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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study examines the renal response to moderate hyperventilation in healthy man. Eight men hyperventilated for 26 hr (PaCO2 approximately 30 to 32 mm Hg) in normoxia (barometric pressure, PB approximately 740 mm Hg) and hypobaric hypoxia (PB approximately530 mm Hg). Anaerobic samples of arterial blood and urine were studied at two-hour intervals. Plasma [HCO3-] fell with time during sustained hypocapnia and after 26 hr was reduced 2.5 mEq/liter, with plasma pH compensated approximately 60%. Statistically significant changes in renal H+ handling were observed within the initial 2 hr of hyperventilation and were evident over the first 12 hr. Over 26 hr, mean total HCO3-excretion in hypocapnia was 10.2 mEq above control and mean total acid excretion (UVTA + UVNH4+) was 17.5 mEq below control. An increased urinary excretion of cations, especially sodium, accompanied the decrease in acid excretion. Plasma lactic acid accumulation was negligible. We conclude that renal mechanisms contribute significantly and relatively quickly to plasma pH compensation during the early phase of adaptation to hypocapnia in man.
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PMID:Renal response to short-term hypocapnia in man. 0 72

Several hypotheses have been put forward to explain postdialysis hypocapnia. Three were tested in this study: impairment of tissue oxygenation by dialysis (D)-induced alkalosis (Bohr effect), the D disequilibrium syndrome, and the loss of carbon dioxide (CO2) in D fluid. In 17 patients pre-DPCO2 was significantly correlated with plasma bicarbonate concentration (HCO3) and no disproportionate reduction of PCO2 was discernible. In 10 patients using a bath acetate concentration of 38 mEq/1 PCO2 was unchanged after D (35.4 versus 35.9 mm Hg before D), and was low relative to HCO3 whic increased from 21.2 to 28.0 mEq/1. After a dialysis using an acetate concentration of 25 mEq/1 HCO3 remained constant (20.4 versus 21.1 mEq/1 pre-D), whereas PCO2 fell from 35.3 to 30.8 mm Hg (P less than 0.001). Consequently PCO2 was again low relative to HCO3. Removal of CO2 by D fluid was excluded as a cause for low blood PCO2: addition of gaseous CO2 to the bath had no influence on arterial blood gases. Since post-D hypocapnia was not prevented when HCO3 was kept constant, it was concluded that post-D alkalosis cannot be the main reason for post-D hyperventilation, and that other factors related to the process of D are responsible.
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PMID:Mechanism of post dialysis hyperventilation in patients with chronic renal insufficiency. 0 52

We have previoulsy shown pH compensation to be similar in CSF and arterial blood during chronic hypoxemic hypocapnia in man and pony, and postulated that the compensatory reduction in CSF [HCO3] was dependent upon corresponding changes in [HCO3]a. We tested this hypothesis in anesthetized, paralyzed dogs by determining the effects of 7 or 14 hours of hypocapnia (PaCO2 20 and 30 mm Hg), hypoxemia (PaO2 30, 38 and 48 mm Hg) and hypocapnic hypoxemia on CSF acid-base status. [hco3]a was either permitted to fall normally or was held near control levels by NaHCO3 infusion. In hypocapnia and hypoxemic hypocapnia, the decrease in [HCO3] and % pH compensation in CSF were less than or equal to that in arterial blood. Most (51-89%) of the compensatory decrease in CSF [HCO3] was prevented by preventing the corresponding reduction in [HCO3]a. This dependence of changes in CSF on plasma [HCO3] required a concurrent decrease in CSF PCO2, but was largely independent of variations in plasma pH. A minor but significant portion of the decrease in CSF [HCO3] was achieved independently of corresponding changes in [HCO3]a. The contribution of this local mechanism to CSF [HCO3] regulation increased with increasing severity of hypocapnia or hypoxemia and was usually associated with a selective increase in CSF lactate. It was concluded that [HCO3] regulation in the CSF during hypoxemic hypocapnia was primarily dependent upon, and therefore limited by, the concomitant decrease in plasma [HCO3].
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PMID:Dependence of CSF on plasma bicarbonate during hypocapnia and hypoxemic hypocapnia. 0 65

It is generally believed that the reduction in plasma [HCO3] characteristic of chronic hypocapnia results from renal homeostatic mechanisms designed to minimize the alkalemia produced by.the hypocapneic state. To test this hypothesis, we have induced chronic hypocapnia in dogs in which plasma [HCO3] had previously been markedly reduced (from 21 to 15 meq/liter) by the prolonged feeding of HCl. The PaCO2 of chronically acid-fed animals was reduced from 32 to 15 mm Hg by placing the animials in a large environmental chamber containing 9% oxygen. In response to this reduction in PaCO2, mean plasma [HCO3] fell by 8.6 meq/liter, reaching a new steady-state level of 6.4 meq/liter. This decrement in plasma [HCO3] is almost identical to the 8.1 meq/liter decrement previously observed in normal (nonacid-fed) animals in which the same degree of chronic hypocapnia had been induced. Thus, in both normal and HCl-fed animals, the renal response to chronic hypocapnia causes plasma [HCO3] to fall by approximately 0.5 meq/liter for each millimeter of Hg reduction in CO2 tension. By contrast, the response of plasma [H+] in the two groups was markedly different. Instead of the fall in [H+] which is seen during chronic hypocapnia in normal animals, [H+] in HCl-fed animals rose significantly from 53 to 59 neq/liter (pH 7.28-7.23). This seemingly paradoxical response is, of course, an expression of the constraints imposed by the Henderson equation and reflects the fact that the percent fall in [HCO3] in the HCl-fed animals was greater than the percent fall in PaCO2. These findings clearly indicate that in chronic hypocapnia the kidney cannot be regarded as the effector limb in a homeostatic feedback system geared to the defense of systemic acidity.
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PMID:Regulation of acid-base equilibrium in chronic hypocapnia. Evidence that the response of the kidney is not geared to the defense of extracellular (H+). 0 88

In respiratory alkalosis the fall in CSF bicarbonate is in part due to increased CSF lactate. The rest of CSF HCO3 fall may be actively regulated or as more recent evidence suggests is dependent on plasma HCO3 fall. Therefore, the relationship between plasma and CSF HCO3 changes was studied during 4 hours of respiratory alkalosis (PaCO2=20 mm Hg) in anesthetized dogs when plasma HCO3: (1) fell normally, (2) kept 'normal' by NaHCO3 infusion, (3) increased by infusing more NaHCO3, and (4) reduced by infusing HCl. In respiratory alkalosis plasma and CSF HCO3 fell 4.6 and 3.8 mEQ/L, respectively. In hypocapnia and 'normal' plasma HCO3 CSF HCO3 fell 2 mEq/L and lactate increased 1.33 mEq/L. In hypocapnia and metabolic alkalosis plasma HCO3 increased 6.5 mEq/L and CSF HCO3 remained unchanged and lactate increased 2.12 mEq/L. In combined hypocapnia and metabolic acidosis plasma HCO3 fall 10.5 mEq/L but CSF HCO3 fell 3.1 mEq/L and CSF pH returned to normal at 4 hours. Therefore CSF HCO3 fall in hypocapnia is primarily and critically dependent on the simultaneous fall in plasma HCO3 content, with a minimal contribution from CNS lactate increase. When CSF PH has returned to normal, however, CSF HCO3 fall is stopped despite further falls in plasma HCO3.
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PMID:Importance of changes in plasma HCO-3 on regulation of CSF HCO-3 in respiratory alkalosis. 0 12

1. The regulation of cerebrospinal fluid (c.s.f.) bicarbonate concentration was studied using the cat choroid plexus isolated in a chamber in situ. 2. Decreases in plasma bicarbonate concentration caused relatively small changes in the c.s.f. bicarbonate concentration. 3. Alterations in c.s.f. bicarbonate concentration (c.s.f. HCO3-=9 or 28 m-equiv/l.) were countered by changes in the bicarbonate concentration of the fluid produced by the plexus or in the rate of bicarbonate transport which returned c.s.f. bicarbonate towards normal. 4. There was significant regulation of pH in the choroid plexus fluid during hypocapnia and hypercapnia. 5. Alterations of plasma acid-base status did not significantly alter the potential difference across the choroid plexus. However, the potential difference increased when c.s.f. bicarbonate was increased and decreased when c.s.f. bicarbonate was decreased. 6. The data indicate that the bicarbonate concentration in the c.s.f. is actively regulated by the choroid plexus during acid-base disturbances occurring either systemically or in the c.s.f.
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PMID:Regulation of cerebrospinal fluid bicarbonate by the cat choroid plexus. 1 33

Graded degrees of both chronic hyper- and hypocapnia are known to induce renal responses that significantly alter plasma bicarbonate concentration. These findings have raised the possibility that even normal variations in PaCO2 play an important role in determining the exact level of bicarbonate in plasma. To test this hypothesis, we examined the relationship between resting levels of PaCO2 and the plasma bicarbonate concentration in two groups of normal dogs, one ingesting a normal salt diet and the other a salt-restricted diet. The results indicate that values for bicarbonate within the normal range are highly dependent on the prevaling level of carbon dioxide tension ([HCO3-] = 0.35 PaCO2 + 9.0, r = 0.72). Accordingly, approximately 50% of the normal variance in bicarbonate concentration is explained simply by the variance in PaCO2. The joint confidence region for bicarbonate concentration and PaCO2, which can be derived from these data, provides a new and more rigorous definition of the normal range for acid-base values in the dog.
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PMID:Effect of natural variations in PaCO2 on plasma [HCO3-] in dogs: a redefinition of normal. 3 8

The effects of 26 h of normoxic hypocapnia (PaCO2, 31 MMHg) vs. 26 h of hypocapnia plus hypobaric hypoxia (PaCO2 32, PaO2 57 mmHg) were compared with respect to: a) CSF acid-base status; and b) the spontaneous ventilation (at PIO2 145 mmHg) which followed the imposed (voluntary) hyperventilation. For each condition of prolonged hypocapnia, PaCO2 was held constant throughout and pHa and [HCO3-]a were constant over the final 6-10 h. We assumed that measured changes in lumbar CSF acid-base status paralleled those in cisternal CSF. Spontaneous hyperventilation followed both normoxic and hypoxic hypocapnia but was significantly greater following hypoxic hypocapnia. In the CSF, pH compensation after 26 h of hyperventilation was incomplete (similar to 45-50%), was similar to that in arterial blood, and was unaffected by a superimposed hypoxemia. These data were inconsistent with current theory which proposes the regulation of CSF [HCO2] via local mechanisms and, in turn, the mediation of ventilatory acclimatization to hypoxemia and/or hypocapnia via CSF [H+]. Alternative mediators of ventilatory acclimatization were postulated, including mechanisms both dependent on and independent of "chemoreceptor" stimuli.
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PMID:Effects of moderate hypoxemia and hypocapnia on CSF [H+] and ventilation in man. 23 66

This study has assessed the regulation of arterial blood and cerebrospinal fluid acid-base status in seven healthy men, at 250 m altitude and after 5 and 10-11 days sojourn at 4,300 m altitude (PaO2 = 39 mmHg day 1 to 48 mmHg day 11). We assumed that observed changes in lumbar spinal fluid acid-base status paralleled those in cisternal CSF, under these relatively steady-state conditions. Ventilatory acclimatization during the sojourn (-14 mmHg PaCO2 at day 11) was accompanied by: 1) reductions in [HCO3-] (-5 to -7 meq/1) which were similar in arterial blood and CSF; 2) substantial, yet incomplete, compensation (70-75%) of both CSF and blood pH; and 3) a level of CSF pH which was maintained significantly alkaline (+0.05 +/- 0.01) to normoxic control values. These data at 4,300 m confirmed and extended our previous findings for more moderate conditions of chronic hypoxia. It was postulated that the magnitude and time course of pH compensation in the CSF during chronic hypoxia and/or hypocapnia are determined by corresponding changes in plasma [HCO2-].
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PMID:Incomplete compensation of CSF [H+] in man during acclimatization to high altitude (48300 M). 23 69

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.
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PMID:[Cerebrospinal fluid changes in severe craniocerebral injury and their therapy]. 101 May 21


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