Brain hypoxia and control of breathing: role of the vagi

1982 ◽  
Vol 53 (1) ◽  
pp. 212-217 ◽  
Author(s):  
R. W. Chapman ◽  
T. V. Santiago ◽  
N. H. Edelman
Keyword(s):  
Ventilatory Response ◽  
Control Of Breathing ◽  
Inspiratory Time ◽  
Small Magnitude ◽  
Lung Inflation ◽  
Brain Hypoxia ◽  
And Control ◽  
Respiratory Responses ◽  
Spontaneous Breath

Vagally mediated reflexes play an important role in the generation of respiratory responses to various stimuli. This study examined the role of vagally mediated mechanisms in the generation of the respiratory responses to progressive brain hypoxia secondary to carboxyhemoglobinemia (HbCO 013;55%) in six unanesthetized goats. Ventilation, respiratory cycle timing, and the lung inflation reflex were measured before and during CO inhalation in intact and bilaterally vagotomized animals. Our results indicate that vagal reflexes contribute a small magnitude of the hyperpnea caused by carboxyhemoglobinemia. Furthermore, in contrast to that reported for CO2 inhalation, the tachypneic nature of the ventilatory response to CO is not a vagally mediated phenomenon. CO inhalation had a biphasic influence on the strength of the lung inflation reflex measured as the ratio of inspiratory time during occlusion (TIoccl) to inspiratory time of the preceding spontaneous breath (TIspont). At HbCO levels of 35%, TIoccl/TIspont was enhanced, whereas at HbCO levels of 55% of ratio fell to unity, indicating abolition of the reflex. After vagotomy, this ratio was unity at all levels of carboxyhemoglobinemia.

Brain hypoxia and control of breathing: neuromechanical control

1980 ◽  
Vol 49 (3) ◽  
pp. 497-505 ◽  
Author(s):  
R. W. Chapman ◽  
T. V. Santiago ◽  
N. H. Edelman
Keyword(s):  
Neural Function ◽  
Resistive Load ◽  
Inspiratory Time ◽  
Lung Inflation ◽  
Brain Hypoxia ◽  
Load Compensation ◽  
Airway Occlusion ◽  
Airway Occlusion Pressure ◽  
Unanesthetized Animals ◽  
And Control

The effects of graded brain hypoxia on respiratory cycle timing, the lung inflation reflex, and respiratory compensation for an inspiratory flow-resistive load were studied in unanesthetized goats. Two models, inhalation and CO and acute reduction of brain blood flow (BBF) were used to produce comparable levels of brain hypoxia. The lung inflation reflex was assessed as the ratio of inspiratory time of an occluded breath to that of the preceding spontaneous breath (TIoccl/TIspont). Compensation for flow-resistive loading was assessed as the effect of the load upon the airway occlusion pressure response to rebreathing CO2 (delta P 0.1/delta PCO2). Major findings were 1) severe brain hypoxia (HbCO of 60% or BBF of 42%) caused tachypnea due to a 50% or more reduction of expiratory time but only a 20% or less reduction of inspiratory time; 2) moderate carboxyhemoglobinemia (HbCO of 25-30%) enhanced TIoccl/TIspont from 1.5 +/- 0.1 at control to 2.1 +/- 0.1, while severe brain hypoxia (HbCO of 60% and BBF of 42%) reduced the ratio to 1.0 +/- 0.2; and 3) compensation for a flow-resistive load, manifested by increases of delta P 0.1/delta PCO2 of 75-300% in the control state, was abolished at HbCO of 45-50% and BBF of 60%. The data suggest that in unanesthetized animals brain hypoxia elicits tachypnea largely by an effect on the expiratory phase of the bulbopontine timing mechanism. The observed enhancement of the lung inflation reflex and abolition of flow-resistive load compensation are best explained by hypoxic depression of higher than brain stem neural function.

Role of N-methyl-D-aspartate receptors in the pontine pneumotaxic mechanism in the cat

1994 ◽  
Vol 76 (3) ◽  
pp. 1138-1143 ◽  
Author(s):  
L. Ling ◽  
D. R. Karius ◽  
D. F. Speck
Keyword(s):  
Nmda Receptor ◽  
Nmda Receptors ◽  
Partial Recovery ◽  
Inspiratory Time ◽  
Systemic Injection ◽  
Lung Inflation ◽  
Mk 801 ◽  
Efferent Limb ◽  
Adult Cats

Systemic injection of MK-801, an N-methyl-D-aspartate (NMDA) receptor-associated channel blocker, induces an apneusis in vagotomized cats similar to that produced by pontine respiratory group (PRG) lesions, suggesting the possible involvement of NMDA receptors in the pontine pneumotaxic mechanism. Previous results from our laboratory indicate that the efferent limb of the pontine pneumotaxic mechanism is unlikely to require NMDA receptor-mediated neurotransmission. Therefore, the present study examined the potential involvement of PRG NMDA receptors in the pontine pneumotaxic mechanism. Experiments were conducted in decerebrate, paralyzed, and ventilated adult cats. The effects on inspiratory time (TI) of MK-801 microinjection into PRG were tested in 12 cats. Pressure microinjection of MK-801 (15 mM, 80–3,000 nl) significantly prolonged TI in all animals when lung inflation was withheld. TI progressively increased in most animals for > or = 30 min. After this period, partial recovery of the effect occurred in eight cats as TI shortened toward predrug levels. In three animals, microinjection of MK-801 induced a complete apneusis in the absence of lung inflation from which there was no detectable recovery. Microinjections into regions approximately 2 mm distant from PRG produced little or no effect. These results provide evidence that NMDA receptors located in the region of PRG play an important functional role in the control of the breathing cycle.

Role of lung inflation in control of air breath duration in African lungfish (Protopterus annectens)

1992 ◽  
Vol 262 (5) ◽  
pp. R879-R884 ◽  
Author(s):  
A. I. Pack ◽  
R. J. Galante ◽  
A. P. Fishman
Keyword(s):  
Tidal Volume ◽  
Neural Circuits ◽  
Inspiratory Time ◽  
Timing Control ◽  
Lung Inflation ◽  
Protopterus Annectens ◽  
African Lungfish ◽  
The Relationship ◽  
Different Levels

Studies were conducted in the African lungfish (Protopterus annectens) to investigate the role of lung inflation on control of the duration of the lung breath. The studies were done in decerebrate spinalectomized animals. Two types of tests were performed: 1) a no-inflation test (airway occluded) in which the lungs were not inflated during an air breath, and 2) an inflation test in which the lungs were inflated at the onset of the lung breath to different levels of intrapulmonary pressure (2.5, 5.0, 7.5, and 10.0 cmH2O). Lung inflation shortened the duration of the lung breath. The relationship between intrapulmonary pressure and breath duration was curvilinear and similar to the relationship between tidal volume and inspiratory duration in mammals. Likewise, the relationship could be described by a hyperbola with a linear relationship between intrapulmonary pressure and the inverse of breath duration. This relationship was essentially not affected by changing the composition of the gas used to inflate the lungs: air, oxygen, or nitrogen. Vagotomy, however, largely abolished the effect of lung inflation on breath duration. Because there is such similarity between these results and effect of lung inflation on control of inspiratory time in mammals, it is postulated that neural circuits for control of respiratory timing were already developed and similar in the lungfish. Because the muscles used in the lungfish to ventilate the lung are totally different (buccal force pump) from those in mammals, the neural circuits for timing control and those for shaping the pattern of motor output appear to be separate.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of cerebral fluids in control of respiration as studied in unanesthetized goats

1965 ◽  
Vol 208 (3) ◽  
pp. 436-450 ◽  
Author(s):  
J. R. Pappenheimer ◽  
V. Fencl ◽  
S. R. Heisey ◽  
D. Held
Keyword(s):  
Cerebrospinal Fluid ◽  
Ventilatory Response ◽  
Alveolar Ventilation ◽  
Capillary Blood ◽  
Concentration Profiles ◽  
Tissue Fluid ◽  
Control Of Respiration ◽  
Cerebral Tissue ◽  
Respiratory Responses

Respiratory responses to inhaled CO2 were measured in unanesthetized goats during repeated perfusions of the ventriculocisternal system through chronically implanted cannulas. [HCO3–] and pH were measured in carotid loop blood and cisternal outflow. Average steady-state alveolar ventilation increased fourfold when cerebrospinal fluid (CSF)-[HCO3–] was reduced from 30 to 15 mm/liter at constant, normal CO2 pressure or threefold when CSF pH changed from 7.32 to 7.21 at constant, normal CSF-[HCO3–]. Sensitivity was two- to sevenfold greater than reported for anesthetized animals. At constant CSF pH the ventilatory response to inhaled CO2 was 60% of the isobicarbonate response. Pco2 in cisternal outflow was shown to approximate that in cerebral tissue. HCO3– flux was measured as a function of CSF-[HCO3–] and concentration profiles between CSF and capillary blood were considered. Alveolar ventilation is a single linear function of [H+] in tissue fluid located two-thirds to three-fourths of the distance along the functional concentration gradient of HCO3– between CSF and blood at all values of Pco2 and CSF-[HCO3–] which we investigated.

The role of prostaglandins in the realization of respiratory effects of TNF-α in case of hypoxia

2021 ◽  
Author(s):  
G.А. Danilova ◽  
A.A. Klinnikova ◽  
N.P. Aleksandrova
Keyword(s):  
Ventilatory Response ◽  
Minute Volume ◽  
Respiratory Effects ◽  
Cox Inhibitor ◽  
Tnf Α ◽  
Before And After ◽  
Factor Α ◽  
And Control ◽  
Rebreathing Method

At the present time very little is known about interactions between systemic inflammation and control of respiration. The aim of this study was to compare the respiratory effects of the main inflammatory cytokine TNF - α before and after pretreatment with diclofenac, a nonspecific cyclooxygenase (COX) inhibitor. In experiments on anesthetized, tracheostomized rats, pneumotachometry method was used to measure peak airflow and respiratory rate. The ventilatory response to hypoxia was investigated by the rebreathing method. It is shown that an increase in the systemic level of TNF – α causes a significant increase in the minute volume of respiration, tidal volume, the average speed of the inspiratory flow. In contrast the slope of the hypoxic ventilatory response decreased after administration of TNF-α. Diclofenac pretreatment eliminated these respiratory effects of TNF - α. The data indicate that the ability of TNF - α to enhance basal ventilation and to reduce the ventilatory hypoxic response is mediated by the cyclooxygenase pathway. Key words: tumor necrosis factor – α, hypoxia, prostaglandins, peripheral chemoreception, respiration.

Prostaglandins and control of breathing in newborn piglets

1988 ◽  
Vol 64 (1) ◽  
pp. 409-418 ◽  
Author(s):  
W. A. Long
Keyword(s):  
Neural Activity ◽  
Prostaglandin E1 ◽  
Control Of Breathing ◽  
Co2 Production ◽  
Mechanically Ventilated ◽  
Newborn Piglets ◽  
End Tidal ◽  
And Control ◽  
End Tidal Co2

To investigate the possible role of prostaglandins in regulation of postnatal breathing, phrenic neural activity (PMO) was recorded as an index of breathing in 42 anesthetized, paralyzed piglets less than 30 days of age (weight 2.4 +/- 0.2 kg, age 9.9 +/- 1.5 days) who were mechanically ventilated with 100% O2 at a fixed tidal volume (8-10 ml/kg). End-tidal CO2 was held constant by an electronic servocontroller which adjusted ventilator rate; ventilator rate was monitored as an index of CO2 production. Rectal temperature was maintained at 39.0 +/- 0.2 degrees C. The effects on PMO of intravenous and brain ventricular injections of NaCl and agents active in the prostaglandin cascade were compared. Intravenous (0.25-1.0 mg/kg, n = 9) and brain (5-33 micrograms/kg, n = 6) indomethacin, a cyclooxygenase inhibitor, doubled PMO within 30 min. Intravenous (1-10 micrograms/kg, n = 6) and brain (1-40 micrograms/kg, n = 6) prostaglandin E1 inhibited PMO by one-half at 10 and 30 min.

Morphogenesis of a New Human Herpes-Type Virus Isolate (Sasha Virus)

1973 ◽  
Vol 31 ◽  
pp. 592-593
Author(s):  
R. F. Zeigel ◽  
W. Munyon
Keyword(s):  
Virus Isolate ◽  
Calf Serum ◽  
Uranyl Acetate ◽  
Human Herpes ◽  
Human Embryonic Lung ◽  
Human Herpes Virus ◽  
Intracytoplasmic Inclusions ◽  
Hel Cells ◽  
And Control

In continuing studies on the role of viruses in biochemical transformation, Dr. Munyon has succeeded in isolating a highly infectious human herpes virus. Fluids of buccal pustular lesions from Sasha Munyon (10 mo. old) uiere introduced into monolayer sheets of human embryonic lung (HEL) cell cultures propagated in Eagles’ medium containing 5% calf serum. After 18 hours the cells exhibited a dramatic C.P.E. (intranuclear vacuoles, peripheral patching of chromatin, intracytoplasmic inclusions). Control HEL cells failed to reflect similar changes. Infected and control HEL cells were scraped from plastic flasks at 18 hrs. of incubation and centrifuged at 1200 × g for 15 min. Resultant cell packs uiere fixed in Dalton's chrome osmium, and post-fixed in aqueous uranyl acetate. Figure 1 illustrates typical hexagonal herpes-type nucleocapsids within the intranuclear virogenic regions. The nucleocapsids are approximately 100 nm in diameter. Nuclear membrane “translocation” (budding) uias observed.

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