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Query: UMLS:C0001127 (respiratory acidosis)
 1,501 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experiments were conducted on cats under nembutal anesthesia; a study was made of pulse activity of bulbar respiratory neurons, electrical activity of the diaphragm and of the intercostal muscles; pO2, pCO2, pH, arterial blood oxygen saturation were determined in combined action of hypoxia and hypercapnia. When hypoxic gaseous mixture was given for respiration the developing hypocapnia disturbed the discharge rhythmic activity of the respiratory neurons, the respiration acquiring a pathological character of the Cheyne--Stokes type. After addition to the hypoxic gaseous mixture of 2% CO2 the gaseous composition of the arterial blood approached the initial values; this addition prevented the development of hypercapnia and disturbances of rhythmic discharge activity of the respiratory neurons. Addition of 5% CO2 to the hypoxic gaseous mixture produced a negative effect: at first it intensified and then depressed the pulse activity of the respiratory neurons, caused metabolic and respiratory acidosis, and promoted asphyxia.
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PMID:[Combined effects of hypoxia and hypercapnia on the functional state of the respiratory center]. 0 Jan 3

Perfusion of the small intestine of anesthetized cats with a solution having excessive CO2 and H+ concentration (pCO2 60 mm Hg; pH; 7.2; [HCO3-] 25 MM) produced a threshold reflex increase in the blood pressure. The subsequent increase of pCO2 to 380 mm Hg and decrease of pH to 6.4 evoked a gradual raise of the blood pressure (8.0+/-0.6 mm Hg) followed by the sharp increase of pressor reflexes amplitude within the range of pH 6.4--6.1. Tissue receptors were found to be essentially sensitive to solutions imitating metabolic acidosis (decrease of [HCO3-] within the physiological range of pH changes (pH 7.1--6.8). Solutions with pH 6.4--6.1 imitating respiratory acidosis (increase of pCO2) were more effective than those imitating metabolic acidosis. The possible role of interstitial pH changes in responses of the tissue chemoreceptors to CO2, is discussed.
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PMID:[Responses of small intestine tissue chemoreceptors to change in the pCO2, pH and (HCO3-) in perfusion solutions]. 0 46

The effect of metabolic and hypercapnic acidosis on myocardial blood flow was studied during intravenous infusions of hydrochloric acid solutions (n = 12) and during passive ventilation with 5% CO2 (n = 5) in anaesthetized, closed chest dogs. Below a pH of 7.2 metabolic acidosis at normal arterial CO2-tensions caused an increase of coronary blood flow and a decrease of coronary vascular resistance associated with a narrowed myocardial arteriovenous O2-difference, indicating vasodilation at unchanged myocardial oxygen consumption. In propranolol-pretreated dogs myocardial blood flow and coronary oxygen AV difference remained unaffected, suggesting that the coronary dilatory effect of metabolic acidemia involves beta adrenergic stimulation. Coronary vasodilation induced by increasing arterial pCO2 was found to the significantly greater as compared with the dilatory effect of metabolic acidosis at the same blood pH level. Blocking of beta receptors did not reduce the coronary response to increased arterial CO2-tensions. It is concluded that the coronary vasodilation observed during hypercapnic acidosis is neither mediated by a beta adrenergic stimulation nor dependent of the concomitant change in blood pH. The possible sites of the coronary dilatory actions of increased arterial CO2-tensions are discussed.
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PMID:Blood pH and PaCO2 as chemical factors in myocardial blood flow control. 0 55

10 Blood acid-base changes were studied at 17 degrees C in immersed crabs (Carcinus maenas) exposed to hypoxic and hyperoxic conditions, by measuring the pH and the CO2 partial pressure, PbCO2, and by calculating the bicarbonate concentration. 20 Hyperoxia first induces a marked respiratory acidosis with a rise of PbCO2. This acidosis is compensated thereafter by a non-ventilatory increase of the blood buffer base concentration. These results are discussed in relation to the general problems concerning the control of the blood acid-base balance in aquatic animals.
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PMID:[Blood acid-base changes produced by variations of water oxygenation in the crab Carcinus maenas (author's transl)]. 0 15

Pulmonary and cutaneous O2 consumption (Vo2) and CO2 production (Vco2) were measured simultaneously in bullfrogs Rana catesbeiana at 20 degrees C. The lungs were responsible for 77.3-91.0% of the total Vo2 and 28.5-74.9% of the total VCO2. The distribution of the total exchange between the lungs and skin depended on metabolic rate; frogs with higher rates relied more heavily on the pulmonary mode for both Vo2 and Vco2. When prevented from ventilating their lungs in an O2-rich environment, bullfrogs developed severe respiratory acidosis, demonstrating the importance of lung exchange in normal acid-base balance. When frogs were totally submerged in an O2-saturated medium, skin Vco2 increased linearly to a steady-state value which approximated the preapneic total Vco2. In these same animals, arterial Pco2 increased proportionately to the increase in skin Vco2, indicating that skin diffusion capacity for CO2 was unaffected. We conclude that the control of breathing in the bullfrog in response to changes in metabolic rate relies predominantly on changes in lung ventilation while the skin plays a more passive role.
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PMID:Importance of pulmonary ventilation in respiratory control in the bullfrog. 0 76

The effects of flunitrazepam (0.03 mg/kg administered intravenously over a two-minute period) was investigated in 11 healthy volunteers with normal pulmonary function. Spirometer tracings were recorded continuously by the Siregnost FD 40 and blood gas measurements were performed by the Harnoncourt AVL gas analyzer. Flunitrazepam produced a characteristic cyclical hypoventilation/hyperventilation pattern lasting 15 min., followed by quiet sleeping rhythms. The duration of action was 20 min. There was a significant fall in PCO2, whilst the CO2 tension showed a significant rise. Changes in pH were in accordance with respiratory acidosis. Apnoea did not occur after the administration of flunitrazepam.
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PMID:[The effects of flunitrazepam (rohypnol) on respiration (author's transl)]. 0 13

Previous work in our laboratory has shown that respiratory acidosis (RA) impaired mechanical function in canine tracheal smooth muscle (TSM). Since an intracellular acidosis could be brought on by the increased CO2 content of the bathing medium and alter the Km's of rate-limiting glycolytic enzymes in the pathway of energy production for contractile function, we have investigated the effects of RA on the intracellular pH (pHi) of TSM. Using the DMO method, paired unstimulated or resting TSM strips were incubated under normocapnic conditions (PO2 600 Torr, PCO2 40 Torr, pH 7.40) and RA (PO2 550 Torr, PCO2 110 Torr, pH 6.95) with 14C-labeled DMO and 3H-labeled inulin or PEG-4000. In another set of paired experiments, TSM strips were tetanized electrically every 5 min or pharmacologically throughout the incubation period ("active" muscle strips). The tissue and an aliquot of bathing medium were counted for 3H and 14C content and the values entered into the Wadell and Butler equation. The pHi's of "resting" normocapnic and acidotic strips were 7.041 +/- 0.017 (SE) and 6.752 +/- 0.012, respectively. However, the pHi's of "active" normocapnic and acidotic strips were 7.275 +/- 0.017 and 7.017 +/- 0.015, respectively. We conclude that respiratory acidosis lowers intracellular pH in both resting and mechanically active TSM's; however, "active" preparations whether exposed to normocapnia or acidosis were unexpectedly more alkaline than their "resting" counterparts.
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PMID:Effect of respiratory acidosis and activity on airway smooth muscle intracellular pH. 1 3

To study the role of carbonic anhydrase in the CSF [HCO3] increase in respiratory acidosis and its effect on brain ammonia, anesthetized rats were subjected to hypercapnia (7% CO2) for 2 hours. The animals received periodic intraventricular injections of either 'mock' CSF or 'mock' CSF and acetazolamide for 45 minutes prior and during hypercapnia when: (a) plasma [HCO3-] was allowed to increase normally and (2) plasma [HCO3] increase was prevented by i.v. HC1 infusion, CSF [HCO3] increased 8.5 mM/L after 2 hours of hypercapnia (delta PCO2 40) in the rats with intraventricular 'mock' CSF injections, and only 6 mM/L in the animals with acetazolamide injections. CSF [HCO3-] increased 7 mM/L during hypercapnia and HCl infusion with intraventricular 'mock' CSF injections, but only 2 mM/L with acetazolamide injections. Changes in total brain CO2 (increase) and brain glutamic acid (decrease) in hypercapnia were not affected by intraventricular acetazolamide and i.v. HCl. The increase of brain NH4+ and glutamine in hypercapnia was reduced in these conditions. It is concluded that there are at least two sources for the CSF [HCO3-] increase in hypercapnia; one formed in the CNS and dependent on carbonic anhydrase, and the other derived from plasma [HCO3-] increase.
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PMID:The CSF HCO3 increase in hypercapnia relationshp to HCO3, glutamate, glutamine and NH3 in brain. 1 66

The respiratory system is described as a feedback control system. The controller consists of the peripheral chemoreceptors and the central chemosensitive structures, the respiratory centre in the medulla oblongata and the thorax-lung pump which they drive. The controlled system is comprised of three compartments (lung, brain and the remaining tissue) connected by the blood circulation. The controlled values are arterial pH and arterial O2 partial pressure and cerebral extracellular pH. Earlier models have been improved by: (1) the dead space description, (2) the thermodynamic formulation of the CO2 dissociation equation and the simple but accurate O2 dissociation equation of the blood, (3) the alteration of the CO2 dissociation equation for the brain and the remaining tissue to accommodate recent results, (4) the application of the one-receptor-theory of central chemosensitivity, (5) the pH dependence of brain circulation, (6) the bicarbonate exchange between blood and extracellular fluid of the brain and (7) the introduction of variable circulation times. Respiratory and metabolic disturbances of the respiratory system are analyzed. The mathematical formulation of the respiratory system is a differential difference equation system. In the steady state the experimental results are reproduced fairly well. A slight discrepancy is found in the simulation of metabolic acidosis. Apparently we have assumed the sensitivity of the peripheral chemoreceptors to be too large so that the respiratory response is not correctly predicted. In the numerical solution there is an overshoot in the on-transient and a damped oscillation in the off-transient of the alveolar CO2 partial pressure during respiratory acidosis. We have varied the parameters to make deviations small. The best agreement seems to result, if the central threshold is near the normal extracellular pH of the brain. A further deviation from experimental findings is that the cerebral CO2 and H+ concentration, the blood circulation of the brain, the alveolar O2 partial tension and the ventilation show a slight oscillation in the off-transient. Except for these discrepancies the experimental results, especially the stability of the extracellular pH of the brain, are reproduced fairly well. During hypoxia there are deviations form the experimental results if the central residual activity is constant and the central threshold deviates from the normal extracellular pH of the brain. But if the central residual activity is pH dependent and if the central threshold is equal to the normal extracellular pH of the brain, then the time course of VE and the other variables agree fairly well with experimental results. There is also a good correspondence between the theoretical and experimental data during hyperoxia. During metabolic acidosis the time constant of the bicarbonate exchange between blood and extracellular fluid of the brain is important. If a time constant of one minute is assumed, then the predicted and the experimental results correspond sufficiently well.
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PMID:[Mathematical simulation of the respiratory system (author's transl)]. 1 39

The effect of local hypercapnic acidosis or local hypocapnic alkalosis on pial arterioles were studied in anesthetized cats equipped with a cranial window for the direct observation of the pial microcirculation of the parietal cortex. Changes in PCO2 and pH of the extracellular fluid were induced by perfusing the space under the cranial window with artificial cerebrospinal fluid equilibrated with different concentrations of CO2, while PaCO2 was maintained constant. Hypercapnic acidosis dilated and hypocapnic alkalosis constricted pial arteioles markedly. The results indicate that a basis exists for considering CO2 as a mediator for local regulation of brain blood flow. The vasodilation associated with arterial hypercapnia was abolished by a reduction in CSF PCO2 equal in magnitude to the rise in arterial blood PCO2, suggesting that the action of CO2 is entirely local.
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PMID:Local mechanism of CO2 action of cat pial arterioles. 1 34


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