Ventilation during prolonged hypercapnia in the rat

1981 ◽  
Vol 51 (1) ◽  
pp. 78-83 ◽  
Author(s):  
Y. L. Lai ◽  
J. E. Lamm ◽  
J. Hildebrandt
Keyword(s):  
Respiratory Acidosis ◽  
Blood Gases ◽  
Alveolar Ventilation ◽  
O2 Consumption ◽  
Arterial Blood Gases ◽  
Inspiratory Time ◽  
Arterial Blood ◽  
Metabolic Compensation ◽  
Ventilatory Drive ◽  
Awake Rats

Awake rats, with chronically implanted arterial catheters and abdominal thermistors, were continuously exposed to 5 or 7% CO2 in air in an environmental chamber for up to 3 wk. To obtain measurements, rats were transferred to a body plethysmograph flushed with the same CO2 mixture, and, after stabilization, O2 consumption (Vo2), ventilation (VE), and arterial blood gases (ABG) were determined. After 2-h exposure, VE, tidal volume/inspiratory time (VT/TI), and VO2 were significantly increased. Thereafter, VE and VT/TI fell gradually with time, the largest decrease occurring within the 1st day of exposure. The increase in VO2 was maintained up to 3 days and then declined. ABG revealed extensive metabolic compensation for respiratory acidosis within 3–7 days. delta(VT/TI) correlated well with delta VE and delta [HCO3]a (P less than 0.05). It is likely that the gradual return toward normal pHa reduces ventilatory drive (VT/TI), which in turn lowers VE. Estimated alveolar ventilation did not decrease consistently with time in parallel with VE, suggesting that the early ventilatory overshoot might also be due to an increase in dead space.

Anesthetic effects on liver and muscle glycogen concentrations: rest and postexercise

1989 ◽  
Vol 66 (6) ◽  
pp. 2895-2900 ◽  
Author(s):  
T. I. Musch ◽  
B. S. Warfel ◽  
R. L. Moore ◽  
D. R. Larach
Keyword(s):  
Skeletal Muscles ◽  
Respiratory Acidosis ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Acid Base ◽  
Arterial Lactate ◽  
Arterial Pco2 ◽  
Arterial Blood ◽  
Acid Base Status ◽  
Gastrocnemius Muscles

We compared the effects of three different anesthetics (halothane, ketamine-xylazine, and diethyl ether) on arterial blood gases, acid-base status, and tissue glycogen concentrations in rats subjected to 20 min of rest or treadmill exercise (10% grade, 28 m/min). Results demonstrated that exercise produced significant increases in arterial lactate concentrations along with reductions in arterial Pco2 (PaCO2) and bicarbonate concentrations in all rats compared with resting values. Furthermore, exercise produced significant reductions in the glycogen concentrations in the liver and soleus and plantaris muscles, whereas the glycogen concentrations found in the diaphragm and white gastrocnemius muscles were similar to those found at rest. Rats that received halothane and ketamine-xylazine anesthesia demonstrated an increase in Paco2 and a respiratory acidosis compared with rats that received either anesthesia. These differences in arterial blood gases and acid-base status did not appear to have any effect on tissue glycogen concentrations, because the glycogen contents found in liver and different skeletal muscles were similar to one another cross all three anesthetic groups. These data suggest that even though halothane and ketamine-xylazine anesthesia will produce a significant amount of ventilatory depression in the rat, both anesthetics may be used in studies where changes in tissue glycogen concentrations are being measured and where adequate general anesthesia is required.

Arterial blood gases and acid-base status of dogs during graded dynamic exercise

1986 ◽  
Vol 61 (5) ◽  
pp. 1914-1919 ◽  
Author(s):  
T. I. Musch ◽  
D. B. Friedman ◽  
G. C. Haidet ◽  
J. Stray-Gundersen ◽  
T. G. Waldrop ◽  
...  
Keyword(s):  
Steady State ◽  
Blood Gases ◽  
Respiratory Alkalosis ◽  
Submaximal Exercise ◽  
O2 Consumption ◽  
Arterial Blood Gases ◽  
Acid Base ◽  
Vo2 Max ◽  
Arterial Blood ◽  
Acid Base Status

The objective of this study was to determine whether arterial PCO2 (PaCO2) decreases or remains unchanged from resting levels during mild to moderate steady-state exercise in the dog. To accomplish this, O2 consumption (VO2) arterial blood gases and acid-base status, arterial lactate concentration ([LA-]a), and rectal temperature (Tr) were measured in 27 chronically instrumented dogs at rest, during different levels of submaximal exercise, and during maximal exercise on a motor-driven treadmill. During mild exercise [35% of maximal O2 consumption (VO2 max)], PaCO2 decreased 5.3 +/- 0.4 Torr and resulted in a respiratory alkalosis (delta pHa = +0.029 +/- 0.005). Arterial PO2 (PaO2) increased 5.9 +/- 1.5 Torr and Tr increased 0.5 +/- 0.1 degree C. As the exercise levels progressed from mild to moderate exercise (64% of VO2 max) the magnitude of the hypocapnia and the resultant respiratory alkalosis remained unchanged as PaCO2 remained 5.9 +/- 0.7 Torr below and delta pHa remained 0.029 +/- 0.008 above resting values. When the exercise work rate was increased to elicit VO2 max (96 +/- 2 ml X kg-1 X min-1) the amount of hypocapnia again remained unchanged from submaximal exercise levels and PaCO2 remained 6.0 +/- 0.6 Torr below resting values; however, this response occurred despite continued increases in Tr (delta Tr = 1.7 +/- 0.1 degree C), significant increases in [LA-]a (delta [LA-]a = 2.5 +/- 0.4), and a resultant metabolic acidosis (delta pHa = -0.031 +/- 0.011). The dog, like other nonhuman vertebrates, responded to mild and moderate steady-state exercise with a significant hyperventilation and respiratory alkalosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Arterial blood gases and acid-base status in awake rats

1982 ◽  
Vol 48 (1) ◽  
pp. 45-57 ◽  
Author(s):  
M. Brun-Pascaud ◽  
C. Gaudebout ◽  
M.C. Blayo ◽  
J.J. Pocidalo
Keyword(s):  
Blood Gases ◽  
Arterial Blood Gases ◽  
Acid Base ◽  
Arterial Blood ◽  
Acid Base Status ◽  
Awake Rats

Effect of naloxone on ventilation in newborn rabbits

1981 ◽  
Vol 50 (4) ◽  
pp. 713-717 ◽  
Author(s):  
T. A. Hazinski ◽  
M. M. Grunstein ◽  
M. A. Schlueter ◽  
W. H. Tooley
Keyword(s):  
Blood Gases ◽  
Postnatal Life ◽  
Respiratory Drive ◽  
Arterial Blood Gases ◽  
Inspiratory Time ◽  
Ether Anesthesia ◽  
Respiratory Effect ◽  
Artery Cannulation ◽  
Arterial Blood ◽  
Before And After

Endorphins have been isolated from amniotic fluid and cord blood of mammals. To determine if these agents influence ventilation after birth, we measured ventilation (VE), tidal volume, inspiratory time, and respiratory frequency (f) in 19 rabbit pups before and after administration of naloxone (NLX), an endorphin antagonist. Tracheostomy and carotid artery cannulation were performed under light ether anesthesia. After 30-90 min for recovery the pups were placed in a body plethysmograph. Rectal temperature was kept at 37 +/- 0.5 degrees C. After 15 min of control measurements we infused saline, which had no respiratory effect. NLX (4 microgram/g) was then infused and measurements continued for 30 min. In 6 of 7 pups less than or equal to 4 days old, VE increased to 140-180% of control values and remained elevated for the remainder of the study period. Increased VE was due solely to increased f. By contrast, only 1 of 12 pups greater than or equal to 5 days old responded in this fashion. This difference was significant (P less than 0.005). Arterial blood gases were measured before and after NLX in 10 pups. In those pups who increased their ventilation after NLX, arterial CO2 tension fell and pH rose above pre-NLX values (P less than 0.05) for both variables). Blood gases of the group whose ventilation was uneffected remained unchanged. These results indicate that early in postnatal life endorphins probably modulate central respiratory drive in rabbits but that these agents become less important with maturation.

Respiratory acidosis in carbonic anhydrase II-deficient mice

1998 ◽  
Vol 274 (2) ◽  
pp. L301-L304 ◽  
Author(s):  
Yeong-Hau H. Lien ◽  
Li-Wen Lai
Keyword(s):  
Metabolic Acidosis ◽  
Carbonic Anhydrase ◽  
Respiratory Acidosis ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Arterial Blood ◽  
Blood Ph ◽  
Type Ii Pneumocytes ◽  
Deficient Mice

To investigate the role of carbonic anhydrase (CA) II on pulmonary CO2 exchange, we analyzed arterial blood gases from CA II-deficient and normal control mice. CA II-deficient mice had a low arterial blood pH (7.18 ± 0.06) and[Formula: see text] concentration ([[Formula: see text]]; 17.5 ± 1.9 meq/l) and a high [Formula: see text](47.4 ± 5.3 mmHg), consistent with mixed respiratory and metabolic acidosis. To eliminate the influence of metabolic acidosis on arterial blood gases, NaHCO3 (4 mmol/kg body weight) was given intraperitoneally, and arterial blood gases were analyzed 4 h later. Normal mice had a small increase in pH and were able to maintain [Formula: see text] and [[Formula: see text]]. The metabolic acidosis in CA II-deficient mice was corrected ([[Formula: see text]], 22.9 ± 2.4 meq/l), and respiratory acidosis became more profound ([Formula: see text], 50.4 ± 2.4 mmHg). These results indicate that CA II-deficient mice have a partial respiratory compensation for metabolic acidosis. We conclude that CA II-deficient mice have a mixed respiratory and metabolic acidosis. It is most likely that CO2 retention in these animals is due to CA II deficiency in both red blood cells and type II pneumocytes.

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.

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