Response of newborn lambs to CO-induced hypoxia

1988 ◽  
Vol 64 (5) ◽  
pp. 1870-1877 ◽  
Author(s):  
M. A. Bureau ◽  
J. L. Carroll ◽  
E. Canet
Keyword(s):  
Minute Ventilation ◽  
Blood Gases ◽  
Periodic Breathing ◽  
Respiratory Frequency ◽  
Gas Mixture ◽  
Arterial Blood Gases ◽  
Small Shift ◽  
Arterial Blood ◽  
The Right ◽  
Very High

This study was undertaken to measure the neonate's response to CO-induced hypoxia in the first 10 days of life. CO breathing was used to induce hypoxia because CO causes tissue hypoxia with no or minimal chemoreceptor stimulation. An inspired gas mixture of 0.25 to 0.5% CO in air was used to raise the blood carboxyhemoglobin (HbCO) progressively from 0 to 60% over approximately 20 min. The study, conducted in awake conscious lambs aged 2 and 10 days, consisted in measuring the response of ventilation and the change in arterial blood gases during the rise of HbCO. The results showed that the 2- and 10-day-old lambs tolerated very high HbCO levels without an increase in minute ventilation (VE) and without metabolic acidosis. At both ages, HbCO caused no VE change until HbCO levels rose to between 45 and 50% after which the VE change was exponential in some animals but minimal in others. The VE change was brought about by a rise in tidal volume and respiratory frequency. During the period of maturation from 2 to 10 days, there was a small shift to the right in the VE-HbCO response. In the 10-day-old lambs the VE response to high HbCO was greater than that of the 2-day-olds because of the lambs' higher respiratory frequency response. Six of the 10-day-old lambs but only two of the 2-day-old lambs showed a hypoxic tachypnea to HbCO of 55–65%. None of the lambs developed periodic breathing, dysrhythmic breathing, or recurrent apneas with an HbCO level as high as 60%.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of airway resistance on hypoxia-induced periodic breathing

1992 ◽  
Vol 72 (6) ◽  
pp. 2128-2133 ◽  
Author(s):  
F. Series ◽  
I. Series ◽  
L. Atton ◽  
A. Blouin
Keyword(s):  
Minute Ventilation ◽  
Upper Airway ◽  
Blood Gases ◽  
Random Order ◽  
Periodic Breathing ◽  
Arterial Blood Gases ◽  
Arterial Blood ◽  
Posthypoxic Period ◽  
Index Value ◽  
Spontaneously Breathing

We studied the effects of changing upper airway pressure on the variability of the dynamic response of ventilation to a hypoxic disturbance in 11 spontaneously breathing dogs. Supralaryngeal pressure, instantaneous inspiratory flow, end-expiratory lung volume, and the inspiratory and expiratory O2 and CO2 concentrations were continuously recorded at baseline and after a 1.5-min hypoxic stimulus (abrupt normoxic recovery). Arterial blood gases were obtained at baseline, at the end of the hypoxic period, and after 1 min of recovery. Airway resistances were modified during the recovery by changing the composition of the inspired gas (all with an inspiratory O2 fraction of 20.9%) among four different trials: two trials were realized with air (density 1.12 g/l), and the other two were with He or SF6 (respective density 0.42 and 4.20) in random order. There was no difference between baseline minute ventilation, arterial blood gases, and supralaryngeal resistance values preceding the trials. The hypoxemic and hypocapnic levels and the hypoxia-induced hyperventilation reached during the hypoxic tests were identical for the different hypoxic stimuli. The supralaryngeal resistance measured at peak flow was dramatically influenced by the composition of the inspired gas: 8.8 +/- 1.8 and 6.9 +/- 1.7 (SE) cmH2O.l-1.s with air, 7.2 +/- 2.2 with He, 21.9 +/- 5.5 with SF6 (P less than 0.05). Ventilatory fluctuations were consistently seen during the posthypoxic period. They were characterized by a strength index value (M) (Waggener et al. J. Appl. Physiol. 56: 576–581, 1984).(ABSTRACT TRUNCATED AT 250 WORDS)

Respiratory syncytial virus infection in anesthetized weanling rather than adult rats prolongs the apneic responses to right atrial injection of capsaicin

2007 ◽  
Vol 102 (6) ◽  
pp. 2201-2206 ◽  
Author(s):  
Wenhong Peng ◽  
Jianguo Zhuang ◽  
Kevin S. Harrod ◽  
Fadi Xu
Keyword(s):  
Respiratory Syncytial Virus ◽  
Blood Gases ◽  
Respiratory Frequency ◽  
Right Atrial ◽  
Arterial Blood Gases ◽  
Adult Rats ◽  
Intranasal Inoculation ◽  
Arterial Blood ◽  
Rsv Infection ◽  
Syncytial Virus

Apnea is a common complication in infants infected by respiratory syncytial virus (RSV). A recent study has shown that intranasal inoculation of RSV in conscious weanling rats strengthens the apneic responses to right atrial injection of capsaicin (CAP), leading to 66% mortality. The objectives of the present study were to determine 1) whether RSV infection changes baseline minute ventilation (V̇e) and arterial blood gases in anesthetized rats; 2) what the effects of RSV infection are on the respiratory responses to CAP; and 3) whether the RSV-strengthened apneic responses are age dependent. Our experiments were conducted in anesthetized and spontaneously breathing rats divided into four groups of weanling and adult rats that received either intranasal inoculation of RSV or virus-free medium. Two days after RSV infection (0.7 ml/kg), animal blood gases, baseline V̇e, and V̇e responses to right atrial injection of three doses of CAP (4, 16, and 64 μg/kg) were measured and compared among the four groups. Our results showed that RSV infection increased respiratory frequency (∼25%, P < 0.05) in weanling but not adult rats, with little effect on arterial blood gases. RSV infection amplified the apneic responses to CAP in weanling but not adult rats, characterized by increases in the initial (40%) and the longest apneic duration (650%), the number of apneic episodes (139%), and the total duration of apneas (60%). These amplifications led to 50% mortality ( P < 0.05). We conclude that RSV infection increases respiratory frequency and strengthens the apneic responses to CAP only in anesthetized weanling but not adult rats.

Ventilatory responses of hamsters and rats to hypoxia and hypercapnia

1985 ◽  
Vol 59 (6) ◽  
pp. 1955-1960 ◽  
Author(s):  
B. R. Walker ◽  
E. M. Adams ◽  
N. F. Voelkel
Keyword(s):  
Duty Cycle ◽  
Minute Ventilation ◽  
Natural Habitat ◽  
Blood Gases ◽  
Atmospheric Conditions ◽  
Arterial Blood Gases ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Rat Experiments ◽  
Fossorial Species

As a fossorial species the hamster differs in its natural habitat from the rat. Experiments were performed to determine possible differences between the ventilatory responses of awake hamsters and rats to acute exposure to hypoxic and hypercapnic environments. Ventilation was measured with the barometric method while the animals were conscious and unrestrained in a sealed plethysmograph. Tidal volume (VT), respiratory frequency (f), and inspiratory (TI) and expiratory (TE) time measurements were made while the animals breathed normoxic (30% O2), hypercapnic (5% CO2), or hypoxic (10% O2) gases. Arterial blood gases were also measured in both species while exposed to each of these atmospheric conditions. During inhalation of normoxic gas, the VT/100 g was greater and f was lower in the hamster than in the rat. Overall minute ventilation (VE/100 g) in the hamster was less than in the rat, which was reflected in the lower PO2 and higher PCO2 of the hamster arterial blood. When exposed to hypercapnia, the hamster increased VE/100 g solely through VT; however, the VE/100 g increase was significantly less than in the rat. In response to hypoxia, the hamster and rat increased VE/100 g by similar amounts; however, the hamster VE/100 g increase was through f alone, whereas the rat increased both VT/100 g and f. Mean airflow rates (VT/TI) were no different in the hamster or rat in each gas environment; therefore most of the ventilatory responses were the result of changes in TI and TE and respiratory duty cycle (TI/TT).

Arterial blood gases of the domestic hen

1965 ◽  
Vol 208 (4) ◽  
pp. 798-800 ◽  
Author(s):  
Hugo Chiodi ◽  
James W. Terman
Keyword(s):  
Arterial Oxygen Saturation ◽  
Venous Blood ◽  
Blood Gases ◽  
Arterial Oxygen ◽  
Dissociation Curve ◽  
Arterial Blood Gases ◽  
Blood Samples ◽  
Arterial Blood ◽  
The Right ◽  
Domestic Hen

Individual blood samples were collected anaerobically from the brachial arteries of adult White Rock hens and were analyzed for Po2, Pco2, pH, oxygen content and capacity, and CO2 content and capacity. A dissociation curve was constructed from data on equilibration of pooled venous blood. The average arterial oxygen saturation was 90%, the Pco2 was about 32 mm Hg, the Po2 was between 94 and 99 mm Hg, and the pH averaged 7.49. The dissociation curve, as has been shown before, was shifted to the right of most homeothermic species.

Brain ECF pH and central chemical control of ventilation during anoxia in turtles

1987 ◽  
Vol 252 (5) ◽  
pp. R848-R852 ◽  
Author(s):  
D. G. Davies ◽  
J. A. Sexton
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Control Period ◽  
Extracellular Fluid ◽  
Blood Gases ◽  
Breathing Frequency ◽  
Arterial Blood Gases ◽  
Brain Extracellular Fluid ◽  
Arterial Blood

The role of changes in brain extracellular fluid [H+] in the control of breathing during anoxia was studied in unanesthetized turtles, Chrysemys scripta. Ventilation, [minute ventilation (VE), tidal volume (VT), and breathing frequency (f)], cerebral extracellular fluid (ECF) pH, and arterial blood gases were measured at 25 degrees C during a 30-min control period (room air), 30 min of anoxia (100% N2 breathing), and 60 min of recovery (room air). ECF pH was measured in the cerebral cortex with a glass microelectrode (1-2 micron tip diam). Large changes in ventilation, ECF [H+], and arterial blood gases were observed. The predominant ventilatory response was an increase in f with a slight increase in VT. A correlation was observed between ECF [H+] and f, which suggested that central chemoreceptor stimulation was involved in the ventilatory response.

scholarly journals Effect of dexmedetomidine on cardiorespiratory regulation in spontaneously breathing adult rats

PLoS ONE ◽  
2022 ◽  
Vol 17 (1) ◽  
pp. e0262263
Author(s):  
Yoichiro Kitajima ◽  
Nana Sato Hashizume ◽  
Chikako Saiki ◽  
Ryoji Ide ◽  
Toshio Imai
Keyword(s):  
Normal Saline ◽  
Minute Ventilation ◽  
Blood Gases ◽  
Male Rats ◽  
Arterial Blood Gases ◽  
Adult Rats ◽  
Tail Artery ◽  
Adrenoceptor Antagonist ◽  
Arterial Blood ◽  
Spontaneously Breathing

Purpose We examined the cardiorespiratory effect of dexmedetomidine, an α2- adrenoceptor/imidazoline 1 (I1) receptor agonist, in spontaneously breathing adult rats. Methods Male rats (226−301 g, n = 49) under isoflurane anesthesia had their tail vein cannulated for drug administration and their tail artery cannulated for analysis of mean arterial pressure (MAP), pulse rate (PR), and arterial blood gases (PaO2, PaCO2, pH). After recovery, one set of rats received normal saline for control recording and was then divided into three experimental groups, two receiving dexmedetomidine (5 or 50 μg·kg−1) and one receiving normal saline (n = 7 per group). Another set of rats was divided into four groups receiving dexmedetomidine (50 μg·kg−1) followed 5 min later by 0.5 or 1 mg∙kg−1 atipamezole (selective α2-adrenoceptor antagonist) or efaroxan (α2-adrenoceptor/I1 receptor antagonist) (n = 6 or 8 per group). Recordings were performed 15 min after normal saline or dexmedetomidine administration. Results Compared with normal saline, dexmedetomidine (5 and 50 μg·kg−1) decreased respiratory frequency (fR, p = 0.04 and < 0.01, respectively), PR (both p < 0.01), and PaO2 (p = 0.04 and < 0.01), and increased tidal volume (both p = 0.049). Dexmedetomidine at 5 μg·kg−1 did not significantly change minute ventilation (V′E) (p = 0.87) or MAP (p = 0.24), whereas dexmedetomidine at 50 μg·kg−1 significantly decreased V′E (p = 0.03) and increased MAP (p < 0.01). Only dexmedetomidine at 50 μg·kg−1 increased PaCO2 (p < 0.01). Dexmedetomidine (5 and 50 μg·kg−1) significantly increased blood glucose (p < 0.01), and dexmedetomidine at 50 μg·kg−1 increased hemoglobin (p = 0.04). Supplemental atipamezole or efaroxan administration similarly prevented the 50 μg·kg−1 dexmedetomidine-related cardiorespiratory changes. Principal conclusion These results suggest that dexmedetomidine-related hypoventilation and hypertension are observed simultaneously and occur predominantly through activation of α2-adrenoceptors, but not I1 receptors, in spontaneously breathing adult rats.

Ventilatory and metabolic adaptations to walking and cycling in patients with COPD

2000 ◽  
Vol 88 (5) ◽  
pp. 1715-1720 ◽  
Author(s):  
Paolo Palange ◽  
Silvia Forte ◽  
Paolo Onorati ◽  
Felice Manfredi ◽  
Pietro Serra ◽  
...  
Keyword(s):  
Minute Ventilation ◽  
Venous Blood ◽  
Blood Gases ◽  
Peak Exercise ◽  
Chronic Obstructive ◽  
Arterial Blood Gases ◽  
Physiological Dead Space ◽  
Arterial Blood ◽  
Ergometer Exercise ◽  
Walking Capacity

To test the hypothesis that in chronic obstructive pulmonary disease (COPD) patients the ventilatory and metabolic requirements during cycling and walking exercise are different, paralleling the level of breathlessness, we studied nine patients with moderate to severe, stable COPD. Each subject underwent two exercise protocols: a 1-min incremental cycle ergometer exercise (C) and a “shuttle” walking test (W). Oxygen uptake (V˙o 2), CO2output (V˙co 2), minute ventilation (V˙e), and heart rate (HR) were measured with a portable telemetric system. Venous blood lactates were monitored. Measurements of arterial blood gases and pH were obtained in seven patients. Physiological dead space-tidal volume ratio (Vd/Vt) was computed. At peak exercise, W vs. CV˙o 2,V˙e, and HR values were similar, whereasV˙co 2 (848 ± 69 vs. 1,225 ± 45 ml/min; P < 0.001) and lactate (1.5 ± 0.2 vs. 4.1 ± 0.2 meq/l; P < 0.001) were lower, ΔV˙e/ΔV˙co 2(35.7 ± 1.7 vs. 25.9 ± 1.3; P < 0.001) and ΔHR/ΔV˙o 2values (51 ± 3 vs. 40 ± 4; P < 0.05) were significantly higher. Analyses of arterial blood gases at peak exercise revealed higher Vd/Vt and lower arterial partial pressure of oxygen values for W compared with C. In COPD, reduced walking capacity is associated with an excessively high ventilatory demand. Decreased pulmonary gas exchange efficiency and arterial hypoxemia are likely to be responsible for the observed findings.

Fluid leaks from extra-alveolar vessels in living dog lungs

1978 ◽  
Vol 44 (5) ◽  
pp. 759-762 ◽  
Author(s):  
R. K. Albert ◽  
S. Lakshminarayan ◽  
T. W. Huang ◽  
J. Butler
Keyword(s):  
Venous Pressure ◽  
Blood Gases ◽  
Alveolar Pressure ◽  
Arterial Blood Gases ◽  
Fluid Accumulation ◽  
Lung Weight ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
The Right ◽  
Lung Base

Edema transudation from extra-alveolar vessels was investigated in anesthetized, open-chested dogs. Fluid accumulation at different alveolar and extra-alveolar vascular pressures was assessed by continuous lung weighing and microscopy. The left (experimental) lung was distended with 6% CO2 and air while normal arterial blood gases were maintained by separately ventilating the right lung. Extra-alveolar vessels were isolated by compressing alveolar vessels with alveolar pressures high enough to stop blood flow. Weight increased steadily (edemogenesis) when pulmonary arterial and/or pulmonary venous pressure was 1 cmH2O below this pressure. Because some alveolar vessels at the lung base could have remained open and leaked, extra-alveolar vessels were also separated from alveolar vessels by glass bead embolization sufficient to stop perfusion. Lung weight gains followed selective pulmonary arterial or venous pressure elevations. Electron microscopy demonstrated edema in experimental lobes which was not present in control lobes with undistended extra-alveolar vessels at the same alveolar pressure. Thus pulmonary edema can be caused by fluid leaking from extra-alveolar vessels.

scholarly journals Pathophysiology and clinical consequences of arterial blood gases and pH after cardiac arrest

2020 ◽  
Vol 8 (S1) ◽  
Author(s):  
Chiara Robba ◽  
Dorota Siwicka-Gieroba ◽  
Andras Sikter ◽  
Denise Battaglini ◽  
Wojciech Dąbrowski ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Mechanical Ventilation ◽  
Cardiac Arrest ◽  
Oxygen Demand ◽  
Blood Gases ◽  
Metabolic Energy ◽  
High Morbidity ◽  
Arterial Blood Gases ◽  
Arterial Blood ◽  
Clinical Consequences

AbstractPost cardiac arrest syndrome is associated with high morbidity and mortality, which is related not only to a poor neurological outcome but also to respiratory and cardiovascular dysfunctions. The control of gas exchange, and in particular oxygenation and carbon dioxide levels, is fundamental in mechanically ventilated patients after resuscitation, as arterial blood gases derangement might have important effects on the cerebral blood flow and systemic physiology.In particular, the pathophysiological role of carbon dioxide (CO2) levels is strongly underestimated, as its alterations quickly affect also the changes of intracellular pH, and consequently influence metabolic energy and oxygen demand. Hypo/hypercapnia, as well as mechanical ventilation during and after resuscitation, can affect CO2 levels and trigger a dangerous pathophysiological vicious circle related to the relationship between pH, cellular demand, and catecholamine levels. The developing hypocapnia can nullify the beneficial effects of the hypothermia. The aim of this review was to describe the pathophysiology and clinical consequences of arterial blood gases and pH after cardiac arrest.According to our findings, the optimal ventilator strategies in post cardiac arrest patients are not fully understood, and oxygen and carbon dioxide targets should take in consideration a complex pattern of pathophysiological factors. Further studies are warranted to define the optimal settings of mechanical ventilation in patients after cardiac arrest.

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