Arterial blood gases in conscious rats exposed to hypoxia, hypercapnia, or both

1975 ◽  
Vol 38 (4) ◽  
pp. 581-587 ◽  
Author(s):  
W. E. Pepelko ◽  
G. A. Dixon
Keyword(s):  
Control Period ◽  
Blood Gases ◽  
Barometric Pressure ◽  
Male Rats ◽  
Arterial Blood Gases ◽  
Blood Samples ◽  
Air Breathing ◽  
Breathing Control ◽  
Arterial Blood ◽  
Caudal Artery

Adult male rats were anesthetized and catheters were implanted in the caudal artery. Soon after recovery from short-lasting anesthesia, a total of 20 groups of six each were individually exposed to five different oxygen levels varying from 21.0 to 9.0% combined with four CO2 levels ranging from 0 to 12.9% at a mean barometric pressure of 744 Torr. Arterial blood samples were collected and analyzed for pH, Po2, and Pco2 before and near the end of 20-min exposures. During an air-breathing control period, pH averaged 7.466 plus or minus 0.020 SD, Paco2 41.2 plus or minus 1.9 Torr and Pao2 91.8 plus or minus 3.5 Torr. During hypoxia, Pao2 levels were similar to that of acutely hypoxic humans. Rats apparently differ from man in that blood buffering is greater, resulting in a higher pH during air breathing and a smaller [H-+] increase with increasing Paco2. Differences between arterial and inspired CO2 were about 10 Torr at 60 and 90 Torr Plco2 and were not influenced by Plo2.

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.

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.

Arterial Blood Gases in Pranayama Practice

1978 ◽  
Vol 46 (1) ◽  
pp. 171-174 ◽  
Author(s):  
V. Pratap ◽  
W. H. Berrettini ◽  
C. Smith
Keyword(s):  
Blood Gases ◽  
Neural Mechanism ◽  
Arterial Blood Gases ◽  
Arterial Blood ◽  
Yogic Breathing ◽  
The Mind ◽  
Calming Effect

Pranayama is a Yogic breathing practice which is known experientially to produce a profound calming effect on the mind. In an experiment designed to determine whether the mental effects of this practice were accompanied by changes in the arterial blood gases, arterial blood was drawn from 10 trained individuals prior to and immediately after Pranayama practice. No significant changes in arterial blood gases were noted after Pranayama. A neural mechanism for the mental effects of this practice is proposed.

Blood gas changes during panting in a small East African antelope, the dik-dik

1978 ◽  
Vol 44 (4) ◽  
pp. 534-537 ◽  
Author(s):  
M. Maskrey ◽  
P. P. Hoppe ◽  
O. S. Bamford
Keyword(s):  
Heat Stress ◽  
Heat Exposure ◽  
Blood Gases ◽  
Respiratory Alkalosis ◽  
Second Phase ◽  
Blood Gas ◽  
Climatic Chamber ◽  
East African ◽  
Blood Samples ◽  
Arterial Blood

Five adult male dik-dik (Madoqua kirkii) were exposed in a climatic chamber to an air temperature of 45 degrees C. Measurements were made of rectal temperature (Tre) and respiratory frequency (f) and arterial blood samples taken before and during heat exposure were analyzed for pH, PCO2 and PO2. During exposure, Tre and f increased in all animals. In the first 80 min dik-dik displayed thermal tachypnea and minor changes in blood gases. Continued exposure lead to hyperpnea accompanied by a fall in PaCO2 and a rise in pH. PaCO2 at first fell and then increased toward or above control levels. The dik-dik did not display second phase breathing. This observation confirms that second phase breathing is not essential to the development of respiratory alkalosis. The main conclusion of the study is that the dik-dik, unlike another heat-adapted antelope, the wildebeest (Taylor, Robertshaw, and Hoffmann. Am. J. Physiol. 217:907–910, 1969), is unable to resist alkalosis during heat stress.

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.

Fetal cardiac bypass alters regional blood flows, arterial blood gases, and hemodynamics in sheep

1992 ◽  
Vol 263 (3) ◽  
pp. H919-H928 ◽  
Author(s):  
S. M. Bradley ◽  
F. L. Hanley ◽  
B. W. Duncan ◽  
R. W. Jennings ◽  
J. A. Jester ◽  
...  
Keyword(s):  
Blood Flow ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Blood Flows ◽  
Arterial Blood ◽  
Cardiac Bypass ◽  
Regional Blood Flows ◽  
Placental Blood ◽  
Fetal Organs ◽  
Placental Blood Flow

Successful fetal cardiac bypass might allow prenatal correction of some congenital heart defects. However, previous studies have shown that fetal cardiac bypass may result in impaired fetal gas exchange after bypass. To investigate the etiology of this impairment, we determined whether fetal cardiac bypass causes a redistribution of fetal regional blood flows and, if so, whether a vasodilator (sodium nitroprusside) can prevent this redistribution. We also determined the effects of fetal cardiac bypass with and without nitroprusside on fetal arterial blood gases and hemodynamics. Eighteen fetal sheep were studied in utero under general anesthesia. Seven fetuses underwent bypass without nitroprusside, six underwent bypass with nitroprusside, and five were no-bypass controls. Blood flows were determined using radionuclide-labeled microspheres. After bypass without nitroprusside, placental blood flow decreased by 25–60%, whereas cardiac output increased by 15–25%. Flow to all other fetal organs increased or remained unchanged. Decreased placental blood flow after bypass was accompanied by a fall in PO2 and a rise in PCO2. Nitroprusside improved placental blood flow, cardiac output, and arterial blood gases after bypass. Thus fetal cardiac bypass causes a redistribution of regional blood flow away from the placenta and toward the other fetal organs. Nitroprusside partially prevents this redistribution. Methods of improving placental blood flow in the postbypass period may prove critical to the success of fetal cardiac bypass.

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