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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ionic compensatory response to CO2 breathing for 3 days was studied on intact and cystectomized turtles at 10 and 20 degrees C. Arterial blood gases, pH, ionized calcium, and the plasma concentrations of Na+, K+, Cl-, total Ca2+, and total Mg2+ were measured periodically. At 20 degrees C, ureteral urine was also collected from bladderless turtles and was analyzed for pH, ions, NH3+, total CO2, osmolality, and titratable acid. When CO2 was breathed there was a compensatory change in the strong-ion difference as manifest by an increase in plasma [HCO3-] that was approximately 10 meq/l both in the 10 and 20 degrees C turtles. The only significant associated strong-ion changes observed consistent with the ionic compensatory response were increases in total and ionized Ca2+ and total Mg2+. These results were unaffected at either temperature by surgical removal of the urinary bladder. Urine collected from cystectomized turtles showed no compensatory increase in acid excretion during hypercapnia; in fact, changes occurred in the opposite direction. Urinary excretion of HCO3- and urine pH increased significantly, whereas titratable acidity decreased significantly. No significant change occurred in ammonia excretion over the three days of hypercapnia. These data argue against compensatory roles for the kidneys and urinary bladder in this species and point to internal ionic exchanges involving bone and shell.
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PMID:Ionic compensation with no renal response to chronic hypercapnia in chrysemys picta bellii. 378 4

In unanaesthetized fetal lambs at 125-135 days gestation in utero central acidosis caused by perfusion of the cerebral ventricular system with a solution containing less than 1 mM-HCO3- (cerebrospinal fluid (c.s.f.) pH 6.98) or intravenous infusion of ammonium chloride (c.s.f. pH 7.1) produced an increase in the depth and frequency of episodic breathing but no change in electrocortical activity, heart rate or arterial pressure. Administration of prostaglandin synthetase inhibitors, sodium meclofenamate (0.8-10 mg/kg I.V. or 0.6-2.6 mg/kg intracerebrally) or acetylsalicylic acid (6.7 mg/kg I.V.) caused prolonged episodes of fetal breathing during low and high voltage electrocortical activity, with a large increase in breath amplitude. Blood gas values, heart rate, blood pressure, electrocortical activity and eye movements were not altered. In fetuses whose brain stems had been sectioned in the upper pons or the inferior colliculus, sodium meclofenamate induced prolonged deep breathing. Intravenous prostaglandin E2 abolished the continuous breathing induced by meclofenamate, but not breathing movements enhanced by hypercapnia or hypoxia. It is concluded that the central chemoreceptors respond to acidosis in near-term lamb fetuses qualitatively as in adult animals. Secondly, the results suggest that prostaglandin E2 and the inhibitors of prostaglandin synthesis also act centrally in the lower pons or medulla to modulate fetal breathing.
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PMID:Central stimulation of breathing movements in fetal lambs by prostaglandin synthetase inhibitors. 392 89

This article reviews normal acid-base regulation, related laboratory tests, and the potential disorders if the body's ability to compensate is disrupted. Acid derived from the oxidation of proteins and through tissue metabolism must be excreted or neutralized daily by the kidneys and lungs to maintain a proper acid-base balance. Acid-base homeostasis is normally maintained by chemical buffering, changes in renal hydrogen-ion excretion, and alterations in the rate and volume of alveolar ventilation. Metabolic disorders are characterized by disturbances in bicarbonate (HCO3-) concentration, and respiratory disorders develop with primary alterations in the partial pressure of carbon dioxide (Pco2). Metabolic acidosis is characterized by low pH, low serum HCO3- concentrations, and a compensatory decrease in Pco2 with hyperventilation. Bicarbonate administration can correct this disorder, and equations for calculating the necessary amount of HCO3- are presented. Metabolic alkalosis is characterized by a primary increase in HCO3-, compensatory hypoventilation, and an increase in Pco2 (hypercapnia). The drug therapy for this disorder is directed at either saline-responsive alkalosis or saline-resistant alkalosis. Formulas for estimating the volume requirements of patients and appropriate doses of acidifying agents are presented. Respiratory acidosis and alkalosis are also discussed. The initial therapy for the hypercapnia associated with respiratory acidosis requires reversing the underlying pulmonary disease with steroids, bronchodilators, or antibiotics. The increased Pco2 in this conditions must be lowered slowly to avoid precipitating cardiac arrhythmias and seizures. The correction of respiratory alkalosis requires elevating the Pco2 and again treating the underlying disease. Pharmacists should be knowledgeable about acid-base regulation and the disorders that frequently occur with disease because drugs are capable of inducing or exacerbating these disorders and are often key elements in therapy.
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PMID:Simple acid-base disorders. 393 55

The increased plasma bicarbonate concentration seen in hypercapnia implies that tubular bicarbonate reabsorption must be increased in the presence of an elevated Paco2. In contrast to early reports, more recent experimental data in acute hypercapnia have been interpreted to show that the observed increment in tubular reabsorption of bicarbonate factored for glomerular filtration rate (THCO3/GFR) is largely related to the concurrent changes in renal sodium reabsorption and to the increment in the filtered load of bicarbonate, and that acute hypercapnia per se causes little or no change in the tubular handling of bicarbonate. We reexamined this question by observing the changes in renal function occurring in the presence of a moderate elevation of plasma bicarbonate concentration in two groups of dogs. In group I, the elevation occurred as a result of acute hypercapnia during the administration of an "isometric" solution; in group II, it was caused by the infusion of identical amounts of an isotonic solution with the same concentration of sodium as in group I, but a higher bicarbonate concentration, in the presence of eucapnia. A subset of group II provided controls for the decrease in renal perfusion pressure that occurred spontaneously in group I. With increasing filtered loads of bicarbonate, fractional excretion (FE) of HCO3 increased in group II, whereas it dropped markedly in group I. Furthermore, the relative reabsorption rate of HCO3 compared with that of Cl (assessed by changes in fractional reabsorption (FR) of HCO3/Cl) decreased in group II, whereas it increased in group I. Although FENa also decreased in group II, the opposite changes in FR(HCO3/Cl) could not be attributed solely to concurrent changes in sodium handling, indicating that in the presence of acute hypercapnia there is a preferential reabsorption of bicarbonate that tends to perpetuate the increase in plasma bicarbonate concentration. By contrast, THCO3/GFR rose in both groups. The data are interpreted to reveal that acute hypercapnia, although causing a drop in renal perfusion pressure and in natriuresis, also has an additional specific effect on raising preferential bicarbonate reabsorption. This effect can be detected best by monitoring changes in the anionic composition of tubular reabsorbate, whereas it may not be unveiled by following changes in THCO3/GFR. Changes in THCO3/GFR may not yield useful information regarding the integrated response of the kidney to acid-base perturbations, and the conclusions of previous studies based on changes in this parameter must be carefully reexamined.
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PMID:Effect of acute hypercapnia on renal bicarbonate reabsorption in the dog. 393 72

The relative importance of pCO2 versus pH in regulating myocardial blood-flow (MBF) is not settled. Therefore, the influence of hypocapnia, hypercapnia and sodium carbonate infusion, on MBF and myocardial metabolism, has been investigated in 10 closed-chest pentobarbital anaesthetized dogs. The animals were hyperventilated, and CO2 was added to the inspiratory gas to induce normocapnia and hypercapnia. A mass spectrograph continuously measured the ventilatory gas components, and MBF was measured by the hydrogen desaturation technique with a catheter positioned in the coronary sinus. During the experiments, there were no significant alterations in heart rate, mean aortic blood-pressure, myocardial oxygen consumption or uptake of glucose and free fatty acids. During hypocapnia MBF was insignificantly reduced, while myocardial oxygen extraction increased significantly. During hypercapnia, however, MBF increased more than 40%. This increase in MBF was abolished following an infusion of sodium carbonate. Thus, in the present study, increased MBF, observed during hypercapnia, was due to the reduction in pH and not to the increase in pCO2.
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PMID:Effects of carbon dioxide and pH on myocardial blood-flow and metabolism in the dog. 393 53

Ureters were cannulated in specimens of Bufo marinus (L.) in order to partition the regulatory contributions of the kidney and skin. The in vivo roles of the kidney, skin and internal calcareous deposits in the response of these animals to chronic hypercapnia were then evaluated. There was no compensatory adjustment by the skin and only a minimal regulatory response by the kidney. Major adjustments which have been attributed to combined skin and urinary tract in previous studies must therefore come from the urinary bladder. Removal of the bladder as a regulatory site in these animals completely eliminated the compensatory elevation of HCO3- in the extracellular fluid. Mobilization of internal calcareous deposits as a source of HCO3- was found to contribute 50% of the compensatory response of these animals during hypercapnia.
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PMID:Partitioning of regulatory sites in Bufo marinus during hypercapnia. 393 85

An estimate of the total mass of bone in the Channel catfish Ictalurus punctatus Rafinesque, was obtained by dissection. The wet weight of bone constituted 16.3 +/- 1.9% (+/- S.D.) of the total (live) wet weight, and 25.0 +/- 2.1% of the dry weight. Of the dry skeletal material, 66.3 +/- 11.1% was soluble in strong acid. The acid-soluble material was about half mineral salts, consisting of 19.5 +/- 2.21% Ca2+ and 27.6 +/- 3.22% PO4(3-), with minor fractions of Mg2+ (0.33%) and CO3(2-) (1.67%). The pH values of fluid compartments associated with skull and vertebral bone tissues were 7.420 +/- 0.026 and 7.444 +/- 0.017 (+/- S.E.), respectively, at a normocapnic plasma pH of 7.868 +/- 0.020. In response to external hypercapnia (7.5 Torr), the blood response consisted of an immediate decrease in pH, and a subsequent compensatory rise in both pH and [HCO3-]. This compensatory phase was accompanied by a net apparent H+ excretion to the water. The participation of the mineral salts of the bone compartment in compensation appeared to be negligible, since there was no significant change in either blood [Ca2+] or [PO4(3-)], nor any significant increase in calcium efflux to the water. The intracellular pH values of the bone compartments were only slightly higher than other tissues, and the changes in pHi during hypercapnia were similar in bone and white muscle. Thus, the bone compartment in the fish appears to be well regulated, relatively refractory to acute acid-base disturbance, and does not serve as an ion source during acid-base compensation.
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PMID:The bone compartment in a teleost fish, Ictalurus punctatus: size, composition and acid-base response to hypercapnia. 406

Disorders of systemic acid-base balance have recently been shown to markedly alter intestinal electrolyte transport. These studies were based on earlier acid balance studies in humans and animals, data suggesting the presence of intestinal mucosal Na+-H+ and Cl-HCO-3 exchange processes and the reported effects of acid-base variables on other epithelia. In vivo studies have shown that intestinal net sodium and chloride absorption is markedly affected by systemic pH and carbon dioxide tension (Pco2). Specifically, systemic acidemia (in the rat ileum) and hypercapnia (in the rat colon) increase sodium and chloride absorption, while alkalemia and hypocapnia decrease absorption. In addition, net bicarbonate secretion (in both segments) varies directly with the plasma HCO3 concentration. The rabbit ileum has been studied both in vivo and in vitro and is affected in a similar way. The rat jejunum and rabbit distal colon and gallbladder do not respond to changes in blood pH and Pco2, consistent with the apparent absence of a mucosal Na+-H+ exchange process in these segments. Evidence suggests important roles for cellular carbonic anhydrase activity and the intracellular concentrations of hydrogen, bicarbonate, and calcium ions and calcium-calmodulin in mediating or modulating the effects of the systemic acid-base disorders. In addition, systemic pH may alter the effects of the neural and humoral mediators of intestinal transport.
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PMID:Systemic acid-base disorders and intestinal electrolyte transport. 633 Nov 93

Arterial blood samples were taken from adult healthy patients before and 24 hours after bilateral nasal packing. The blood samples were investigated for PO2, PCO2, HCO3, pH and Hb. It was found that there is (i) an increase of high significance of PCO2 and HCO3-, (ii)) a significant increase of percentage of Hb., (iii) a highly significant decrease of PO2 in patients after nasal packing; (iv) as regards the pH, no significant difference was found. What we suggest is that bilateral anterior nasal pack results in hypoxia and hypercapnia due to hypoventilation.
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PMID:The effect of nasal packing on arterial blood gases and acid-base balance and its clinical importance. 640 76

Electrolyte composition of the cerebral spinal fluid (CSF) is important in central respiratory drive. The relationship between [Cl-] and [HCO3-] is of particular interest in maintenance of electrolyte balance. Therefore, the effect of furosemide, an inhibitor of sodium-coupled chloride transport, on CSF electrolyte homeostasis was studied under conditions of normocapnia and hypercapnia in anesthetized dogs. The drug was given intravenously (IV) or in the lateral cerebral ventricles (CV). With normocapnia, there was no change in CSF or arterial PCO2, pH, [K+], [Cl-], or [HCO3-], while CSF [NA+] decreased 1.7 mM in dogs receiving IV furosemide. With 5% CO2 breathing and IV furosemide, CSF PCO2, pH, [K+], [Cl-], and [HCO3-] changed as has been reported for 5% CO2 breathing alone. 5% CO2 and CV furosemide, however, led to a greater reduction in CSF [Cl-] and no change in CSF [HCO3-]. Thus CV furosemide alters the CSF [Cl-] and [HCO3-] in hypercapnia, suggesting that sodium-coupled chloride transport plays a role in regulation of CSF acid-base homeostasis.
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PMID:Effect of furosemide on cerebrospinal fluid composition. 643 18


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