Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: UMLS:C0085383 (hypocapnia)
1,697 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.
...
PMID:[Combined effects of hypoxia and hypercapnia on the functional state of the respiratory center]. 0 Jan 3

After summarizing the phenomena of respiratory physiology involved in the hyperpnea test, the author studies the quantitative relation between the drop in PECO2 (pressure of CO2 in expired air) and changes in the EEG during hyperpnea. Normal subjects are divided into two groups of a hundred (6 to 19 1/2 years of age; 20 to 59 1/2 years of age). The PECO2 at rest is higher among the young subjects than among the adults, and its decline during hyperpnea is sharper. Thus, children show discrete respiratory acidosis in comparison with adults. The EEG of normal adults is practically unchanged during hyperpnea whereas, in the young group, moderate changes in the profile were observed in 45 out of 100 cases (classified empirically as normal). The PECO2 reaches a lower level in subjects showing EEG changes than in those showing none. All the reported differences are statistically significant (p less than 0.01). The probability of hyperpnea modifying the EEG profile becomes progressively less with age, and may be related to the reduced production of CO2 in older subjects. Epileptic subjects (primary generalized epilepsy) produce more CO2 than normal subjects during the hyperpnea test. The statistical data reported in the study show the importance of the size of the drop in ventilatory CO2 in the determination of EEG changes. The rest of hyperpnea in EEG can therefore be validly interpreted only if capnographic variations are measured. A standard quantitative hyperpnea test of this type should be devised, with specification of the hypocapnia level to be achieved.
...
PMID:[Quantitative hyperpnea in EEG (author's transl)]. 2 61

The sign of a traumatically caused alveolar hyperventilation in severe cranio-cerebral injury is a respiratory alcalosis as well as hypoxia and hypoxemia in the arterial as well in the cerebral veneous blood. The combination of decreased oxygen tension or saturation and hypocapnia can exist for several days and in a lethal course transform into a combined metabolic respiratory acidosis with increasing carbonic acid tension and so initiate the prefinal state. The extremely pathological blood gases are usually the first sign of shock-specific changes of the lung. The most impressing changes of the cerebrospinal fluid are the metabolic acidosis in combination with a diminished oxygen tension and tissue hypoxia of the brain. The acidosis of cerebrospinal fluid in severe brain injury is not only of prognostic but also of therapeutical importance. The treatment of the acidosis of cerebrospinal fluid by intrathecal administration of buffering substances in severe brain injuries and its sequelae can have a favourable influence on the cerebral circulation and brain metabolism.
...
PMID:[Cerebrospinal fluid changes in severe craniocerebral injury and their therapy]. 101 May 21

Deviations of the alveolar ventilation rate from normality induce respiratory acid-base disturbances. Alveolar hyperventilation leads to hypocapnia and thus respiratory alkalosis whereas alveolar hypoventilation induces hypercapnia leading to respiratory acidosis. The changes in CO2 induce compensatory alterations of renal bicarbonate transport: Hypercapnia stimulates renal reabsorption of bicarbonate whereas hypocapnia enhances urinary bicarbonates. The plasma bicarbonate concentration rises in response to hypercapnia and falls following hypocapnia. Renal regulation of plasma bicarbonate results in a characteristic dependence on systemic PCO2 permitting the formation of diagnostic criteria for respiratory imbalance of acid-base homeostasis. In chronic respiratory acidosis plasma bicarbonate should rise by 0.35 mmol/l per mmHg increase in PCO2. In chronic respiratory alkalosis, on the other hand, plasma bicarbonate should fall by 0.4 mmol/l for every mmHg decrease in PCO2. If the measured bicarbonate values do not fall into this expected range, acute respiratory or mixed (respiratory and metabolic) acid-base disturbances should be suspected. The clinical significance and application of these diagnostic criteria are illustrated by examples.
...
PMID:[Hypo- and hyperventilation: consequences for acid-base balance]. 192 34

In the intact rat kidney, bicarbonate reabsorption in the early proximal tubule (EP) is strongly dependent on delivery. Independent of delivery, metabolic acidosis stimulates EP bicarbonate reabsorption. In this study, we investigated whether systemic pH changes induced by acute or chronic respiratory acid-base disorders also affect EP HCO3- reabsorption, independent of delivery (FLHCO3, filtered load of bicarbonate). Hypercapnia was induced in rats acutely (1-3 h) and chronically (4-5 d) by increasing inspired PCO2. Hypocapnia was induced acutely (1-3 h) by mechanical hyperventilation, and chronically (4-5 d) using hypoxemia to stimulate ventilation. When compared with normocapneic rats with similar FLHCO3, no stimulation of EP or overall proximal HCO3 reabsorption was found with either acute hypercapnia (PaCO2 = 74 mmHg, pH = 7.23) or chronic hypercapnia (PaCO2 = 84 mmHg, pH = 7.31). Acute hypocapnia (PaCO2 = 29 mmHg, pH = 7.56) did not suppress EP or overall HCO3 reabsorption. Chronic hypocapnia (PaCO2 = 26 mmHg, pH = 7.54) reduced proximal HCO3 reabsorption, but this effect was reversed when FLHCO3 was increased to levels comparable to euvolemic normocapneic rats. Thus, when delivery is accounted for, we could find no additional stimulation of proximal bicarbonate reabsorption in respiratory acidosis and, except at low delivery rates, no reduction in bicarbonate reabsorption in respiratory alkalosis.
...
PMID:Delivery dependence of early proximal bicarbonate reabsorption in the rat in respiratory acidosis and alkalosis. 199 47

We studied the relationship between contractile function and intracellular pH (pHi) in the isolated rat diaphragm when superfusate PCO2 was changed during hyperoxia or hypoxia. Superfused diaphragm strips were field stimulated at 0.5 Herz, and twitch tension (TT) was recorded. The pHi was calculated from the volume distribution of a weak acid, dimethyl-oxazolidinedione. In hyperoxia, hypercapnic acidosis (pH 7.06-6.63) depressed diaphragm pHi and TT, whereas hypocapnic alkalosis (pH 7.82-8.15) increased pHi but did not significantly affect TT. TT was maximum at physiological pHi (7.06), but in hyperoxic hypercapnic muscles substantial force was still generated at pHi values as low as 6.44. Hypoxia (PO2 30-38 mm Hg) markedly reduced TT; this effect was slightly exacerbated by hypercapnia and attenuated by hypocapnia. Hypoxia lowered pHi by about 0.2 units, which was insufficient to account for the hypoxic contractile failure. Knowledge of the hyperoxic muscle TT/pHi relationship suggests that, in other contexts, caution should be exercised in attributing severe muscle fatigue or force loss to modest falls in pHi.
...
PMID:The effect of pH and hypoxia on function and intracellular pH of the rat diaphragm. 210 18

Acid-base derangements are encountered frequently in clinical practice and many have life-threatening implications. Treatment is dependent on correctly identifying the acid-base disorder and, whenever possible, repairing the underlying causal process. Bicarbonate is the agent of choice for the treatment of acute metabolic acidosis. Controversy surrounds the use of alkali therapy in lactic acidosis and diabetic ketoacidosis, but bicarbonate should clearly be administered for severe acidosis. In most patients with mild to moderate chloride-responsive metabolic alkalosis, providing an adequate amount of a chloride salt will restore acid-base balance to normal over a matter of days. In contrast, therapy of the chloride-resistant metabolic alkalosis is best directed at the underlying disease. When alkalemia is severe, administering hydrochloric acid or a hydrochloric acid precursor may be necessary. Treatment of respiratory acidosis should be targeted at restoring ventilation; alkali should be administered only for superimposed metabolic acidosis. The therapy of respiratory alkalosis is centred on reversal of the root cause; short of this goal, there is no effective treatment of primary hypocapnia. The coexistence of more than one acid-base disorder (i.e. a mixed disorder) is not uncommon. When plasma bicarbonate concentration and arterial carbon dioxide tension (paCO2) are altered in opposite directions, extreme shifts in pH may occur. In such cases, it is imperative that the nature of the disturbance is identified early and therapy directed at both disorders.
...
PMID:Rational treatment of acid-base disorders. 219 65

To examine whether CPB influences pulmonary vascular sensitivity to CO2, we compared the effect of slight induced hypocarbia and hypercarbia on pulmonary circulation before and after CPB in ten mechanically ventilated patients undergoing CABG. Hypocarbia was produced by increasing tidal volume slightly and hypercarbia was then induced by adding CO2 to the inspired gas mixture. In another ten patients, hypercarbia was produced after CPB by decreasing ventilator rate and the cardiopulmonary responses to hypercarbia, produced by the two methods of CO2 elevation, were compared. Slight respiratory acidosis induced by CO2 inhalation did not change PVR before CPB but effected a 50 percent increase after CPB. Hypercarbia induced by alveolar hypoventilation after CPB increased PVR by 40 percent. During the increased CO2 production after hypothermic CPB, pulmonary vasoconstriction would be expected to occur and impair right ventricular performance. Therefore, tight control of PaCO2 with appropriate adjustment of ventilatory support is mandatory.
...
PMID:Pulmonary vascular resistance before and after cardiopulmonary bypass. The effect of PaCO2. 249 21

We have compared the ventilatory responses of intact and carotid body-denervated (CBD) goats to moderate [partial pressure of O2 in arterial blood; (Pao2) approximately 44 Torr] and severe (Pao2 approximately 33 Torr) many time points for up to 7 days of hypobaria. In the intact group there were significant time-dependent decreases in partial pressure of CO2 in arterial blood (PaCO2) in both moderate and severe hypoxemia (approximately-7 and -11 Torr) that were largely complete by 8 h of hypoxemia and maintained throughout. Acute restoration of normoxia in chronically hypoxic intact animals produced time-dependent increases in Paco2 over 2 h, but hypocapnia persisted relative to sea-level control. Arterial plasma [HCO3-] and [H+] decreased, and [Cl-] increased with a time course and magnitude consistent with developing hypocapnia. Chronic CBD, per se, resulted in a sustained, partially compensated respiratory acidosis, as PaCO2 rose 6 Torr and base excess rose 3 mEq/1, [Cl-] fell 1 mEq/1, and pHa fell 0.01 units. During exposure to identical levels of arterial hypoxemia as in the intact group. CBD animals showed no significant changes in PaCO2, [H+]a, or [HCO3-]a at any time during moderate or severe hypoxemia. Plasma [C1-] remained within the normal range throughout exposure to moderate hypoxia and increased in severe hypoxia. In a few instances some hypocapnia was observed, but this was highly inconsistent and was always less than one-third of that observed in intact goats. In contrast to intact goats, acute restorations of normoxia in the chronically hypoxic CBD goats always caused hyperventilation.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Carotid bodies are required for ventilatory acclimatization to chronic hypoxia. 308 45

The study pertains to a series of investigations on the effects of CO2 inhalation as used for pre-slaughter anaesthesia in swine. Acid/base parameters, blood oxygen tension, plasma Na, K, Ca and stress hormone concentrations were monitored in Yorkshire swine before, during, and for 10 min after the animals were descended for 1 min into 80% CO2 in air. Severe respiratory acidosis (PaCO2 approximately 50 kPa, arterial pH approximately 6.6) and hypoxia (PaO2 approximately 4kPa) had developed after 45 s of the CO2 inhalation. The corresponding changes in venous blood were less drastic (PvCO2 approximately 17 kPa, pH 7.1, PvO2 approximately 4 kPa). Readjustment to PaCO2 approximately II kPa, arterial pH 7.2, and PaO2 approximately 13 kPa had occurred at 1 min post CO2. Four minutes later the respiratory acidosis had become converted into metabolic acidosis subjected to partial respiratory compensation (arterial pH 7.3 in the presence of moderate hypocapnia and hyperoxaemia). The cause of this metabolic acidosis (present also at 10 min post CO2) was apparently hypoxia-induced anaerobic metabolism (= lactic acid production). Apparently due to hydrogen ion transport into the cells in exchange for other cations, hyperkalaemia (K approximately 6.6 mmol l-1), and a 7 mmol l-1 increase in plasma Na had developed at 1.5 min later. The CO2 inhalation did not change the total plasma Ca significantly. The transport of the swine from the stable to the immediate pre-experimental situation induced a 3-fold increase in plasma cortisol concentration (PC, to approximately 130 mmol l-1). No further increase in PC occurred in response to the CO2 inhalation. It indicates that no additional emotional strain was imposed upon the animals during the CO2 exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Acidosis, hypoxia and stress hormone release in response to one-minute inhalation of 80% CO2 in swine. 314 71


1 2 3 Next >>

---