Role of pulmonary reflexes in ventilation and respiratory control of acutely obstructed dogs during assisted ventilation

Lung ◽  
1980 ◽  
Vol 158 (1) ◽  
pp. 1-8
Author(s):  
Zab Mohsenifar ◽  
David Campisi ◽  
Daniel H. Simmons
Keyword(s):  
Respiratory Control ◽  
Assisted Ventilation

Role of ATP in respiratory control and active transport in tobacco hornworm midgut

1980 ◽  
Vol 238 (1) ◽  
pp. C10-C14 ◽  
Author(s):  
L. J. Mandel ◽  
T. G. Riddle ◽  
J. M. Storey
Keyword(s):  
Active Transport ◽  
Respiratory Control ◽  
Intermediate Form ◽  
Decay Kinetics ◽  
Kinetic Rates ◽  
Fresh Frozen ◽  
The Difference ◽  
Redox Level ◽  
K Transport

The intracellular ATP, ADP, AMP, and orthophosphate (Pi) levels were measured in the midgut of Manduca sexta. The nucleotide levels were identical in tissues either “fresh” frozen or equilibrate in regular (32 mM) K or low (8 mM) K solutions. The calculated [ATP]/[ADP][Pi]ratio was approximately 300 M-1, which is low compared to other tissues. Given the ability of this ratio to control the respiratory rate, it is speculated that this low value may cause the maximal uncontrolled respiration normally observed in the midgut. The kinetics to anoxia of active transport (Isc) and the redox level of the mitochondrial cytochromes were measured simultaneously in the midgut. The cytochromes became reduced with a time constant of 0.75 +/- 0.15 min, whereas that for Isc inhibition was 2.1 +/- 0.15 min after a delay of 0.25 min. The difference between these two kinetic rates indicates that an intermediate form of energy exists in this tissue to energize active K transport. Measurements of ATP levels during the transition to anoxia indicate that its decay kinetics are sufficiently slow for ATP to be the immediate energy source for active transport in this tissue.

Excretion of a Toxic Dose of Thallium

1990 ◽  
Vol 36 (8) ◽  
pp. 1506-1509 ◽  
Author(s):  
H A Chandler ◽  
G P R Archbold ◽  
J M Gibson ◽  
P O'Callaghan ◽  
J N Marks ◽  
...  
Keyword(s):  
Blood Serum ◽  
Whole Blood ◽  
Assisted Ventilation ◽  
Toxic Dose ◽  
Serum And Urine

Abstract We report a successfully treated case of severe thallium intoxication that required 95 days of assisted ventilation and 224 days of hospitalization. Monitoring of the patient for 500 days by measuring thallium in whole blood, serum, and urine is documented, and the role of the laboratory and utility of the measurements are considered.

scholarly journals Development of central respiratory control in anurans: The role of neurochemicals in the emergence of air-breathing and the hypoxic response

2019 ◽  
Vol 270 ◽  
pp. 103266 ◽  
Author(s):  
Tara A. Janes ◽  
Jean-Philippe Rousseau ◽  
Stéphanie Fournier ◽  
Elizabeth A. Kiernan ◽  
Michael B. Harris ◽  
...  
Keyword(s):  
Respiratory Control ◽  
Hypoxic Response ◽  
Air Breathing

scholarly journals Succinate Accumulation Is Associated with a Shift of Mitochondrial Respiratory Control and HIF-1α Upregulation in PTEN Negative Prostate Cancer Cells

2018 ◽  
Vol 19 (7) ◽  
pp. 2129 ◽  
Author(s):  
Anja Weber ◽  
Helmut Klocker ◽  
Herbert Oberacher ◽  
Erich Gnaiger ◽  
Hannes Neuwirt ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Mitochondrial Respiration ◽  
Respiratory Control ◽  
Phosphatase And Tensin Homolog ◽  
Permeabilized Cells ◽  
Tensin Homolog ◽  
Viable Cells ◽  
Sodium Dependent

The idea of using metabolic aberrations as targets for diagnosis or therapeutic intervention has recently gained increasing interest. In a previous study, our group discovered intriguing differences in the oxidative mitochondrial respiration capacity of benign and prostate cancer (PCa) cells. In particular, we found that PCa cells had a higher total respiratory activity than benign cells. Moreover, PCa cells showed a substantial shift towards succinate-supported mitochondrial respiration compared to benign cells, indicating a re-programming of respiratory control. This study aimed to investigate the role of succinate and its main plasma membrane transporter NaDC3 (sodium-dependent dicarboxylate transporter member 3) in PCa cells and to determine whether targeting succinate metabolism can be potentially used to inhibit PCa cell growth. Using high-resolution respirometry analysis, we observed that ROUTINE respiration in viable cells and succinate-supported respiration in permeabilized cells was higher in cells lacking the tumor suppressor phosphatase and tensin-homolog deleted on chromosome 10 (PTEN), which is frequently lost in PCa. In addition, loss of PTEN was associated with increased intracellular succinate accumulation and higher expression of NaDC3. However, siRNA-mediated knockdown of NaDC3 only moderately influenced succinate metabolism and did not affect PCa cell growth. By contrast, mersalyl acid—a broad acting inhibitor of dicarboxylic acid carriers—strongly interfered with intracellular succinate levels and resulted in reduced numbers of PCa cells. These findings suggest that blocking NaDC3 alone is insufficient to intervene with altered succinate metabolism associated with PCa. In conclusion, our data provide evidence that loss of PTEN is associated with increased succinate accumulation and enhanced succinate-supported respiration, which cannot be overcome by inhibiting the succinate transporter NaDC3 alone.

Role of NMDA receptors in development of respiratory control

2005 ◽  
Vol 149 (1-3) ◽  
pp. 123-130 ◽  
Author(s):  
Karen A. Waters ◽  
Rita Machaalani
Keyword(s):  
Nmda Receptors ◽  
Respiratory Control

scholarly journals Direct evidence for a role of intramitochondrial Ca2+ in the regulation of oxidative phosphorylation in the stimulated rat heart. Studies using31P n.m.r. and ruthenium red

1989 ◽  
Vol 262 (1) ◽  
pp. 293-301 ◽  
Author(s):  
J F Unitt ◽  
J G McCormack ◽  
D Reid ◽  
L K MacLachlan ◽  
P J England
Keyword(s):  
Oxidative Phosphorylation ◽  
Direct Evidence ◽  
Respiratory Control ◽  
Ruthenium Red ◽  
Phosphorylation Potential ◽  
Mitochondrial Inner Membrane ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Inotropic Stimulation

1. The concentrations of free ATP, phosphocreatine (PCr), Pi, H+ and ADP (calculated) were monitored in perfused rat hearts by 31P n.m.r. before and during positive inotropic stimulation. Data were accumulated in 20 s blocks. 2. Administration of 0.1 microM-(-)-isoprenaline resulted in no significant changes in ATP, transient decreases in PCr, and transient increases in ADP and Pi. However, the concentrations of all of these metabolites returned to pre-stimulated values within 1 min, whereas cardiac work and O2 uptake remained elevated. 3. In contrast, in hearts perfused continuously with Ruthenium Red (2.5 micrograms/ml), a potent inhibitor of mitochondrial Ca2+ uptake, administration of isoprenaline caused significant decreases in ATP, and also much larger and more prolonged changes in the concentrations of ADP, PCr and Pi. In this instance values did not fully return to pre-stimulated concentrations. Administration of Ruthenium Red alone to unstimulated hearts had minor effects. 4. It is proposed that, in the absence of Ruthenium Red, the transmission of changes in cytoplasmic Ca2+ across the mitochondrial inner membrane is able to maintain the phosphorylation potential of the heart during positive inotropic stimulation, through activation of the Ca2+-sensitive intramitochondrial dehydrogenases (pyruvate, NAD+-isocitrate and 2-oxoglutarate dehydrogenases) leading to enhanced NADH production. 5. This mechanism is unavailable in the presence of Ruthenium Red, and oxidative phosphorylation must be stimulated primarily by a fall in phosphorylation potential, in accordance with the classical concept of respiratory control. However, the full oxidative response of the heart to stimulation may not be achievable under such circumstances.

Mitochondrial dysfunction and respiratory chain defects in a rodent model of methotrexate-induced enteritis

2013 ◽  
Vol 33 (10) ◽  
pp. 1051-1065 ◽  
Author(s):  
VK Kolli ◽  
K Natarajan ◽  
B Isaac ◽  
D Selvakumar ◽  
P Abraham
Keyword(s):  
Critical Role ◽  
Respiratory Control ◽  
Mitochondrial Damage ◽  
Intestinal Injury ◽  
Chain Complexes ◽  
Diphenyltetrazolium Bromide ◽  
Small Intestinal Injury ◽  
Chain Defects ◽  
Small Intestinal

The efficacy of methotrexate (MTX), a widely used chemotherapeutic drug, is limited by its gastrointestinal toxicity and the mechanism of which is not clear. The present study investigates the possible role of mitochondrial damage in MTX-induced enteritis. Small intestinal injury was induced in Wistar rats by the administration of 7 mg kg−1 body wt. MTX intraperitoneally for 3 consecutive days. MTX administration resulted in severe small intestinal injury and extensive damage to enterocyte mitochondria. Respiratory control ratio, the single most useful and reliable test of mitochondrial function, and 3-(4,5-dimethylthiazol-2-yll)-2,5-diphenyltetrazolium bromide reduction, a measure of cell viability were significantly reduced in all the fractions of MTX-treated rat enterocytes. A massive decrease (nearly 70%) in the activities of complexes II and IV was also observed. The results of the present study suggest that MTX-induced damage to enterocyte mitochondria may play a critical role in enteritis. MTX-induced alteration in mitochondrial structure may cause its dysfunction and decreases the activities of the electron chain complexes. MTX-induced mitochondrial damage can result in reduced adenosine triphosphate synthesis, thereby interfering with nutrient absorption and enterocyte renewal. This derangement may contribute to malabsorption of nutrients, diarrhea, and weight loss seen in patients on MTX chemotherapy.

Sign in / Sign up

Export Citation Format

Share Document