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.

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.

scholarly journals The Influence of CO2 Production and Physiological Deadspace on End-Tidal CO2 During Controlled Ventilation: A Study Using a Mechanical Model

1989 ◽  
Vol 17 (4) ◽  
pp. 482-486 ◽  
Author(s):  
M. A. Stockwell ◽  
W. Bruce ◽  
N. Soni
Keyword(s):  
Carbon Dioxide ◽  
Mechanical Model ◽  
Carbon Dioxide Production ◽  
Lung Model ◽  
Co2 Production ◽  
Controlled Ventilation ◽  
End Tidal Carbon Dioxide ◽  
Carbon Dioxide Levels ◽  
End Tidal ◽  
End Tidal Co2

A mechanical lung model was used to investigate the effect of varying carbon dioxide production and deadspace on the end-tidal carbon dioxide levels achieved during mechanical ventilation when using the Bain, Humphrey ADE, and circle systems. Both factors had significant influence on end-tidal cardon dioxide concentration and could result in values in excess of those considered acceptable in clinical practice. The implications of the results are discussed.

scholarly journals EARLY PROBIOTICS IN PREVENTING VENTILATOR-ASSOCIATED PNEUMONIA AFTER MULTIPLE TRAUMA

2020 ◽  
pp. 83-85
Author(s):  
TAMER HABIB ◽  
AMIRA B KASSEM ◽  
ISLAM AHMED
Keyword(s):  
Multiple Trauma ◽  
University Hospital ◽  
Control Group ◽  
Trauma Patients ◽  
Ventilator Associated Pneumonia ◽  
Mechanically Ventilated ◽  
Significant Difference ◽  
Multiple Trauma Patients ◽  
And Control

Objective: Using probiotics in preventing ventilator-associated pneumonia (VAP) remain controversial due to different intensive care unit (ICU) populations included in such studies. The aim of this study is to evaluate the role of probiotics in prophylaxis of VAP after multiple trauma. Methods: Sixty-five adult multiple trauma patients on mechanical ventilator (expected ≥48 h) after admission to the Critical Care Medicine Department, Alexandria Main University Hospital from June to November 2018. Patients were randomly assigned using computer sheet into two groups; probiotics group (32 patients received one Lacteol Forte® sachet through orogastric/nasogastric tube 3 times daily during their ICU stay) and control group (33 patients received similar regimen of placebo sachets). All patients were followed up and subjected to all possible strategies of the diagnosis of microbiologically confirmed VAP. Results: Sixty-five patients were enrolled with a mean of age (39.48±7.692) years, 80% of them were male. Regarding the incidence of VAP, it was 18.46% of all patients without statistically significant difference between probiotics group (15.63%) and control group (21.21%) (p=0.751). Conclusion: Routine use of early probiotics in mechanically ventilated multiple trauma patients was not associated with lower incidence of VAP, duration of MV, or ICU mortality.

Is hypercapnia necessary for the ventilatory response to exercise in man?

1987 ◽  
Vol 73 (6) ◽  
pp. 617-625 ◽  
Author(s):  
K. Murphy ◽  
R. P. Stidwill ◽  
Brenda A. Cross ◽  
Kathryn D. Leaver ◽  
E. Anastassiades ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Co2 Production ◽  
Moderate Exercise ◽  
Arterial Ph ◽  
Arteriovenous Shunts ◽  
Exercise Period ◽  
Leg Exercise ◽  
End Tidal ◽  
Response To Exercise ◽  
End Tidal Co2

1. Continuous recordings of arterial pH, ventilation, airway CO2 and heart rate were made during rest and during 3–4 min periods of rhythmic leg exercise in four renal patients with arteriovenous shunts. 2. The patients were anaemic (haemoglobin 6.5–9.0 g/dl) but had a normal ventilatory response to exercise as judged by the ratio of the change in ventilation to the change in CO2 production. 3. Breath-by-breath oscillations in arterial pH disappeared for the majority of the exercise period in each patient. 4. Changes in mean arterial pH and end-tidal CO2 tension with exercise were inconsistent between subjects but consistent within a given subject. On average, mean arterial pH rose by 0.011 pH unit. Changes in end-tidal CO2 tension reflected changes in mean pHa by falling on average by 1 mmHg (0.13 kPa). 5. Hypercapnia and acidaemia were not found to be necessary for the ventilatory response to moderate exercise.

The Ventilatory Effects of Doxapram in Normal Man

1983 ◽  
Vol 65 (1) ◽  
pp. 65-69 ◽  
Author(s):  
P. M. A. Calverley ◽  
R. H. Robson ◽  
P. K. Wraith ◽  
L. F. Prescott ◽  
D. C. Flenley
Keyword(s):  
Oxygen Uptake ◽  
Ventilatory Response ◽  
Co2 Production ◽  
Central Action ◽  
Ventilatory Responses ◽  
Ventilatory Effects ◽  
Normal Man ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Ventilatory Response To Co2

1. To determine the mode of action of doxapram in man we have measured ventilation, oxygen uptake, CO2 production, hypoxic and hypercapnic ventilatory responses in six healthy men before and during intravenous infusion to maintain a constant plasma level. 2. Doxapram changed neither resting oxygen uptake nor CO2 production but produced a substantial increase in resting ventilation at both levels of end-tidal CO2 studied. 3. Doxapram increased the ventilatory response to isocapnic hypoxia from − 0.8 ± 0.4 litre min−1 (%Sao2)−1 to −1.63 ± 0.9 litres min−1 (%Sao2)−1. This was similar to the increase in hypoxic sensitivity which resulted from raising the end-tidal CO2 by 0.5 kPa without adding doxapram. 4. The slope of the ventilatory response to rebreathing CO2 rose from 11.6 ± 5.3 litres min−1 kPa−1 to 20,4 ± 9.8 litres min−1 kPa−1 during doxapram infusion. 5. The marked increase in the ventilatory response to CO2 implies that doxapram has a central action, but the potentiation of the hypoxic drive also suggests that the drug acts on peripheral chemoreceptors, or upon their central connections, at therapeutic concentrations in normal unanaesthetized subjects.

Respiratory monitoring

2011 ◽  
Author(s):  
Carl Waldmann ◽  
Neil Soni ◽  
Andrew Rhodes
Keyword(s):  
Pulmonary Function ◽  
Pulmonary Function Tests ◽  
Test Results ◽  
Mechanical Ventilators ◽  
Mechanically Ventilated ◽  
Ventilatory Parameters ◽  
Co2 Monitoring ◽  
Function Test ◽  
End Tidal ◽  
End Tidal Co2

Pulmonary function tests in critical illness 90End-tidal CO2 monitoring 92Pulse oximetry 94Pulmonary function test results in critically ill patients can be important prognostically and guide ventilatory and weaning strategies. However, they are not straightforward to measure in mechanically ventilated patients and remain limited to dynamic volumes. Fortunately, most modern mechanical ventilators are able to calculate and display static and dynamic lung volumes, together with derived values for airway resistance, compliance and flow/volume/time curves. The ability to monitor these changes after altering ventilatory parameters has enabled more sophisticated adjustments of ventilation, to prevent potentially damaging mechanical ventilation....

Effect of aerosolized histamine on occlusion pressure and ventilation in humans

1982 ◽  
Vol 53 (3) ◽  
pp. 690-697 ◽  
Author(s):  
R. P. Millman ◽  
D. A. Silage ◽  
D. D. Peterson ◽  
A. I. Pack
Keyword(s):  
Smooth Muscle ◽  
Neural Activity ◽  
Occlusion Pressure ◽  
Bronchial Smooth Muscle ◽  
Co2 Partial Pressure ◽  
Residual Capacity ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Airway Conductance ◽  
Stimulation Of

To define further the mechanism by which inspiratory neural activity is increased in asthma, we studied the effect of aerosolized histamine on occlusion pressure (P100) and ventilation in conscious humans while end-tidal CO2 partial pressure was maintained at a constant, slightly hypercapnic level. The dose of histamine we employed varied from subject to subject but was such that it produced a 70% reduction in specific airway conductance in each subject. In 9 of the 13 subjects tested, inhaled histamine significantly increased P100. This increase was not due to changes in functional residual capacity, which was not affected by aerosolized histamine. Inhalation of isoproterenol abolished the effects of histamine on specific airway conductance and P100. Anesthesia of the airways by lidocaine eliminated the effect of histamine on P100 but did not alter the magnitude of the change in specific airway conductance produced by histamine. We conclude that the increase in occlusion pressure seen after the inhalation of histamine in humans depends on both contraction of bronchial smooth muscle and stimulation of airway receptors.

Relation between work output of respiratory muscles and end-tidal CO2 tension

1963 ◽  
Vol 18 (3) ◽  
pp. 497-504 ◽  
Author(s):  
J. Milic-Emili ◽  
J. M. Tyler
Keyword(s):  
Carbon Dioxide ◽  
Pulmonary Ventilation ◽  
Respiratory Muscles ◽  
Normal Subjects ◽  
Work Output ◽  
Inspiratory Muscles ◽  
Expiratory Muscles ◽  
End Tidal ◽  
End Tidal Co2

End-tidal CO2 tension, pulmonary ventilation, and work output of respiratory muscles were determined in six normal subjects breathing various mixtures of carbon dioxide in air, with three graded resistances added to both inspiration and expiration. In two individuals, the resistances were also added separately to inspiration or expiration. A linear relationship was found between work output of inspiratory muscles and end-tidal CO2 tension; this relationship was uninfluenced by added resistance. No consistent relationship was observed between either ventilation or work output of expiratory muscles and end-tidal CO2 tension. These results suggest that carbon dioxide controls directly the activity of inspiratory muscles alone and that the activity of expiratory muscles is only coincidentally involved. The possible role of intrinsic properties of respiratory muscles and of nervous mediation in the control of breathing is discussed. Submitted on October 22, 1962

Naloxone enhances respiratory output in cats

1979 ◽  
Vol 47 (5) ◽  
pp. 1105-1111 ◽  
Author(s):  
E. E. Lawson ◽  
T. G. Waldrop ◽  
F. L. Eldridge
Keyword(s):  
Phrenic Nerve ◽  
Opiate Receptors ◽  
Physiological Role ◽  
Opiate Antagonist ◽  
Nerve Activity ◽  
Phrenic Nerve Activity ◽  
End Tidal ◽  
Decerebrate Cats ◽  
End Tidal Co2

To investigate the physiological role of opiate receptors and opiatelike neurotransmitters, which are present in brain-stem respiratory centers, we administered naloxone to 10 cats by intravenous injection. These animals were vagotomized, paralyzed, and servo-ventilated to maintain constant end-tidal CO2; in addition, their carotid sinus nerves were sectioned bilaterally. Respiratory output was assessed by integration of phrenic nerve activity. Control saline infusions had no effect on respiratory output. However, administration of naloxone (0.4 mg/kg) caused phrenic minute output to increase significantly in each of five anesthetized cerebrate cats (control 7,272 +/- 1,615 U/min; 30 min postnaloxone 12,920 +/- 3,857 U/min; P less than 0.05) and five unanesthetized decerebrate cats (control 10,368 +/- 1,222 U/min; naloxone 14,648 +/- 3,225 U/min; P less than 0.05). In addition to the effect on phrenic minute output, naloxone infusion resulted in an increase of the inspiratory rate of rise of phrenic nerve activity in each cat. There was no change in the ratio of inspiratory duration to total respiratory period (TI/Ttot). Because naloxone is a specific opiate antagonist, we suggest that endogenous opiatelike neurotransmitters (endorphins) may modulate central inspiratory drive.

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