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.

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.

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.

31P-NMR in vivo measurement of renal intracellular pH: effects of acidosis and K+ depletion in rats

1986 ◽  
Vol 251 (5) ◽  
pp. F904-F910 ◽  
Author(s):  
W. R. Adam ◽  
A. P. Koretsky ◽  
M. W. Weiner
Keyword(s):  
Metabolic Acidosis ◽  
Intracellular Ph ◽  
Respiratory Acidosis ◽  
Resonance Spectroscopy ◽  
Ph Effects ◽  
Potassium Depletion ◽  
Chronic Metabolic Acidosis ◽  
Arterial Blood ◽  
Blood Ph

Renal intracellular pH (pHi) was measured in vivo from the chemical shift (sigma) of inorganic phosphate (Pi), obtained by 31P-nuclear magnetic resonance spectroscopy (NMR). pH was calculated from the difference between sigma Pi and sigma alpha-ATP. Changes of sigma Pi closely correlated with changes of sigma monophosphoesters; this supports the hypothesis that the pH determined from sigma Pi represents pHi. Renal pH in control rats was 7.39 +/- 0.04 (n = 8). This is higher than pHi of muscle and brain in vivo, suggesting that renal Na-H antiporter activity raises renal pHi. To examine the relationship between renal pH and ammoniagenesis, rats were subjected to acute (less than 24 h) and chronic (4-7 days) metabolic acidosis, acute (20 min) and chronic (6-8 days) respiratory acidosis, and dietary potassium depletion (7-21 days). Acute metabolic and respiratory acidosis produced acidification of renal pHi. Chronic metabolic acidosis (arterial blood pH, 7.26 +/- 0.02) lowered renal pHi to 7.30 +/- 0.02, but chronic respiratory acidosis (arterial blood pH, 7.30 +/- 0.05) was not associated with renal acidosis (pH, 7.40 +/- 0.04). At a similar level of blood pH, pHi was higher in chronic metabolic acidosis than in acute metabolic acidosis, suggesting an adaptive process that raises pHi. Potassium depletion (arterial blood pH, 7.44 +/- 0.05) was associated with a marked renal acidosis (renal pH, 7.17 +/- 0.02). There was a direct relationship between renal pH and cardiac K+. Rapid partial repletion with KCl (1 mmol) significantly increased renal pHi from 7.14 +/- 0.03 to 7.31 +/- 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)

Use of Evacuated Collection Tubes for Routine Determination of Arterial Blood Gases and pH

1971 ◽  
Vol 17 (7) ◽  
pp. 610-613 ◽  
Author(s):  
Martin Fleisher ◽  
Morton K Schwartz
Keyword(s):  
Blood Gases ◽  
Arterial Blood Gases ◽  
Nitrogen Gas ◽  
Simple Method ◽  
Atmospheric Contamination ◽  
Arterial Blood ◽  
Blood Ph ◽  
Specimen Collection ◽  
Analytical Equipment

Abstract There is a well-recognized need for a reliable, convenient, and simple method for determining whole blood pH, PaCOaCO2, and PaOaO2. We have designed a specimen collection set that facilitates collection of the specimen and permits convenient and reliable analysis by the laboratory. Specimens are collected in newly designed "Vacutainer" tubes containing heparin and nitrogen gas. Without removing the Vacutainer stopper, the specimen may be anaerobically introduced into the analytical equipment through a unique aspirating needle. Atmospheric contamination of the specimen is eliminated.

scholarly journals The Role of Lactate Dehydrogenase (LDH) Compared to Arterial Blood Gases (ABG) in Diagnosing Pneumocystis Carinii Pneumonia (PCP) in HIV/AIDS Patients on Routine Antiretroviral Therapy

2021 ◽  
Vol 8 (10) ◽  
pp. 1-7
Author(s):  
Aulia Rahman ◽  
Tambar Kembaren ◽  
Endang Sembiring
Keyword(s):  
Lactate Dehydrogenase ◽  
Pneumocystis Carinii Pneumonia ◽  
Predictive Value ◽  
Pneumocystis Carinii ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Aids Patients ◽  
Arterial Blood ◽  
Hiv Aids

Background: The lungs are one of the primary target organs for HIV disease and a major source of morbidity and mortality, among others, caused by Pneumocystis carinii pneumonia (PCP) or recurrent bacterial pneumonia. In developing countries, the incidence of PCP infection has soared, with high mortality rates ranging from 20% to 80%. The increase in serum LDH plays an important role in determining the severity of the disease. This study aims to determine the role of LDH examination as a diagnostic tool for PCP and Arterial Blood Gases (ABG) in HIV and AIDS patients. Method: This research is an analytical study using an observational diagnostic test design, conducted from November 2020-January 2021 at the HIV Treatment Room at H. Adam Malik Hospital, Medan with 158 subjects. We calculate the value of sensitivity, specificity, positive predictive value, and negative predictive value. Results: 75.3% of the total sample was male, with the highest age group being 30-39 years old (46.2%) 126 samples (79.7%) had CD4 levels 200 cells/mm3, 98 samples (62%) had LDH levels > 500 U/L. In this study, 113 samples (71.5%) fell into the ABG criteria [PaO2] <70 mmHg). LDH has superior sensitivity and specificity value compared to ABG examination. In this case PaO2 or A-A DO2 in diagnosing PCP in HIV-AIDS patients. Conclusion: LDH examination combined with clinical and radiological examinations has good sensitivity and specificity in the diagnosis of PCP. Keywords: HIV, AIDS, Lactate dehydrogenase, PCP.

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 Can Venous Blood Gases Replace Arterial Blood Gases in Diabetic Ketoacidosis/Renal Failure Induced Metabolic Acidosis?

2015 ◽  
Vol 3 (3) ◽  
pp. 65-69
Author(s):  
Naveen Mohan ◽  
Gireesh Kumar K. P ◽  
Sreekrishnan T. P ◽  
Ajith Kumar J ◽  
Ajith V. ◽  
...  
Keyword(s):  
Renal Failure ◽  
Metabolic Acidosis ◽  
Diabetic Ketoacidosis ◽  
Venous Blood ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Arterial Blood
Sign in / Sign up

Export Citation Format

Share Document