CO2-sensitive olfactory and pulmonary receptor modulation of episodic breathing in bullfrogs

1996 ◽  
Vol 270 (1) ◽  
pp. R134-R144 ◽  
Author(s):  
R. Kinkead ◽  
W. Milsom
Keyword(s):  
Breathing Pattern ◽  
Olfactory Receptors ◽  
Breathing Frequency ◽  
Receptor Modulation ◽  
Arterial Blood ◽  
Pulmonary Receptor ◽  
Sudden Release ◽  
Kinetics Of ◽  
Tonic Stimulation ◽  
Stimulation Of

Breathing was monitored during normocarbia, hypercarbia (6% CO2 in air), and the period immediately after the return to normocarbic conditions in intact, olfactory-denervated, and vagotomized bullfrogs. In intact frogs, ventilation increased during hypercarbia, but the breathing pattern remained episodic. Immediately upon return to air, there was a further paradoxical increase in breathing frequency, and breathing became continuous in most frogs. Results obtained from animals after olfactory receptor denervation indicate that tonic stimulation of olfactory receptors by airway CO2 inhibited breathing during hypercarbia. Measurements of the kinetics of changes in airway and arterial blood CO2 levels support the suggestion that the sudden release of this inhibition on the return to normocarbic conditions was responsible for the posthypercarbic hyperpnea. Vagotomy increased ventilation during normocarbia. Hypercarbia now caused a change in breathing pattern but had no net effect on total ventilation, suggesting that pulmonary vagal feedback inhibited ventilation during normocarbia but stimulated ventilation during hypercarbia. Although olfactory and pulmonary receptor feed-back shape the breathing pattern, they were not responsible for initiating or terminating the episodes of breathing.

Thromboxane A2 mimetic U-46619 induces systemic and pulmonary hypertension and delayed tachypnea in the goat

1994 ◽  
Vol 77 (3) ◽  
pp. 1466-1473 ◽  
Author(s):  
J. A. Carrithers ◽  
D. Brown ◽  
F. Liu ◽  
J. A. Orr
Keyword(s):  
Sodium Nitroprusside ◽  
Pressor Response ◽  
Thromboxane A2 ◽  
Relative Increase ◽  
Breathing Frequency ◽  
Systemic Arterial Hypertension ◽  
Arterial Blood ◽  
Before And After ◽  
Pulmonary Arterial ◽  
Stimulation Of

Cardiorespiratory variables were measured continuously in five conscious goats before and after the infusion of U-46619 at a dose of either 2, 4, or 6 micrograms.kg-1.5 min-1. Infusion of U-46619 led to immediate increases in pulmonary arterial blood pressure (ABP) that were sustained for up to 15 min after the end of the infusion. Systemic ABP also increased, but the relative increase from control was less than the pulmonary pressor response. At the highest dose, U-46619 elicited a delayed tachypneic response that was greatest several minutes after the infusion was stopped. U-46619 was also infused simultaneously with sodium nitroprusside to clamp ABP pressure at baseline levels to determine whether stimulation of baroreceptors might contribute to the latency of the tachypneic response. Although sodium nitroprusside infusion prevented the increase in ABP, the increase in breathing frequency was still delayed 3–4 min from the start of the infusion. We conclude that U-46619 elicits pulmonary and systemic arterial hypertension in the conscious goat. At the higher dose U-46619 also elicits a delayed tachypnea that remains delayed even if ABP is normal.

α-Adrenergic receptor modulation of the intrathoracic efferent sympathetic nervous system regulating the canine heart

1989 ◽  
Vol 67 (10) ◽  
pp. 1199-1204 ◽  
Author(s):  
J. A. Armour
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Blocking Agent ◽  
Sympathetic Ganglia ◽  
Canine Heart ◽  
Receptor Modulation ◽  
Adrenergic Antagonist ◽  
Cervical Ganglia ◽  
Β Adrenergic Receptors ◽  
Stimulation Of

The augmentation of ventricular inotropism induced by electrical stimulation of acutely decentralized efferent sympathetic preganglionic axons was reduced, but still present, following administraiton of hexamethonium (10 mg/kg i.v.). While hexamethonium continued to be administered, the cardiac augmentations so induced were enhanced significantly following administration of the α-adrenergic receptor blocking agent, phentolamine myselate (1 mg/kg i.v.). Stimulation of the sympathetic efferent postganglionic axons in cardiopulmonary nerves induced cardiac augmentations that were unchanged following administration of these agents singly or together. The cardiac augmentations induced by stimulation of efferent preganglionic sympathetic axons were unchanged when phentolamine was administered alone. The augmentations of cardiac inotropism induced by efferent postganglionic sympathetic axonal stimulation were decreased following local administration of the β-adrenergic antagonist timolol into the ipsilateral stellate and middle cervical ganglia. Thereafter, these augmentations were unchanged following the subsequent intravenous administration of phentolamine. It is concluded that the activation of cardiac neurons in the stellate and middle cervical ganglia by stimulation of efferent preganglionic sympathetic axons can be modified by α-adrenergic receptors and that these effects are dependent upon β-adrenergic receptors, not nicotinic ones, in intrathoracic ganglia.Key words: α-adrenergic inotropism, sympathetic ganglia, hexamethonium, phentolamine.

The relative roles of external and internal CO2versusH+ in eliciting the cardiorespiratory responses ofSalmo salarandSqualus acanthiasto hypercarbia

2001 ◽  
Vol 204 (22) ◽  
pp. 3963-3971 ◽  
Author(s):  
S. F. Perry ◽  
J. E. McKendry
Keyword(s):  
Cardiac Output ◽  
Sea Water ◽  
Buccal Cavity ◽  
Respiratory Acidosis ◽  
Systemic Resistance ◽  
Measured Variable ◽  
Cardiorespiratory Responses ◽  
Arterial Blood ◽  
Water Ph ◽  
Stimulation Of

SUMMARYFish breathing hypercarbic water encounter externally elevated PCO2 and proton levels ([H+]) and experience an associated internal respiratory acidosis, an elevation of blood PCO2 and [H+]. The objective of the present study was to assess the potential relative contributions of CO2versus H+ in promoting the cardiorespiratory responses of dogfish (Squalus acanthias) and Atlantic salmon (Salmo salar) to hypercarbia and to evaluate the relative contributions of externally versus internally oriented receptors in dogfish.In dogfish, the preferential stimulation of externally oriented branchial chemoreceptors using bolus injections (50 ml kg–1) of CO2-enriched (4 % CO2) sea water into the buccal cavity caused marked cardiorespiratory responses including bradycardia (–4.1±0.9 min–1), a reduction in cardiac output (–3.2±0.6 ml min–1 kg–1), an increase in systemic vascular resistance (+0.3±0.2 mmHg ml min–1 kg–1), arterial hypotension (–1.6±0.2 mmHg) and an increase in breathing amplitude (+0.3±0.09 mmHg) (means ± s.e.m., N=9–11). Similar injections of CO2-free sea water acidified to the corresponding pH of the hypercarbic water (pH 6.3) did not significantly affect any of the measured cardiorespiratory variables (when compared with control injections). To preferentially stimulate putative internal CO2/H+ chemoreceptors, hypercarbic saline (4 % CO2) was injected (2 ml kg–1) into the caudal vein. Apart from an increase in arterial blood pressure caused by volume loading, internally injected CO2 was without effect on any measured variable.In salmon, injection of hypercarbic water into the buccal cavity caused a bradycardia (–13.9±3.8 min–1), a decrease in cardiac output (–5.3±1.2 ml min–1 kg–1), an increase in systemic resistance (0.33±0.08 mmHg ml min–1 kg–1) and increases in breathing frequency (9.7±2.2 min–1) and amplitude (1.2±0.2 mmHg) (means ± s.e.m., N=8–12). Apart from a small increase in breathing amplitude (0.4±0.1 mmHg), these cardiorespiratory responses were not observed after injection of acidified water.These results demonstrate that, in dogfish and salmon, the external chemoreceptors linked to the initiation of cardiorespiratory responses during hypercarbia are predominantly stimulated by the increase in water PCO2 rather than by the accompanying decrease in water pH. Furthermore, in dogfish, the cardiorespiratory responses to hypercarbia are probably exclusively derived from the stimulation of external CO2 chemoreceptors, with no apparent contribution from internally oriented receptors.

scholarly journals Arterial blood sampling in male CD-1 and C57BL/6J mice with 1% isoflurane is similar to awake mice

2018 ◽  
Vol 125 (6) ◽  
pp. 1749-1759 ◽  
Author(s):  
Ashley M. Loeven ◽  
Candace N. Receno ◽  
Caitlin M. Cunningham ◽  
Lara R. DeRuisseau
Keyword(s):  
Cardiovascular Responses ◽  
Blood Chemistry ◽  
Blood Sampling ◽  
Optimal Time ◽  
Mouse Strains ◽  
Breathing Frequency ◽  
Breathing Patterns ◽  
Suitable Alternative ◽  
Arterial Blood Sampling ◽  
Arterial Blood

Isoflurane (ISO) is a commonly used anesthetic that offers rapid recovery for laboratory animal research. Initial studies indicated no difference in arterial Pco2 ([Formula: see text]) or pH between conscious (NO ISO) and 1% ISO-exposed CD-1 mice. Our laboratory investigated whether arterial blood sampling with 1% ISO is a suitable alternative to NO ISO sampling for monitoring ventilation in a commonly studied mouse strain. We hypothesized similar blood chemistry, breathing patterns, and cardiovascular responses with NO ISO and 1% ISO. C57BL/6J mice underwent unrestrained barometric plethysmography to quantify the pattern of breathing. Mice exposed to hypoxic and hypercapnic gas under 1% ISO displayed blunted responses; with air, there were no breathing differences. Blood pressure and heart rate were not different between NO ISO and 1% ISO-exposed mice breathing air. Oxygen saturation was not different between groups receiving 2% ISO, 1% ISO, or air. Breathing frequency stabilized at ~11 min of 1% ISO following 2% ISO exposure, suggesting that 11 min is the optimal time for a sample in C57BL/6J mice. Blood samples at 1% ISO and NO ISO revealed no differences in blood pH and [Formula: see text] in C57BL/6J mice. Overall, this method reveals similar arterial blood sampling values in awake and 1% ISO CD-1 and C57BL/6J mice exposed to air. Although this protocol may be appropriate in other mouse strains when a conscious sample is not feasible, caution is warranted first to identify breathing frequency responses at 1% ISO to tailor the protocol. NEW & NOTEWORTHY Conscious arterial blood sampling is influenced by extraneous factors and is a challenging method due to the small size of mice. Through a series of experiments, we show that arterial blood sampling with 1% isoflurane (ISO) is an alternative to awake sampling in C57BL/6J and CD-1 male mice breathing air. Monitoring breathing frequency during 1% ISO is important to the protocol and should be closely followed to confirm adequate recovery after the catheter implantation.

Unrestrained video-assisted plethysmography: a noninvasive method for assessment of lung mechanical function in small animals

2008 ◽  
Vol 104 (1) ◽  
pp. 253-261 ◽  
Author(s):  
Jason H. T. Bates ◽  
John Thompson-Figueroa ◽  
Lennart K. A. Lundblad ◽  
Charles G. Irvin
Keyword(s):  
Airway Resistance ◽  
Breathing Pattern ◽  
Small Animals ◽  
Mechanical Function ◽  
Direct Link ◽  
Breathing Frequency ◽  
Noninvasive Method ◽  
Noninvasive Methods ◽  
Mean Values ◽  
Video Assisted

The assessment of lung mechanical function in small animals, particularly mice, is essential for investigations into the pathophysiology of pulmonary disease. The most accurate and specific methods for making this assessment are highly invasive and so provide data of questionable relevance to normality. By contrast, present noninvasive methods based on unrestrained plethysmography have no direct link to the mechanical properties of the lung. There is thus a need for a completely noninvasive method for determining lung mechanical function in small animals. In the present study, we demonstrate an extension of unrestrained plethysmography in which changes in lung volume are estimated via orthogonal video imaging of the thorax. These estimates are combined with the pressure swings recorded as mice breathe inside a heated and humidified chamber to yield an estimate of specific airway resistance (sRaw). We used this new technique, which we term “unrestrained video-assisted plethysmography” (UVAP), to measure sRaw in 11 BALB/c mice exposed to aerosols of saline, methacholine, and albuterol and obtained mean values of 0.71, 1.23 and 1.10 cmH2O·s, respectively. Mean breathing frequency was 4.3, 3.4, and 3.6 breaths/s, respectively, while the corresponding mean tidal volumes were 0.36, 0.44 and 0.37 ml, respectively. We conclude that UVAP, a noninvasive method, is able to provide usefully accurate estimates of sRaw and breathing pattern parameters in mice.

Stimulation of the nigrostriatal dopamine system produces hypertension and tachycardia in rats

1994 ◽  
Vol 266 (6) ◽  
pp. H2489-H2496 ◽  
Author(s):  
M. T. Lin ◽  
J. J. Yang
Keyword(s):  
Corpus Striatum ◽  
Substantia Nigra Pars Compacta ◽  
Dopamine System ◽  
Arterial Blood ◽  
Nigrostriatal Dopamine ◽  
Induced Hypertension ◽  
Bilateral Vagotomy ◽  
6 Hydroxydopamine ◽  
Da Release ◽  
Stimulation Of

To test for the ability of the nigrostriatal dopamine (DA) system to influence cardiovascular function, experiments were carried out to assess the effects of electrical or chemical stimulation of the nigrostriatal DA system on arterial blood pressure, heart rate, and striatal DA release in anesthetized rats. Electrical stimulation of the substantia nigra pars compacta (SNC), in addition to enhancing the DA release in the corpus striatum (CS), elicited proportional hypertension and tachycardia. This could be mimicked by microinjection of two excitatory amino acids, kainic acid and glutamate, into the SNC area of rat brain. The SNC stimulation-induced hypertension, tachycardia, and increased striatal DA release were attenuated by prior destruction of the nigrostriatal DA system produced by intramedial forebrain bundle injection of 6-hydroxydopamine and by prior blockade of postsynaptic DA receptors produced by intra-CS injection of DA receptor antagonists, haloperidol or pimozide. The SNC stimulation-induced hypertension was attenuated by spinal transection, whereas the SNC stimulation-induced tachycardia was attenuated by bilateral vagotomy. The data suggest that stimulation of the nigrostriatal DA system produces both hypertension and tachycardia in rats.

Reconfiguration of the Respiratory Network at the Onset of Locust Flight

1998 ◽  
Vol 80 (6) ◽  
pp. 3137-3147 ◽  
Author(s):  
Jan-Marino Ramirez
Keyword(s):  
Respiratory Activity ◽  
Respiratory Rhythm ◽  
Quiescent State ◽  
Suboesophageal Ganglion ◽  
Rhythm Generator ◽  
Locust Flight ◽  
Respiratory Network ◽  
Intracellular Stimulation ◽  
Tonic Stimulation ◽  
Stimulation Of

Ramirez, Jan-Marino. Reconfiguration of the respiratory network at the onset of locust flight. J. Neurophysiol. 80: 3137–3147, 1998. The respiratory interneurons 377, 378, 379 and 576 were identified within the suboesophageal ganglion (SOG) of the locust. Intracellular stimulation of these neurons excited the auxillary muscle 59 (M59), a muscle that is involved in the control of thoracic pumping in the locust. Like M59, these interneurons did not discharge during each respiratory cycle. However, the SOG interneurons were part of the respiratory rhythm generator because brief intracellular stimulation of these interneurons reset the respiratory rhythm and tonic stimulation increased the frequency of respiratory activity. At the onset of flight, the respiratory input into M59 and the SOG interneurons was suppressed, and these neurons discharged in phase with wing depression while abdominal pumping movements remained rhythmically active in phase with the slower respiratory rhythm (Fig. 9 ). The suppression of the respiratory input during flight seems to be mediated by the SOG interneuron 388. This interneuron was tonically activated during flight, and intracellular current injection suppressed the respiratory rhythmic input into M59. We conclude that the respiratory rhythm generator is reconfigured at flight onset. As part of the rhythm-generating network, the interneurons in the SOG are uncoupled from the rest of the respiratory network and discharge in phase with the flight rhythm. Because these SOG interneurons have a strong influence on thoracic pumping, we propose that this neural reconfiguration leads to a behavioral reconfiguration. In the quiescent state, thoracic pumping is coupled to the abdominal pumping movements and has auxillary functions. During flight, thoracic pumping is coupled to the flight rhythm and provides the major ventilatory movements during this energy-demanding locomotor behavior.

Involvement of trigeminal spinal nucleus in parasympathetic reflex vasodilatation in cat lower lip

2002 ◽  
Vol 282 (2) ◽  
pp. R492-R500 ◽  
Author(s):  
Kentaro Mizuta ◽  
Satoshi Kuchiiwa ◽  
Takashi Saito ◽  
Hideaki Mayanagi ◽  
Keishiro Karita ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Kainic Acid ◽  
Local Anesthesia ◽  
Similar Degree ◽  
Dependent Manner ◽  
Lower Lip ◽  
Arterial Blood ◽  
Blood Flow Increase ◽  
Spinal Nucleus ◽  
Stimulation Of

We examined whether the trigeminal spinal nucleus (Vsp) forms part of the central mechanism by which electrical stimulation of the central cut end of the lingual nerve (LN) evokes parasympathetic reflex vasodilatation in the lower lip in artificially ventilated, cervically vagosympathectomized cats deeply anesthetized with α-chloralose and urethane. For this purpose, we made microinjections within the brain stem to produce nonselective, reversible local anesthesia (lidocaine) or soma-selective, irreversible neurotoxic damage (kainic acid). Local anesthesia of Vsp by microinjection of lidocaine (2%; 1 μl/site) reversibly and significantly reduced the ipsilateral-LN-evoked parasympathetic reflex vasodilatation. Unilateral microinjection of kainic acid (10 mM/site; 1 μl) into Vsp ipsilateral to the stimulated LN led to an irreversible reduction in the reflex vasodilatation but had no effect on the vasodilatation elicited by stimulation of the contralateral LN. Such microinjection of kainic acid into Vsp had no effect on the vasodilatation evoked by electrical stimulation of the ipsilateral inferior salivatory nucleus. Electrical stimulation of Vsp elicited a blood flow increase in the lower lip in an intensity- and frequency-dependent manner, regardless of whether systemic arterial blood pressure rose or fell. Hexamethonium (1.0 mg/kg iv) significantly reduced the vasodilator responses elicited by electrical stimulation of the central cut end of LN or of Vsp, each to a similar degree. After hexamethonium, both vasodilator responses showed time-dependent recovery. These results strongly suggest that Vsp is an important bulbar relay for LN-evoked parasympathetic reflex vasodilatation in the cat lower lip.

scholarly journals Kinetic Modelling of [68Ga]Ga-DOTA-Siglec-9 in Porcine Osteomyelitis and Soft Tissue Infections

Molecules ◽  
2019 ◽  
Vol 24 (22) ◽  
pp. 4094 ◽  
Author(s):  
Lars Jødal ◽  
Anne Roivainen ◽  
Vesa Oikonen ◽  
Sirpa Jalkanen ◽  
Søren B. Hansen ◽  
...  
Keyword(s):  
Soft Tissue ◽  
Hind Limb ◽  
Kinetic Modelling ◽  
Compartment Model ◽  
Cell Surface Expression ◽  
Soft Tissue Infections ◽  
Tissue Samples ◽  
Tissue Compartment ◽  
Arterial Blood ◽  
Kinetics Of

Background: [68Ga]Ga-DOTA-Siglec-9 is a positron emission tomography (PET) radioligand for vascular adhesion protein 1 (VAP-1), a protein involved in leukocyte trafficking. The tracer facilitates the imaging of inflammation and infection. Here, we studied the pharmacokinetic modelling of [68Ga]Ga-DOTA-Siglec-9 in osteomyelitis and soft tissue infections in pigs. Methods: Eight pigs with osteomyelitis and soft tissue infections in the right hind limb were dynamically PET scanned for 60 min along with arterial blood sampling. The fraction of radioactivity in the blood accounted for by the parent tracer was evaluated with radio-high-performance liquid chromatography. One- and two-tissue compartment models were used for pharmacokinetic evaluation. Post-mortem soft tissue samples from one pig were analysed with anti-VAP-1 immunofluorescence. In each analysis, the animal’s non-infected left hind limb was used as a control. Results: Tracer uptake was elevated in soft tissue infections but remained low in osteomyelitis. The kinetics of [68Ga]Ga-DOTA-Siglec-9 followed a reversible 2-tissue compartment model. The tracer metabolized quickly; however, taking this into account, produced more ambiguous results. Infected soft tissue samples showed endothelial cell surface expression of the Siglec-9 receptor VAP-1. Conclusion: The kinetics of [68Ga]Ga-DOTA-Siglec-9 uptake in porcine soft tissue infections are best described by the 2-tissue compartment model.

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