Adaptation to Respiratory Acidosis in the Turtle Bladder

Potentially (near) fatal asthma (PFA) defines a subset of patients with asthma who are at increased risk for death from their disease. The diagnosis of PFA should motivate treating physicians, health professionals, and patients to be more aggressive in the monitoring, treatment, and control of this high-risk type of asthma. A diagnosis of PFA is made when any one of the following are present: (1) a history of endotracheal intubation from asthma, (2) acute respiratory acidosis (pH < 7.35) or respiratory failure from acute severe asthma, (3) two or more episodes of acute pneumothorax or pneumomediastinum from asthma, (4) two or more episodes of acute severe asthma, despite the use of long-term oral corticosteroids and other antiasthma medications. There are two predominant phenotypes of near-fatal exacerbations: “subacute” exacerbation and “hyperacute” exacerbation. The best way to “treat” acute severe asthma is 3‐7 days before it occurs (i.e., at the onset of symptoms or change in respiratory function) and to optimize control of asthma by decreasing the number of symptomatic days and the days and/or nights that require rescue therapy and increasing baseline respiratory status in “poor perceivers.” PFA is treated with a multifaceted approach; physicians and health-care professionals should appreciate limitations of pharmacotherapy, including combination inhaled corticosteroid‐long-acting β-agonist products as well as addressing nonadherence, psychiatric, and socioeconomic issues that complicate care.

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Calcium transport in turtle bladder

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1987.253.6.r917 ◽

1987 ◽

Vol 253 (6) ◽

pp. R917-R921

Author(s):

S. Sabatini ◽

N. A. Kurtzman

Keyword(s):

Calcium Transport ◽

Calcium Absorption ◽

Short Circuit ◽

Open Circuit ◽

Calcium Flux ◽

Bladder Epithelium ◽

Control Value ◽

Sodium Calcium ◽

Turtle Bladder ◽

Absorptive Flux

Unidirectional 45Ca fluxes were measured in the turtle bladder under open-circuit and short-circuit conditions. In the open-circuited state net calcium flux (JnetCa) was secretory (serosa to mucosa) and was 388.3 +/- 84.5 pmol.mg-1.h-1 (n = 20, P less than 0.001). Ouabain (5 X 10(-4) M) reversed JnetCa to an absorptive flux (serosal minus mucosal flux = -195.8 +/- 41.3 pmol.mg-1.h-1; n = 20, P less than 0.001). Amiloride (1 X 10(-5) M) reduced both fluxes such that JnetCa was not significantly different from zero. Removal of mucosal sodium caused net calcium absorption; removal of serosal sodium caused calcium secretion. When bladders were short circuited, JnetCa decreased to approximately one-third of control value but remained secretory (138.4 +/- 54.3 pmol.mg-1.h-1; n = 9, P less than 0.025). When ouabain was added under short-circuit conditions, JnetCa was similar in magnitude and direction to ouabain under open-circuited conditions (i.e., absorptive). Tissue 45Ca content was approximately equal to 30-fold lower when the isotope was placed in the mucosal bath, suggesting that the apical membrane is the resistance barrier to calcium transport. The results obtained in this study are best explained by postulating a Ca2+-ATPase on the serosa of the turtle bladder epithelium and a sodium-calcium antiporter on the mucosa. In this model, the energy for calcium movement would be supplied, in large part, by the Na+-K+-ATPase. By increasing cell sodium, ouabain would decrease the activity of the mucosal sodium-calcium exchanger (or reverse it), uncovering active calcium transport across the serosa.

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Effect of calcium ionophore A23187 on electrogenic acid-base transport in turtle bladder Inhibition of acidification and stimulation of alkalinization

Biochimica et Biophysica Acta (BBA) - Biomembranes ◽

10.1016/0005-2736(83)90197-9 ◽

1983 ◽

Vol 732 (1) ◽

pp. 146-153 ◽

Cited By ~ 5

Author(s):

Gerhard Ehrenspeck

Keyword(s):

Calcium Ionophore ◽

Calcium Ionophore A23187 ◽

Ionophore A23187 ◽

Acid Base ◽

Turtle Bladder ◽

Bladder Inhibition ◽

Stimulation Of

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Combined Renal-Pulmonary Extracorporeal Support with Low Blood Flow Techniques: A Retrospective Observational Study (CICERO Study)

Blood Purification ◽

10.1159/000517280 ◽

2021 ◽

pp. 1-10

Author(s):

Guglielmo Consales ◽

Lucia Zamidei ◽

Franco Turani ◽

Diego Atzeni ◽

Paolo Isoni ◽

...

Keyword(s):

Mechanical Ventilation ◽

Observational Study ◽

Multiorgan Failure ◽

Invasive Mechanical Ventilation ◽

Respiratory Acidosis ◽

Kidney Injury ◽

Protective Ventilation ◽

Retrospective Observational Study ◽

Organ Support ◽

Chronic Obstructive

Background: Critically ill patients with acute respiratory failure frequently present concomitant lung and kidney injury, within a multiorgan failure condition due to local and systemic mediators. To face this issue, extracorporeal carbon dioxide removal (ECCO2R) systems have been integrated into continuous renal replacement therapy (CRRT) platforms to provide a combined organ support, with efficient clearance of CO2 with very low extracorporeal blood flows (<400 mL/min). Objectives: To evaluate efficacy and safety of combined ECCO2R-CRRT support with PrismaLung®-Prismaflex® in patients affected by hypercapnic respiratory acidosis associated with AKI in a second level intensive care unit. Methods: We carried out a retrospective observational study enrolling patients submitted to PrismaLung®-Prismaflex® due to mild to moderate acute respiratory distress syndrome (ARDS) or acute exacerbation of chronic obstructive pulmonary disease (aeCOPD). The primary endpoints were the shift to protective ventilation and extubation of mechanically ventilated patients and the shift to invasive mechanical ventilation of patients receiving noninvasive ventilation (NIV). Clinical-laboratoristic data and operational characteristics of ECCO2R-CRRT were recorded. Results: Overall, 12/17 patients on mechanical ventilation shifted to protective ventilation, CO2 clearance was satisfactorily maintained during the whole observational period, and pH was rapidly corrected. Treatment prevented NIV failure in 4 out of 5 patients. No treatment-related complications were recorded. Conclusion: ECCO2R-CRRT was effective and safe in patients with aeCOPD and ARDS associated with AKI.

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The Effects of the Carbonic Anhydrase Inhibitor Acetazoleamide on Chronic Respiratory Acidosis.1

Acta Medica Scandinavica ◽

10.1111/j.0954-6820.1956.tb14299.x ◽

2009 ◽

Vol 154 (1) ◽

pp. 53-64 ◽

Cited By ~ 8

Author(s):

M. M. PLATTS ◽

T. HANLEY

Keyword(s):

Carbonic Anhydrase ◽

Respiratory Acidosis ◽

Carbonic Anhydrase Inhibitor

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Causes, Effects and Methods of Monitoring Gas Exchange Disturbances during Equine General Anaesthesia

Animals ◽

10.3390/ani11072049 ◽

2021 ◽

Vol 11 (7) ◽

pp. 2049

Author(s):

Elżbieta Stefanik ◽

Olga Drewnowska ◽

Barbara Lisowska ◽

Bernard Turek

Keyword(s):

Gas Exchange ◽

General Anaesthesia ◽

Near Infrared ◽

Respiratory Acidosis ◽

Monitoring Methods ◽

Arterial Blood Gas ◽

Complementary Method ◽

Arterial Blood ◽

Operative Complications ◽

Post Operative Complications

Horses, due to their unique anatomy and physiology, are particularly prone to intraoperative cardiopulmonary disorders. In dorsally recumbent horses, chest wall movement is restricted and the lungs are compressed by the abdominal organs, leading to the collapse of the alveoli. This results in hypoventilation, leading to hypercapnia and respiratory acidosis as well as impaired tissue oxygen supply (hypoxia). The most common mechanisms disturbing gas exchange are hypoventilation, atelectasis, ventilation–perfusion (V/Q) mismatch and shunt. Gas exchange disturbances are considered to be an important factor contributing to the high anaesthetic mortality rate and numerous post-anaesthetic side effects. Current monitoring methods, such as a pulse oximetry, capnography, arterial blood gas measurements and spirometry, may not be sufficient by themselves, and only in combination with each other can they provide extensive information about the condition of the patient. A new, promising, complementary method is near-infrared spectroscopy (NIRS). The purpose of this article is to review the negative effect of general anaesthesia on the gas exchange in horses and describe the post-operative complications resulting from it. Understanding the changes that occur during general anaesthesia and the factors that affect them, as well as improving gas monitoring techniques, can improve the post-aesthetic survival rate and minimize post-operative complications.

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Division of the pattern-evoked retinal reponse by respiratory acidosis

Vision Research ◽

10.1016/0042-6989(88)90179-4 ◽

1988 ◽

Vol 28 (3) ◽

pp. 363-369 ◽

Cited By ~ 3

Author(s):

William W. Dawson ◽

Ronald Parmer ◽

G.M. Hope

Keyword(s):

Respiratory Acidosis

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Dialysis-induced Respiratory Acidosis

CHEST Journal ◽

10.1378/chest.98.5.1285 ◽

1990 ◽

Vol 98 (5) ◽

pp. 1285-1288 ◽

Cited By ~ 6

Author(s):

Judith Cohn ◽

Robert A. Balk ◽

Roger C. Bone

Keyword(s):

Respiratory Acidosis

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Hyperinflation-induced cardiorespiratory failure in rats

Journal of Applied Physiology ◽

10.1152/japplphysiol.91342.2008 ◽

2009 ◽

Vol 107 (1) ◽

pp. 275-282 ◽

Cited By ~ 6

Author(s):

Jeremy A. Simpson ◽

Keith R. Brunt ◽

Christine P. Collier ◽

Steve Iscoe

Keyword(s):

Mean Arterial Pressure ◽

Arterial Pressure ◽

Lung Volume ◽

Troponin T ◽

Respiratory Acidosis ◽

Left Ventricular ◽

Cardiovascular Failure ◽

Cardiorespiratory Failure ◽

Arterial Hypoxemia ◽

Ventricular Afterload

We previously showed that severe inspiratory resistive loads cause acute (<1 h) cardiorespiratory failure characterized by arterial hypotension, multifocal myocardial infarcts, and diaphragmatic fatigue. The mechanisms responsible for cardiovascular failure are unknown, but one factor may be the increased ventricular afterload caused by the large negative intrathoracic pressures generated when breathing against an inspiratory load. Because expiratory threshold loads increase intrathoracic pressure and decrease left ventricular afterload, we hypothesized that anesthetized rats forced to breathe against such a load would experience only diaphragmatic failure. Loading approximately doubled end-expiratory lung volume, halved respiratory frequency, and caused arterial hypoxemia and hypercapnia, respiratory acidosis, and increased inspiratory drive. Although hyperinflation immediately reduced the diaphragm's mechanical advantage, fatigue did not occur until near load termination. Mean arterial pressure progressively fell, becoming significant (cardiovascular failure) midway through loading despite tachycardia. Loading was terminated (endurance 125 ± 43 min; range 82–206 min) when mean arterial pressure dropped below 50 mmHg. Blood samples taken immediately after load termination revealed hypoglycemia, hyperkalemia, and cardiac troponin T, the last indicating myocardial injury that was, according to histology, mainly in the right ventricle. This damage probably reflects a combination of decreased O2 delivery (decreased venous return and arterial hypoxemia) and greater afterload due to hyperinflation-induced increase in pulmonary vascular resistance. Thus, in rats breathing at an increased end-expiratory lung volume, cardiorespiratory, not just respiratory, failure still occurred. Right heart injury and dysfunction may contribute to the increased morbidity and mortality associated with acute exacerbations of obstructive airway disease.

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