Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The effects of respiratory gas mass-transfer by high-efficiency hemodialyzers with regard to respiratory status and acid-base balance were studied in three groups of patients. Patients dialyzed with acetate dialysate and a single pass delivery system (group I) and those dialyzed with the same dialysate and a recirculating single pass system (group II) had significant intradialytic decreases in PCO2 (p is less than 0.05), while patients hemodialyzed aginst a carbon dioxide/bicarbonate dialysate (group III) had no significant alterations in arterial PCO2. The massfransfer rate of carbon dioxide was 0.3 mM/min in group I and 0.2 mM/min in group II. The hypocapnia caused by dialyzer mass-transfer of carbon dioxide was associated with a significant drop in minute ventilation volume and a decrease in PO2 which was significant in group I (p is less than 0.05). Although bicarbonate mass-transfer reduced serum bicarbonate levels, the loss of carbon dioxide to the dialysate resulted in an increased arterial pH during dialysis.
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PMID:Respiratory gas exchange by high-efficiency hemodialyzers. 67 97

Hyperammonemia increases brain glutamine levels, causes astrocytic swelling, and depresses cerebral blood flow (CBF) responsivity to CO2. Methionine sulfoximine (MSO) inhibition of glutamine synthetase activity, known to be enriched in astrocytes, prevents ammonia-induced increases in brain glutamine and water content. We tested the hypothesis that inhibition of glutamine accumulation restores CBF responsivity to CO2 during acute hyperammonemia. Pentobarbital-anesthetized rats treated with either vehicle or MSO (150 mg/kg i.p.) received a 6-hour intravenous infusion of either sodium or ammonium acetate. With subsequent induction of hypercapnia, CBF increased from 113 +/- 14 (mean +/- SEM) to 194 +/- 9 ml/min per 100 g in control rats but was unchanged from 107 +/- 13 to 79 +/- 10 ml/min per 100 g in hyperammonemic rats. Treatment with MSO in hyperammonemic rats restored the CBF response to hypercapnia (from 73 +/- 8 to 141 +/- 14 ml/min per 100 g). With induction of hypocapnia, CBF decreased from 114 +/- 11 to 88 +/- 11 ml/min per 100 g in control rats but increased from 112 +/- 13 to 142 +/- 19 ml/min per 100 g in hyperammonemic rats. Treatment with MSO in hyperammonemic rats did not fully restore the response to hypocapnia but prevented the paradoxical increase in CBF (from 80 +/- 8 to 80 +/- 8 ml/min per 100 g). In control rats, MSO did not affect CO2 responsivity. Treatment with MSO prevented ammonia-induced increases in intracranial pressure. Hyposmotic-induced increases in brain water content and intracranial pressure attenuated the CBF response to hypercapnia but, unlike hyperammonemia, did not attenuate the response to hypocapnia. In contrast to hypercapnia, vasodilation in response to arterial hypotension was intact in hyperammonemic rats. We conclude that the grossly abnormal CBF responsivity to CO2 alterations during hyperammonemia is linked to glutamine accumulation rather than ammonia per se. Cerebral edema secondary to glutamine accumulation may contribute in part to abnormal CBF responses, although other aspects of astrocyte dysfunction are likely to be important.
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PMID:Restoration of cerebrovascular CO2 responsivity by glutamine synthesis inhibition in hyperammonemic rats. 139 82

Acute hyperammonemia at normal arterial pH causes selective increases in midbrain blood flow in dogs. Unexpectedly, further increases occur with hypocapnia. We investigated whether metabolic acidemia and alkalemia modulate the distribution of ammonium across the blood-brain barrier and if, in turn, midbrain blood flow is effectively modulated. In dogs anesthetized with pentobarbital sodium, hyperammonemia (approximately 940 microM) was produced by a 210-min infusion of ammonium acetate. Concurrent infusion of NaHCO3 increased arterial pH to 7.53 +/- 0.02 (SE), whereas HCl infusion decreased pH to 7.11 +/- 0.01. Normocapnia was maintained. Cerebrospinal fluid [HCO3-] increased 5 mM with alkalemia (one-half of the increase in blood) and was unchanged with acidemia. Thus cerebrospinal fluid [H+]/blood [H+] was greater with alkalemia than acidemia. The corresponding ratio for ammonium was likewise greater with alkalemia (0.70 +/- 0.06) than acidemia (0.44 +/- 0.08). Microsphere-determined blood flow to midbrain more than doubled in the alkalemic group but was unchanged in the acidemic group. No other region along the neuraxis or in cerebrum showed increased blood flow in either hyperammonemic group. Alkalemia without hyperammonemia did not increase midbrain blood flow. Thus metabolic acidemia-alkalemia significantly alters ammonium partitioning into cerebrospinal fluid, and this alteration is sufficiently great to exert a specific physiological effect manifested by changes in midbrain blood flow.
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PMID:Arterial pH modulation of regional cerebral blood flow during hyperammonemia in dogs. 197 74

We administered chlormadinone acetate (CMA), medroxyprogesterone acetate (MPA), and placebo to 16 normal male subjects using a randomized double-blind crossover study. After CMA administration, minute alveolar ventilation increased by +1.04 +/- 0.22 (SE) 1/min (P less than 0.05) accompanied by decrements of arterial PCO2 (-4.0 +/- 1.0 Torr) (P less than 0.01) and [HCO3-] (-2.1 +/- 0.05 mM/l) (P less than 0.01). On the other hand, in the MPA runs the corresponding changes of the above parameters were +0.71 +/- 0.21 l/min (P less than 0.05), -2.9 +/- 0.6 Torr (P less than 0.01), and -1.3 +/- 0.3 mM/l (P less than 0.01), respectively. The slopes of hypoxic ventilatory and occlusion pressure response lines remained unchanged in hypocapnia after CMA or MPA ingestion, but they increased when entidal PCO2 was adjusted to the predrug level. The hypercapnic ventilatory and occlusion pressure response lines merely shifted to the left without changing their slopes with these agents. No significant differences in all the above parameters were found between CMA and MPA runs. We concluded that in the normal males the effect of CMA on ventilation was similar to that of MPA, despite the fact that the luteinizing activity of CMA was reported to be approximately 10 times higher than the latter.
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PMID:Comparison of two synthetic progesterones on ventilation in normal males: CMA vs. MPA. 244 56

Intravenous infusion in conscious rabbits of Hacetate decreases both arterial CO2 partial pressure PaCO2 and cerebrospinal fluid (CSF) HCO3- more than observed with HCl or HNO3 infusion. These acids did not affect CSF HCO3- in isocapnic conditions, and this study asks whether Hacetate infusion will do so. Arterial, central venous, and cisterna magna catheters were implanted in pentobarbital-anesthetized rabbits and all subsequent measurements were performed in the conscious state. Hacetate was infused intravenously over 6 h to decrease plasma HCO3- the same amount in a group allowed to decrease its PaCO2 in response to the acid (hypocapnic) and one in which PaCO2 was maintained at control levels (isocapnic). CSF HCO3- decreased significantly in isocapnia, although the change was less than in hypocapnia. Stoichiometrically by 6 h the measured CSF HCO3- change was balanced by an increase in acetate in hypocapnia and the sum of an increase in acetate and a decrease in chloride in isocapnia. Mechanistically, net acetate entry into CSF appears to involve an exchange for chloride as proposed for NO3-/Cl- and a process that lowers CSF HCO3-. This process could be competitive replacement of HCO3- by acetate in the CSF production mechanism or nonionic diffusive entry of Hacetate into CSF with subsequent titration of HCO3-. The decreases in CSF HCO3- result from the acetate mechanism and the hypocapnic effect on Cl- and HCO3-. The greater ventilatory response results from the greater CSF acidification or a specific effect of acetate per se.
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PMID:CSF acid-base regulation and ventilation in iso- and hypocapnic Hacetate acidosis. 309 54

Studies of acutely induced hyperammonemia and chronic hyperammonemia associated with liver dysfunction suggest that cerebral blood flow (CBF) and O2 consumption (CMRO2) become uncoupled and that CMRo2 may depend on arterial CO2 tension (PaCO2). We examined CBF (radiolabeled microspheres) and CMRO2 during hypercapnia (PaCO2 congruent to 74 Torr) and hypocapnia (PaCO2 congruent to 21 Torr) both before and during intravenous ammonium acetate infusion in pentobarbital-anesthetized dogs. Continuous infusion over 120 min produced stable increases of arterial ammonia levels (1,400 mumol/l) by 30 min, whereas CBF, CMRO2, and O2 extraction (measured at sagittal sinus) remained unchanged when PaCO2 was held constant (congruent to 35 Torr). Acute hyperammonemia attenuated the increase in CBF during hypercapnia by 44% and abolished the decrease in CBF during hypercapnia. Regional blood flow to pons and midbrain increased under normocapnic conditions, and midbrain blood flow increased further during hypocapnia. Sodium acetate infusion did not affect CBF responses to CO2. Thus we failed to observe an uncoupling of global CBF and CMRO2 during normocapnic hyperammonemia, or an interaction of CO2 and ammonia on CMRO2, although the increased pons and midbrain blood flow may reflect regional effects of ammonia on reticular activating system metabolism. On the basis of the literature, we suggest that the attenuated hypercapnic CBF response may arise from impaired glial regulation of extracellular potassium and bicarbonate concentrations and that lactic acid production, enhanced by combined alkalosis and hyperammonemia, may contribute to the abolition of hypocapnic vasoconstriction.
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PMID:Interaction of CO2 and ammonia on cerebral blood flow and O2 consumption in dogs. 392 Sep 20

In order to elucidate the mechanisms responsible for the hypoxemia observed during acetate dialysis, but not found during bicarbonate dialysis, the authors studied ventilation, blood gases and their exchanges in the lungs and across the dialyzer on 9 patients. Oxygen consumption was similar both in acetate and bicarbonate dialysis. At the beginning of acetate dialysis, hypocapnia, due to CO2 losses through the dialyzer, causes hypoventilation and hypoxemia; afterwards, the worsening of acidosis (due to bicarbonate losses) stimulates ventilation, thus correcting the initial imbalance. Authors also hypothesize a pulmonary mechanism for CO2 "sparing" contributing to compensate CO2 losses through the dialyzer. The absence of hypoxemia during bicarbonate dialysis would be due to the absence of CO2 losses through the dialyzer.
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PMID:[Respiratory response and acid-base equilibrium in acetate dialysis and bicarbonate dialysis]. 666 24

The background of this study is the occurrence during acetate hemodialysis (HDA) of arterial hypoxemia associated with well described vasodilatator hemodynamic changes. Our aim was to evaluate the relationship between these 2 phenomena. Eleven patients (7 males, 4 females, mean age 54 years) were compared in a protocol of HDA and bicarbonate hemodialysis (HDB) as regards their cardiac output measured by the dye dilution method, blood gases and respiratory gas measurements made at the bedside. The results show significant hypoxemia with hypocapnia as soon as the 30th minute of HDA and no significant variation of cardiac index. No significant variation of respiratory response was noted. Arterial prostaglandin levels rose significantly higher during HDA (+ 302%) than HDB (+ 163%; 2 alpha less than 0,05). The absence of a correlation between arterial hypoxemia and hemodynamic changes in HDA compared to HDB suggests that the phenomena are not interdependent. The importance of increased thromboxane activation in HDA will require further investigation.
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PMID:[Hypoxemia in hemodialysis: hemodynamic mechanism? Hemodynamic and spirometric study using acetate and bicarbonate buffers]. 666 25

A high frequency of metabolic acidosis in a group of 30 patients on regular dialysis treatment initiated a study of the effect (and possible side effects) of a higher concentration of acetate in the dialysate. The concentration of acetate in the dialysate was increased from 32.6 ('low ac') to 38.2 mmol/l ('high ac'). The 'low ac' dialysis treatment changes the metabolic acidoses (mean pH = 7.34; base excess, BEb = - 8.3 mmol/l) to chronic hypocapnia (pH = 7.40; BEb = - 5.4 mmol/l). 'High ac' normalized the acid base status (pH = 7.44; BEb = -0.6 mmol/l). No side effects occurred. Since PaCO2 does not change much during hemodialysis it is convenient to look at the linearly related changes of the pH and the logarithmic standard bicarbonate concentration along iso-PCO2 lines in a log standard bicarbonate-pH-nomogram.
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PMID:Improved effect of hemodialysis on acidemic patients from an acetate concentration of 38 mmol/l. 678 71


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