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

The role of the central 5-hydroxytryptamine (5-HT) neuron system in cerebral microcirculation of the rat was examined by immunohistochemical and hydrogen clearance methods. Immunohistochemical studies demonstrated 5-HT-immunoreactive nerve fibers along intraparenchymal blood vessels (arterioles, capillaries, and venules). Ultrastructural observation revealed that 5-HT-immunoreactive terminal boutons (0.3 to 1.0 micron in diameter) made contact with the basement membrane of the capillaries. After an intracerebral injection of 5,7-dihydroxytryptamine (5,7-DHT), a neurotoxin to the 5-HT neuron system, no 5-HT-immunoreactive nerve fibers were found around the injection site with immunohistochemical techniques. With the hydrogen clearance method, the 5,7-DHT-injected cortex showed no significant change in regional cerebral blood flow (rCBF) in the presence of normocapnia, but a significant increase in rCBF with hypercapnia, compared with the untreated cortex. These facts strongly suggest that the central 5-HT neuron system has an important role in carbon dioxide reactivity of the cerebral blood vessels.
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PMID:5-Hydroxytryptamine innervation of vessels in the rat cerebral cortex. Immunohistochemical findings and hydrogen clearance study of rCBF. 391 93

We have recently shown that background presence of chronic metabolic acid-base disorder markedly alters in vivo acute CO2 titration curve. These studies were carried out to assess the influence of chronic respiratory acid-base disorders on response to acute hypercapnia and to explore whether the chronic level of plasma pH is the factor responsible for alterations in the CO2 titration curve. We compared whole-body responses to acute hypercapnia of dogs with preexisting chronic respiratory alkalosis (n = 8) with that of normal animals (n = 4) and animals with chronic respiratory acidosis (n = 13). Chronic respiratory alkalosis and acidosis, as well as the acute CO2 titrations, were produced in unanesthetized dogs within a large environmental chamber. For comparison with our data on chronic metabolic acidosis and alkalosis, plasma bicarbonate levels, which are secondarily altered in chronic respiratory acid-base disorders, were used as an index of chronic acid-base status of the animals. Results indicate that, as with chronic metabolic acid-base disorders, a larger increment in plasma bicarbonate occurs during acute hypercapnia when steady-state plasma bicarbonate is low (respiratory alkalosis) than when it is high (respiratory acidosis). Yet, in further analogy with the metabolic studies, plasma hydrogen ion concentration is better defended at higher plasma bicarbonate levels in accordance with mathematical relationships defined by the Henderson-Hasselbalch equation. Combined results demonstrate that the influence of chronic acid-base status on whole-body response to acute hypercapnia is independent of initial plasma pH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of chronic respiratory acid-base disorders on acute CO2 titration curve. 392 16

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 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

The contribution made by the cerebral inflow arteries to total cerebrovascular resistance (CVR) and their importance in producing alterations in cerebral blood flow (CBF) (i.e., changes in CVR) were investigated. The arterial blood pressure at the circle of Willis was measured in 14 anesthetized rabbits via transorbital retrograde cannulation of the ophthalmic artery. CBF was measured in 21 rabbits under identical experimental conditions, using the hydrogen clearance technique. Inflow artery resistance was calculated from the measurements which were made at both normocapnia and hypercapnia throughout hemorrhagic hypotension. Under resting conditions, the inflow arteries made a relatively minor contribution to total CVR (7%). Hypercapnia resulted in a decrease in CVR and an increase in CBF; however, inflow artery resistance remained constant. Autoregulation and reductions in total CVR were observed as PP was reduced to 35 mm Hg. Inflow artery resistance remained constant at pressures greater than 45 mm Hg and increased slightly at PP less than 45 mm Hg. The relative contribution of inflow artery resistance to total CVR increased under the various conditions studied--increasing by a factor of 2 during hypercapnia, by a factor of 3 during hypotension, and by a factor of 4 during hypotension + hypercapnia. We concluded that the large inflow arteries do not participate in the autoregulatory or CO2 responses of the cerebrovasculature of the rabbit.
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PMID:Contribution of the inflow arteries to alterations in total cerebrovascular resistance in the rabbit. 399 31

Previous studies from this laboratory have demonstrated that the decreased renal bicarbonate reabsorption prevailing during chronic hypocapnia is not mediated by the alkalemia that normally accompanies this acid-base disturbance but by some direct consequence of the change in PaCO2 itself. Based on the reasonable expectation that the mechanisms underlying the kidney's response to primary respiratory disturbances would be similar over the entire spectrum of physiologic carbon dioxide tensions, the present study was designed to assess whether an acidic change in systemic pH is a critical factor in the renal response to chronic hypercapnia. For this purpose, the plasma and renal responses to chronic respiratory acidosis in normal dogs were compared to those in dogs chronically fed a large hydrochloric acid (HCl) load (7 mmoles/kg/day). Exposure to 6% carbon dioxide for 7 days in a large environmental chamber induced a stable increment in PaCO2 which averaged 17 +/- 0.5 and 22 +/- 1.3 mm Hg in normal and HCl-fed animals, respectively. Steady-state plasma bicarbonate concentration rose from 22.0 +/- 0.4 to 27.1 +/- 0.5 mEq/liter in normals and from 14.7 +/- 0.7 to 24.2 +/- 0.8 mEq/liter in the HCl-fed group. As a result of these changes in PaCO2 and plasma bicarbonate, steady-state plasma hydrogen ion concentration rose in normals from 41 +/- 0.8 to 49 +/- 0.9 nEq/liter (pH 7.39 +/- 0.01 vs. 7.31 +/- 0.01) but did not change significantly in the HCl-fed group (55 +/- 1.4 vs. 56 +/- 1.4 nEq/liter; pH 7.26 +/- 0.01 vs. 7.25 +/- 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of acid-base equilibrium in chronic hypercapnia. 399 41

Metabolic balance studies were carried out in normal dogs to define the renal mechanisms responsible for the adaptation to, and recovery from, chronic hypocapnia. A chronic reduction in arterial CO(2) tension (Pa(CO2)) of some 15 mm Hg was achieved by means of chronic exposure of the animals to 9% oxygen in an environmental chamber. The development of hypocapnia was associated with a marked suppression of net acid excretion which, together with a slight accumulation of organic acids, produced a reduction in plasma bicarbonate concentration (8 mEq/liter) that led to nearly full protection of extracellular pH (DeltaH(+) = - 2.5 nmoles/liter). When Pa(CO2) was returned to control levels, an augmentation of acid excretion restored plasma composition to normal after a brief period of "posthypocapneic metabolic acidosis."The changes in renal acid excretion during both adaptation and recovery were accomplished in a fashion notably different from that previously observed in chronic hypercapnia, being linked to changes in cation rather than chloride excretion. Thus, in dogs ingesting a normal NaCl diet, suppression of hydrogen ion excretion during adaptation to hypocapnia was associated with an increased excretion of sodium rather than with a retention of chloride. The fact that this loss of sodium occurred without a concomitant loss of potassium strongly suggests that the hypocapneic state specifically depressed distal sodium reabsorption; if distal sodium reabsorption had not been depressed, a reduction in proximal sodium reabsorption or a diminution in distal hydrogen ion secretion (or both) should have produced an increase in potassium excretion. The interpretation that chronic hypocapnia diminished sodium reabsorption was supported by the finding that when renal sodium avidity was enhanced by restriction of sodium intake, acid retention was accomplished by a loss of potassium rather than of sodium. The accompanying reduction in plasma bicarbonate concentration was slightly less than that observed in dogs ingesting a normal NaCl diet, a finding probably accounted for by a slight difference in the availability of cation for excretion under the two experimental circumstances. These findings, taken together with the observation that augmented acid excretion during recovery from hypocapnia is linked to cation retention, suggest that an adequate intake of cation during both adaptation and recovery from chronic hypocapnia may be critical to the physiologic regulation of acid-base equilibrium.
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PMID:The nature of the renal adaptation to chronic hypocapnia. 503 22

Studies were carried out to determine the influence of the chronic level of arterial carbon dioxide tension upon the buffering response to acute changes in arterial carbon dioxide tension. After chronic adaptation to six levels of arterial CO(2) tension, ranging between 35 and 110 mm Hg, unanesthetized dogs underwent acute whole body CO(2) titrations. In each instance a linear relationship was observed between the plasma hydrogen ion concentration and the arterial carbon dioxide tension. Because of this linear relationship, it has been convenient to compare the acute buffering responses among dogs in terms of the slope, dH(+)/dPaco(2). With increasing chronic hypercapnia there was a decrease in this slope, i.e. an improvement in buffer capacity, which is expressed by the equation dH(+)/dPaco(2)=-0.005 (Paco(2))(chronic) + 0.95. In effect, the ability to defend pH during acute titration virtually doubled as chronic Paco(2) increased from 35 to 110 mm Hg. The change in slope, dH(+)/dPaco(2), was the consequence of the following two factors: the rise in plasma bicarbonate concentration which occurs with chronic hypercapnia of increasing severity, and the greater change in bicarbonate concentration which occurred during the acute CO(2) titration in the animals with more severe chronic hypercapnia. These findings demonstrate the importance of the acid-base status before acute titration in determining the character of the carbon dioxide titration curve. They also suggest that a quantitative definition of the interplay between acute and chronic hypercapnia in man should assist in the rational analysis of acid-base disorders in chronic pulmonary insufficiency.
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PMID:The influence of graded degrees of chronic hypercapnia on the acute carbon dioxide titration curve. 554 76

We have carried out balance studies in normal dogs in order to appraise the effects of chronic hypoxemia on acid-base and electrolyte equilibrium. During the first phase of observation we produced a state of "pure" hypoxemia by reducing the oxygen concentration (utilizing nitrogen as a diluent) and by adding carbon dioxide to the environment in a concentration sufficient to keep arterial CO(2) tension (PCO(2)) within normal limits. The data demonstrate that such a 9-day period of normocapneic hypoxemia has no effect on electrolyte excretion and is virtually without effect on plasma composition. During the second phase of observation we subjected the hypoxemic dogs to stepwise increments in arterial carbon dioxide tension in order to evaluate the effects of the low oxygen tension on the acid-base adjustments to a chronic state of hypercapnia. At least 6 days was allowed for extracellular composition to reach a new steady state at each level of inspired carbon dioxide. The data demonstrate a rise in both plasma bicarbonate concentration and renal acid excretion that was not significantly different from that which has been described previously for hypercapnia without hypoxemia. Just as in these earlier studies, plasma hydrogen ion concentration rose with each increment in carbon dioxide tension, each millimeter Hg increment in PCO(2) leading to an increase in hydrogen ion concentration of 0.32 nmole per L. It thus appears that the chronic"carbon dioxide response curve" is not significantly influenced by moderately severe hypoxemia.
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PMID:The effects of chronic hypoxemia on electrolyte and acid-base equilibrium: an examination of normocapneic hypoxemia and of the influence of hypoxemia on the adaptation to chronic hypercapnia. 602 72

Acute and steady-state responses to hypercapnia of respiratory output, measured as integrated phrenic nerve activity, and medullary extracellular fluid (e.c.f.) pH, measured directly, were determined in paralysed, vagotomized and glomectomized cats. Medullary e.c.f. pH responds within seconds to an acute change of alveolar and arterial PCO2. The respiratory response closely and inversely matches the e.c.f. pH change, but not the cerebrospinal fluid pH change. The medullary e.c.f. pH change following a rapid step-change in end-tidal PCO2 requires at least 5 min for a new steady state to be achieved. Steady-state studies in twenty-six cats show: (a) that the respiratory response to progressive hypercapnic stimulation of the central chemoreceptors is curvilinear (Eldridge, Gill-Kumar & Millhorn, 1981), (b) that the relationship between increasing end-tidal PCO2 and medullary hydrogen ion concentration [(H+]) or changes of pH is linear (r = 0.995); a doubling of PCO2 causes 0.260 units pH change, (c) there is a curvilinear relationship between e.c.f. [H+] and the respiratory response that is the same as that found with CO2. We conclude that medullary e.c.f. pH measured by means of a surface electrode accurately reflects the CO2-induced [H+] stimulus to respiration. The decreasing respiratory responses to identical changes of central chemoreceptor input are due to progressive neuronal saturation of a central pathway between the chemoreceptors and the respiratory controller.
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PMID:Respiratory effects of carbon dioxide-induced changes of medullary extracellular fluid pH in cats. 609 23


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