchial denervation, fg did not differ from that of sham-operated control fish; in addition, fg was not significantly affected by aquatic hypoxia in sham-operated or denervated fish. In sham-operated fish, aquatic hypoxia significantly increased overall air-breathing frequency (fab) and the percentage of type I breaths. In fish with complete IX-X branchial denervation, fab was also significantly increased during aquatic hypoxia, but there were equal percentages of type I and type II air breaths. Branchial denervation did not affect the frequency of type I air breaths during aquatic hypoxia. Gas bladder deflation via an indwelling catheter resulted in type II breaths almost exclusively; furthermore, fab was significantly correlated with the volume removed from the gas bladder, suggesting a volume-regulating function for type II air breaths. These results indicate that chronic (3–4 weeks) branchial denervation does not significantly affect fg or type I air-breathing responses to aquatic hypoxia. Because type I air-breathing responses to aquatic hypoxia persist after IX-X cranial nerve denervation, O2-sensitive chemoreceptors that regulate air-breathing may be carried in other afferent pathways, such as the pseudobranch. Gas bladder deflation reflexly stimulates type II breaths, suggesting that gas bladder volume-sensitive stretch receptors control this particular air-breathing mechanism. It is likely that type II air breaths function to regulate buoyancy when gas bladder volume declines during the inter-breath interval.

Cardiovascular effects of microinjection of low doses of serotonin into the NTS of unanesthetized rats

1997 ◽  
Vol 272 (4) ◽  
pp. R1135-R1142 ◽  
Author(s):  
J. C. Callera ◽  
L. G. Bonagamba ◽  
C. Sevoz ◽  
R. Laguzzi ◽  
B. H. Machado
Keyword(s):  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Cardiovascular Reflexes ◽  
Low Doses ◽  
Reflex Bradycardia ◽  
Baseline Values ◽  
Dose Dependent Decrease ◽  
Baroreceptor Activation ◽  
Dose Dependent

In the present study, we analyzed in conscious rats the effects of microinjections of serotonin (5-HT; pmol range) into the nucleus of the solitary tract (NTS) on basal mean arterial pressure (MAP) and heart rate (HR) and also on the reflex bradycardia induced by the activation of the baro- and chemoreflex evaluated 1 min after 5-HT microinjection into the NTS. The data show that unilateral microinjection of 5-HT in the picomolar range into the NTS of unanesthetized rats produced a dose-dependent decrease in MAP and HR, which was blocked by previous microinjection of ketanserin (250 pmol/50 nl) into the NTS. The changes in MAP and HR induced by 5-HT were of very short duration, with a return to baseline values a few seconds later. The cardiovascular responses to baro- or chemoreflex activation 1 min after 5-HT microinjection into the NTS did not differ from the control, indicating that low doses of 5-HT produced no effect on the cardiovascular reflexes tested at that time. The present data show that, as also observed in anesthetized rats, the microinjection of picomolar doses of 5-HT into the NTS elicits the typical cardiovascular responses to baroreceptor activation. These effects, hypotension and bradycardia, seem to be mediated by 5-HT2 receptors because both were blocked by a selective 5-HT2 receptor antagonist. However, since microinjection of 5-HT (1 pmol) into the NTS produced no changes in the cardiovascular responses to the baro- and chemoreflex activated 1 min later, the role of 5-HT2 receptors in the processing of the cardiovascular afferent messages in the NTS remains to be elucidated.

Ventilation and hypoxic ventilatory responsiveness in Chinese-Tibetan residents at 3,658 m

1997 ◽  
Vol 83 (6) ◽  
pp. 2098-2104 ◽  
Author(s):  
Linda S. Curran ◽  
Jianguo Zhuang ◽  
Shin Fu Sun ◽  
Lorna G. Moore
Keyword(s):  
High Altitude ◽  
Minute Ventilation ◽  
Ambient Air ◽  
Hypoxic Exposure ◽  
Chronic Mountain Sickness ◽  
Air Breathing ◽  
Ventilatory Responses ◽  
Permissive Role

Curran, Linda S., Jianguo Zhuang, Shin Fu Sun, and Lorna G. Moore. Ventilation and hypoxic ventilatory responsiveness in Chinese-Tibetan residents at 3,658 m. J. Appl. Physiol. 83(6): 2098–2104, 1997.—When breathing ambient air at rest at 3,658 m altitude, Tibetan lifelong residents of 3,658 m ventilate as much as newcomers acclimatized to high altitude; they also ventilate more and have greater hypoxic ventilatory responses (HVRs) than do Han (“Chinese”) long-term residents at 3,658 m. This suggests that Tibetan ancestry is advantageous in protecting resting ventilation levels during years of hypoxic exposure and is of interest in light of the permissive role of hypoventilation in the development of chronic mountain sickness, which is nearly absent among Tibetans. The existence of individuals with mixed Tibetan-Chinese ancestry (Han-Tibetans) residing at 3,658 m affords an opportunity to test this hypothesis. Eighteen men born in Lhasa, Tibet, China (3,658 m) to Tibetan mothers and Han fathers were compared with 27 Tibetan men and 30 Han men residing at 3,658 m who were previously studied. We used the same study procedures (minute ventilation was measured with a dry-gas flowmeter during room air breathing and hyperoxia and with a 13-liter spirometer-rebreathing system during the hypoxic and hypercapnic tests). During room air breathing at 3,658 m (inspired O2 pressure = 93 Torr), Han-Tibetans resembled Tibetans in ventilation (12.1 ± 0.6 vs. 11.5± 0.5 l/min btps, respectively) but had HVR that were blunted (63 ± 16 vs. 121 ± 13, respectively, for HVR shape parameter A) and declined with increasing duration of high-altitude residence. During administered hyperoxia (inspired O2 pressure = 310 Torr) at 3,658 m, the paradoxical hyperventilation previously seen in Tibetan but not Han residents at 3,658 m (11.8 ± 0.5 vs. 10.1 ± 0.5 l/min btps) was absent in these Han-Tibetans (9.8 ± 0.6 l/minbtps). Thus, although longer duration of high-altitude residence appears to progressively blunt HVR among Han-Tibetans born and residing at 3,658 m, their Tibetan ancestry appears protective in their maintenance of high resting ventilation levels despite diminished chemosensitivity.

Chemoreflexive responses to hypoxia and NaCN in longnose gar: evidence for two chemoreceptor loci

1986 ◽  
Vol 251 (1) ◽  
pp. R116-R125 ◽  
Author(s):  
N. J. Smatresk ◽  
M. L. Burleson ◽  
S. Q. Azizi
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular Responses ◽  
Dorsal Aorta ◽  
Pressure Amplitude ◽  
Breathing Frequency ◽  
Air Breathing ◽  
Gill Ventilation ◽  
Ventral Aorta ◽  
Hypoxic Water

Interactions between internal and external O2 stimulus levels were assessed by measuring the ventilatory and cardiovascular responses to varying water (PWO2) and air bladder (PabO2) O2 levels and intravascular NaCN in anesthetized spontaneously ventilating Lepisosteus osseus. As PWO2 fell, air-breathing frequency (fab) increased. Buccal pressure amplitude (Pb) also increased as PWO2 fell from hyperoxia to normoxia, but hypoxic water depressed Pb. The PO2 in the ventral aorta (VA) fell as PabO2 fell, which stimulated fab and Pb when the gar was in normoxic or hyperoxic water. Thus gill ventilation and air breathing were normally controlled by both internal and external O2 levels, but aquatic hypoxia uniformly depressed gill ventilation regardless of changes in PabO2 levels. Heart rate and blood pressure were unaffected by these changes. NaCN stimulated hypoxic reflexes and bradycardia more quickly when given into the VA or conus than when given into the dorsal aorta. The animals appear to possess internal chemoreceptors that set the level of hypoxic drive and external chemoreceptors that inhibit gill ventilation and shift the ventilatory emphasis from water to air breathing.

The role of compassionate love in shaping psychological, behavioral, and cardiovascular responses to a partner in distress

2014 ◽  
Author(s):  
Molly Ann Metz ◽  
Heidi Kane ◽  
Thery Prok ◽  
Christena Cleveland ◽  
Nancy Collins
Keyword(s):  
Cardiovascular Responses ◽  
Compassionate Love

Role of paraventricular and supraoptic nuclei in central cardiovascular regulation in the cat

1980 ◽  
Vol 239 (1) ◽  
pp. R137-R142 ◽  
Author(s):  
J. Ciriello ◽  
F. R. Calaresu
Keyword(s):  
Heart Rate ◽  
Cardiovascular Responses ◽  
Inhibitory Influence ◽  
Sympathetic Nervous Systems ◽  
Aortic Depressor Nerve ◽  
Bilateral Lesions ◽  
Alpha Chloralose ◽  
Supraoptic Nuclei ◽  
Stimulation Of

To investigate the role of the paraventricular (PAH) and supraoptic (SON) nuclei in regulation of the cardiovascular system experiments were done in 26 cats anesthetized with alpha-chloralose, paralyzed, and artificially ventilated. Electrical stimulation of histologically verified sites in the region of the PAH and SON elicited increases in arterial pressure in bilaterally vagotomized animals and increases in heart rate both in spinal (C2) animals and in animals bilaterally vagotomized, In addition, stimulation of either the PAH or SON inhibited the reflex vagal bradycardia elicited by stimulation of the carotid sinus nerve (CSN) and bilateral lesions of these areas increased the magnitude of the response. On the other hand, stimulation and lesions of these hypothalamic regions did not alter the magnitude of the cardiovascular responses to stimulation of the aortic depressor nerve. These results demonstrate that stimulation of the PAH and SON elicit cardiovascular responses due to reciprocal changes in activity of the parasympathetic and sympathetic nervous systems and that these structures maintain a tonic inhibitory influence on the heart rate component of the CSN reflex.

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