Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Administration of sodium bicarbonate during cardiopulmonary resuscitation (CPR) is controversial, and our aim was to elucidate whether or not its administration is beneficial by analyzing the acid-base status and the level of carbon dioxide in central venous blood during CPR, and their changes following administration of sodium bicarbonate. Six patients were studied. They had all been admitted to the intensive care unit (ICU), had already had pulmonary arterial or central venous catheters inserted, and had acute episodes of circulatory collapse during their stay in the ICU. The following phenomena were observed: 1) hypercapnia and acidosis of central venous blood were prominent during both cardiogenic shock and CPR, although arterial hypocapnia was maintained by hyperventilation; 2) administration of sodium bicarbonate during cardiogenic shock and CPR induced exacerbation of hypercapnia and acidosis of central venous blood; 3) when arterial hypercapnia was present due to disturbed ventilation, administration of sodium bicarbonate exacerbated hypercapnia and acidosis of both arterial and central venous blood; 4) administration of sodium bicarbonate did not induce hypercapnia of central venous blood in a septic shock patient in whom the septic hyperdynamic state was prevalent in spite of low systemic perfusion pressure. It was concluded that hypercapnia and acidosis of the central venous blood and tissues were exacerbated by administration of sodium bicarbonate during CPR, and that such an effect might be dependent on the severity of the decrease in tissue perfusion.
 ...
PMID:Exacerbation of hypercapnia and acidosis of central venous blood and tissue following administration of sodium bicarbonate during cardiopulmonary resuscitation. 254 21

The present study investigates the nature of tensor veli palatini muscle (TVP) and levator veli palatini muscle (LVP) as accessory respiratory muscles. In the first part of the study, the relation between the muscles' activities as revealed by EMG activities and respiration rhythm was analysed under various combinations of partial pressures of O2 and CO2 in the arterial blood. Furthermore, the effect of sodium cyanide (NaCN) perfused through the carotid sinus was examined. During resting breathing, no EMG activity was recorded from either muscle. In hypercapnic or hypoxemic conditions produced by rebreathing, TVP exhibited a phasic EMG activity during inspiration. LVP showed a phasic EMG activity during expiration in hypoxic conditions (PaO2 less than 40 mmHg). NaCN perfused bilaterally through the carotid sinus induced the phasic EMG activities similar to those observed in hypercapnia and/or hypoxemia. TVP was more sensitive to NaCN than LVP. The second part of the study examined specific roles of the muscles in altered states of breathing. At the time of onset of LVP activity induced by rebreathing, the oral proportion of airflow markedly increased. On the other hand, TVP activity greatly increased in amplitude when negative pressure was applied to the upper airway. The results suggest that both muscles are accessory respiratory muscles and are regulated by chemogenic inputs including those from the carotid body; TVP is an accessory inspiratory muscle that contributes to the maintenance of upper airway patency, and LVP is an accessory expiratory muscle that increases the portion of expiratory airflow through the oral cavity.
 ...
PMID:[Role of the soft palate in respiration: an electromyographic study in the dog]. 263 51

The aim of the present study was to evaluate clinical and laboratory features of acute severe asthma (ASA) in children and their outcome of mechanical ventilation (MV). Twenty ASA episodes admitted to the hospital with hypercapnia (HC) and/or lost of consciousness (LC) and/or severe non reversible bronchial obstruction (NRBO) were retrospectively studied. Long lasting asthma and frequent admissions were registered in the majority of cases. In HC group (14 cases) the PaCO2 was 70 +/- 26 mmHg (X +/- SD). Hypercapnia was associated with intravenous administration of sodium bicarbonate in three cases. In NRBO group (4 cases) the acute response to salbutamol brought out during the first week of treatment and it was associated with increased basal forced expiratory volume in one second (FEV1). Ten cases were treated with MV because of hypercapnia and/or lost of consciousness, seizures (one case), and cardiac arrest (one case). The later patient died in 24 hours. Pneumothorax and atelectasis (one case), and pneumonia (one case) were the complications of mechanical ventilation. Three cases with PaO2 less than 60 mmHg and four cases with FEV1 less than 60% were sent home. After 27 days one patient from the later group had a new episode of ASA. Arterial gases and expiratory flow measurements are paramount tools for close monitoring of children with ASA. It is suggested that normalization of those parameters are an essential criteria for discharging those patients.
 ...
PMID:[Severe asthmatic crisis in children]. 265 54

The intracellular energetic environment of rat hippocampal slices was manipulated by bolstering ATP levels following the addition of adenosine to the incubation medium, or by manipulating intracellular pH. Addition of 8 mM adenosine to the incubation medium increased total tissue adenylate and ATP content, but did not prolong electrical function during anoxia. Further, it resulted in long-lasting alterations in normoxic evoked responses. Intracellular pH (pHi) was changed by manipulating the bicarbonate/CO2 ratio of the incubation medium, or by adding amiloride, a hydrogen/sodium antiport blocker. Estimates of intracellular pH using the creatine kinase equilibrium agree with those obtained by Neutral red scanning spectrophotometry in control conditions. However, only Neutral red indicated an acidification with amiloride treatment, while the creatine kinase equilibrium was preferentially affected by hypercapnia, suggesting the presence of at least two pH compartments in hippocampal brain slices. These manipulations cannot be carried out easily in vivo, and provide a means of determining the importance of metabolic changes on neural function during anoxia.
 ...
PMID:Manipulating the intracellular environment of hippocampal slices: pH and high-energy phosphates. 272 18

We evaluated the effect of general anesthesia induced by 45 mg/kg iv pentobarbital sodium or by 75 mg/kg iv alpha-chloralose plus 500 mg/kg iv urethan on the response of cerebral arterioles to hypercapnia in rabbits equipped with chronically implanted cranial windows for the observation of the cerebral microcirculation. Both types of anesthetic induced approximately comparable anesthesia and depressed the responsiveness to CO2 to an equal extent. There were no changes in resting vessel diameter or in mean arterial blood pressure induced by either anesthetic, but both anesthetics increased end-expiratory PCO2 during room air breathing. The findings show that anesthetics depress the responsiveness of cerebral arterioles to hypercapnia. A decrease in cerebral metabolism and/or direct effects of the anesthetics on cerebral vessels may be involved.
 ...
PMID:Effects of anesthesia on cerebral arteriolar responses to hypercapnia. 275 Sep 51

The pathogenesis of edema in COPD patients is poorly understood. In 50 COPD patients without cor pulmonale, we measured water sodium and potassium excretion in 24 hours, concentration of sodium and potassium in plasma as well as PRA, ATII and aldosterone levels. We found that PRA, ATII, and aldosterone levels in COPD patients with edema are much higher than those in patients without edema and sodium and water excretion decreased significantly in edematous COPD patients. Elevation of PRA, ATII, and aldosterone correlated with inability to excrete sodium and water. These data suggest that, in conjunction with hypercapnia-hypoxia-mediated disturbance in renal function, stimulation of RAAS, especially the resulting increase of aldosterone may contribute to edema formation in COPD patients.
 ...
PMID:[Role of the renin-angiotensin-aldosterone system in the pathogenesis of edema formation in chronic obstructive pulmonary disease]. 280 68

Posthypercapnic metabolic alkalosis has been attributed to decreased HCO3 excretion because of low glomerular filtration rate (GFR), volume contraction, or chloride depletion. We have previously shown that chronic hypercapnia enhances the Vmax of the Na+-H+ antiporter. We reasoned that an increased Vmax of the Na+-H+ antiporter could play a role in the maintenance of posthypercapnic metabolic alkalosis. To test this hypothesis, we measured the kinetics of the Na+-H+ antiporter by the dissipation of the quenching of acridine orange fluorescence in purified brush-border membrane obtained from posthypercapnic rabbits. The kinetic parameters were measured in controls and in rabbits that were exposed to hypercapnia for 48 h and then allowed to breathe room air for 3, 24, or 48 h. In luminal membranes prepared from posthypercapnic animals, the Vmax of the Na+-H+ antiporter was significantly increased after 3 and 24 h but not after 48 h compared with controls. The increase in Vmax was not different from that of hypercapnic animals. There was no difference in the Km of the Na+-H+ antiporter among these five groups. Amiloride inhibited the Vmax equally in membranes from control and posthypercapnic rabbits. Proton permeability was comparable among the groups. These data indicate that the increase in Vmax in posthypercapnic rabbits is mediated through the electroneutral Na+-H+ exchange and not through conductive H+ and Na+ pathway. Glucose uptake was not different in control and posthypercapnia, indicating a selective increase in Na+-H+ antiporter activity. At 3 and 24 h posthypercapnia, HCO3 concentration was higher than control.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Na+-H+ antiporter in posthypercapnic state. 282 35

Several disturbances of acid-base balance, including chronic metabolic and respiratory acidoses and metabolic alkalosis, are associated with enhanced proximal tubule bicarbonate reabsorption. To determine whether augmented brush border Na/H exchange might mediate enhanced proximal tubule bicarbonate reabsorption in these disorders, we measured Na/H exchange activity in cortical brush border membrane vesicles (BBMV) prepared from rats and rabbits adapted to hypercapnia and other chronic acid-base disturbances. BBMV prepared from control animals and animals with chronic acid-base disturbances were similar as judged by marker enzymes, alkaline phosphatase, and ouabain-sensitive phosphatase. Despite profound respiratory acidosis, no increase in Na/H exchange activity could be detected in vesicles prepared from rats adapted to chronic (8 to 10 days) or subacute (24 hr) respiratory acidosis. In addition, vesicles prepared from rabbits exposed to chronic hypercapnia did not show increased Na/H exchange when compared with contemporaneous controls. By contrast, in agreement with previously published results, amiloride-sensitive sodium uptake was increased by 30% in vesicles derived from animals with ammonium chloride-induced acidosis compared with contemporaneous controls. Two models of chronic metabolic alkalosis were also studied; vesicles from alkalotic rats did not show any alteration in Na/H exchange. We conclude that metabolic acidosis, but not respiratory acidosis or metabolic alkalosis, leads to enhanced activity of the luminal Na/H exchanger.
 ...
PMID:Regulation of Na/H exchange in renal microvillus vesicles in chronic hypercapnia. 284 83

Local anaesthetic systemic toxicity is a rare but often dramatic complication of regional anaesthesia. Convulsions often follow warning signs, easily recognized when looked for; but they may occur from the first. They are rapidly followed by hypoxia and hypercapnia which greatly enhance the risk of severe cardiac depression, mainly with bupivacaine or etidocaine. Thiopentone is able to stop convulsions quickly, but may further depress the cardiovascular system. Diazepam has been shown to be effective in the treatment of local anaesthetic-induced convulsions. It gives less myocardial depression, but is much slower in effect. Midazolam, a new short-acting benzodiazepine, should be the best choice. Should tracheal intubation become necessary, suxamethonium can be used. Indeed, the principal use of these drugs is to make ventilation easier, so as to restore rapidly correct oxygenation. Severe cardiac depression, often leading to cardiac arrest, may occur from the first or after the appearance of convulsions. It generally follows a regional block carried out with bupivacaine. A few antiarrhythmic drugs have been used to treat ventricular arrhythmias, either in experimental studies (lidocaine, bretylium) or after clinical accidents (lidocaine). Their efficacy and innocuity have to be proved before they can be proposed to treat these accidents. Bradycardia only needs treatment with atropine when it causes severe haemodynamic disturbances. When cardiac arrest occurs, cardiopulmonary resuscitation must be carried out; its mainstays are: oxygen, sodium bicarbonate, adrenaline, calcium and perhaps glucagon. This must be continued for a long time, as late successes have been published.
 ...
PMID:[How should a toxic accident be treated?]. 290 Jun 15

Bicarbonate reabsorption by the immature kidney in response to acute acid-base changes was assessed in 50 anesthetized newborn rabbits before the end of nephrogenesis. The normal newborn rabbit (age 5-12 days) is in a state of hypochloremic metabolic alkalosis (PHCO3-, 31.9 +/- 0.6 mmol/l; PCl-, 83.1 +/- 1.0) and excretes a hypertonic (Uosmol = 578 +/- 41 mosmol/kgH2O), alkaline (UpH = 7.40 +/- 0.15) urine containing 50 +/- 9 mmol/l Cl- and 13 +/- 4 mmol/l Na+. The alkalosis is probably generated by an alkaline load contained in the mother's milk and maintained by a state of chloride wasting and volume contraction. In this alkalotic model, bicarbonate reabsorption, expressed per milliliter glomerular filtration rate (GFR), correlates positively with arterial CO2 pressure (PaCO2). The ability of the immature kidney to reclaim filtered bicarbonate in response to an elevation of the plasma carbon dioxide tension remains unlimited up to PaCO2 of 110 mmHg (y = 20.7 + 0.15 x, r = 0.82, P less than 0.001). Hypercapnia is associated with a marked fall in GFR, so that the positive correlation between bicarbonate reabsorption and PaCO2 vanishes when the bicarbonate reabsorption rate is expressed in absolute terms. Bicarbonate reabsorption is strongly dependent on the filtered load during both acutely induced metabolic acidosis and alkalosis. The acid-base state of the newborn rabbit is in sharp contrast with that of most animal species, and the renal handling of bicarbonate as a function of GFR does not show signs of tubular immaturity.
 ...
PMID:Bicarbonate reabsorption by the kidney of the newborn rabbit. 291 64


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>