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Query: UMLS:C0001127 (respiratory acidosis)
 1,501 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Regulation of CSF HCO3-in respiratory acidosis was studied in light of the "dual contribution theory," which proposed that there were two sources for the CSF HCO3-increase: 1) HCO3-by diffusion from plasma and 2) HCO3-generated in the CNS and catalyzed by the local carbonic anhydrase (J. Appl. Physiol. 38: 504-512, 1975). In anesthetized dogs with an increase in Paco2 of 30 mmHg for 4 h the plasma HCO3 increased 2 meq/1 and CSF 6 meq/1. In combined respiratory and metabolic acidosis, plasma HCO3-did not increase but CSF HCO3-increased 6 meq/1. In combined acidosis and intraventricular injections of acetazolamide no increase in plasma or CSF HCO3-occurred. In combined respiratory acidosis and metabolic alkalosis and intraventricular acetazolamide, plasma HCO3-increased 15 meq/1 but CSF HCO3-increased 6 meq/1. Brain and CSF ammonia increased linearly and selectively with the increase in the relative contribution of CNS HCO3-increase. Therefore regulation of CSF HCO3-in respiratory acidosis depends on both components of the dual contribution theory, where each component can provide the total CSF HCO3-increase under appropriate experimental conditions. The control mechanism may be sensitive to changes in [H+] on the brain side of the blood-brain barrier.
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PMID:Dual contribution theory of regulation of CSF HCO3 in respiratory acidosis. 0 20

To study the role of carbonic anhydrase in the CSF [HCO3] increase in respiratory acidosis and its effect on brain ammonia, anesthetized rats were subjected to hypercapnia (7% CO2) for 2 hours. The animals received periodic intraventricular injections of either 'mock' CSF or 'mock' CSF and acetazolamide for 45 minutes prior and during hypercapnia when: (a) plasma [HCO3-] was allowed to increase normally and (2) plasma [HCO3] increase was prevented by i.v. HC1 infusion, CSF [HCO3] increased 8.5 mM/L after 2 hours of hypercapnia (delta PCO2 40) in the rats with intraventricular 'mock' CSF injections, and only 6 mM/L in the animals with acetazolamide injections. CSF [HCO3-] increased 7 mM/L during hypercapnia and HCl infusion with intraventricular 'mock' CSF injections, but only 2 mM/L with acetazolamide injections. Changes in total brain CO2 (increase) and brain glutamic acid (decrease) in hypercapnia were not affected by intraventricular acetazolamide and i.v. HCl. The increase of brain NH4+ and glutamine in hypercapnia was reduced in these conditions. It is concluded that there are at least two sources for the CSF [HCO3-] increase in hypercapnia; one formed in the CNS and dependent on carbonic anhydrase, and the other derived from plasma [HCO3-] increase.
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PMID:The CSF HCO3 increase in hypercapnia relationshp to HCO3, glutamate, glutamine and NH3 in brain. 1 66

The effect of local hypercapnic acidosis or local hypocapnic alkalosis on pial arterioles were studied in anesthetized cats equipped with a cranial window for the direct observation of the pial microcirculation of the parietal cortex. Changes in PCO2 and pH of the extracellular fluid were induced by perfusing the space under the cranial window with artificial cerebrospinal fluid equilibrated with different concentrations of CO2, while PaCO2 was maintained constant. Hypercapnic acidosis dilated and hypocapnic alkalosis constricted pial arteioles markedly. The results indicate that a basis exists for considering CO2 as a mediator for local regulation of brain blood flow. The vasodilation associated with arterial hypercapnia was abolished by a reduction in CSF PCO2 equal in magnitude to the rise in arterial blood PCO2, suggesting that the action of CO2 is entirely local.
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PMID:Local mechanism of CO2 action of cat pial arterioles. 1 34

The mathematical model of the respiratory control system in man of Middendorf and Loeschcke (1976 a, b) opens the possibility to stimulate the constellation of parameters in non-respiratory acidosis. Several investigators agree that the pH in CSF or in the extracellular fluid of the brain stays remarkably constant in this situation and it can be shown that this is a result of a precise control rather than the consequence of a sluggishly reacting system. Application of the model assuming constant extracellular brain pH allowed to calculate the relative sensitivities to pH changes of the central and the peripheral sensory mechanisms generating respiratory drive. Assuming air breathing and a normal critical arterial O2-pressure and otherwise normal parameters of respiration, circulation and blood composition (except diminished buffer base) the central chemosensitivity to a pH change turned out to be 25 times the peripheral. This factor is critically dependent on the ratio of the bicarbonate change in extracellular brain fluid to that in arterial blood. The coinciding data of Fencl (1971) and of Kronenberg and Cain (1968) were used for the calculation.
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PMID:Cooperation of peripheral and central chemosensitive mechanisms in the control of the extracellular pH in brain in non-respiratory acidosis. 2 79

To evaluate the regulation of (H+) and (HCO3 minus) in brain extracellular fluid during respiratory acidosis, the changes in cisternal and lumbar CSF acid-base state were assessed in six anteshetized, paralyzed, mechanically ventilated dogs rendered hypercapnic by increase in FIco2. Arterial (HCO3 minus) was held constant. The electrochemical potential difference (mu) between CSF and blood for H+ and HCO3 minus was calculated from values for (H+) and (HCO3 minus) in CSF and arterial plasma and the simultaneously measured CSF/plasma DC potential difference. Measurements were made at pHa equal to 7.40, after stable arterial values of pHa of about 7.2 were attained and 3, 4.5, and 6 h thereafter. A steady state for ion distribution was attained by 4.5 h. Values of mu for H+ and HCO3 minus at 6 h had returned to +0.7 and minus 0.7 mV of control for cisternal CSF and +1.3 and minus 0.6 mV of control for lumbar CSF. The attainment of steady-state values for mu close to control is comparable with passive distribution of these ions between CSF and blood.
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PMID:Distribution of H+ and HCO3 minus between CSF and blood during respiratory acidosis in dogs. 23 64

CSF bicarbonate regulation was studied in respiratory acidosis and alkalosis of 4h duration in antsthetized dogs. PCO2, pH, HCO3, ammonia, and lactate in CSF and arterial and safittal sinus bloof were measured when equal volumes of saline or acetazolamide (8 mg) were injected into lateral cerebral ventricles. The brain CO2 dissociation curve was determined at the end of all experiments. CSF and arterial bicarbonate increased 11.8 and 5.9 meg/l, respectively, in acidosis. Acetazolamide limited the rise in CSF bicarbonate to 4.2 meg/l, and prevented the CSF bicarbonate increase associated with hyperammonemia. During alkalosis CSF bicarbonate fell 6.5 meg/l and CSF lactate increased almost 2 meg/l while arterial bicarbonate fell 5.7 meg/l and lactate remained unchanged. Thus plasma bicarbonate changes account for some of the CSF unchanged. Thus plasma bicarbonate changes account for some of the CSF bicarbonate alterations in respiratory acid-base-disturbances. In acidosis additional CSF bicarbonate is formed by the choroid plexus and glial cells on the inner and outer surfaces of the brain--a reaction catalyzed by the locally present carbonic anhydrase. In alkalosis the greater fall in CSF bicarbonate than blood is due to selective brain and CSF lactic acidosis.
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PMID:CSF bicarbonate regulation in respiratory acidosis and alkalosis. 23 31

Direct assessment of tracheal circumference, which permits evaluation of constriction and dilatation in vivo, was made continuously in intact, pentobarbital-anesthetized, spontaneously breathing dogs. Immediate response to induction of hypercapnia included tracheal constriction and cessation of normal, vagus-dependent rhythmicity of airway tone. The characteristic constrictor response to acetylcholine was exaggerated significantly during hypercapnic acidosis and returned to normal when arterial pH, but not CSF pH, was corrected by NaHCO3 infusion. Epinephrine produced significant tracheal dilatation (infrequently followed by constriction) and isoproterenol produced only dilatation at normal pH. The catecholamine-induced dilatation was decreased significantly during hypercapnic acidosis, but improved after NaHCO3 infusion. Responses to acetylcholine and epinephrine were the the same as control during alkalemia, whereas the response to isoproterenol was unexplainedly diminished. Thus alkalemia may inhibit the action of isoproterenol; acidemia enhances parasympathomimetic constriction and reduces sympathomimetic dilatation; and correction of arterial pH returns these responses to normal, even if hypercapnia and CSF acidosis persist.
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PMID:Arterial pH, airway caliber and response to acetylcholine and catecholamines in vivo. 50 32

In 48 patients the acid-base equilibrium in the CSF and blood was determined on the 2nd day after intracranial operation. In the postopertive period various disturbances of this equilibrium were found which were probably various stages of metabolic acidosis compensation in the CSF which was a reflection of metabolic (lactate) acidosis developing primarily in the damaged brain area. On the basis of determinations it was found that changes in the CSF of the type of metabolic acidosis (21 cases) corresponded most frequently to respiratory alkalosis in the blood (11 cases). Changes of the type of respiratory acidosis in the CSF(13 cases) corresponded usually to metabolic alkalosis in the blood (7 cases). The development of metabolic acidosis in patients in severe and moderately severe condition (19 cases) was associated with poor prognosis as to survival since the mortality in this group was 10 (about 53%). The favourable effect of dehydrating treatment may be due also to facilitation of passage of bicarbonates from the blood into the cerebral tissue and CSF since their level is increased in the blood during metabolic alkalosis (during a decrease in the extracellular space) resulting from dehydration.
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PMID:[Acid-base equilibrium in cerebrospinal fluid following intracranial surgery]. 116 40

Case records of 32 neonatal calves with the antemortem diagnosis of meningitis were reviewed. Mean age at admission was 6 days (range, 11 hours to 30 days), and the most common concurrent clinical problem was diarrhea (16/32). Twenty-seven of the calves were available for necropsy. At postmortem, there was evidence of septicemia in 22 (81%) of these calves. Escherichia coli was the organism most frequently isolated (11/16; 69%) from the CNS. The major clinical signs of CNS disturbance observed over the course of hospitalization were lethargy, recumbency, anorexia, loss of suckle reflex, and coma. Leukocytosis and a left shift was evident in 11 of 15 (73%) calves. Concurrent metabolic problems that could have aggravated the CNS disturbance included hyperkalemia and respiratory acidosis. Analysis cerebrospinal of fluid from 22 of the calves, revealed pleocytosis, xanthochromia, turbidity, and high total protein concentration. Cytologically, neutrophils predominated in the CSF in calves with acute disease. Mononuclear cells dominated in calves with chronic disease. Microscopically, bacteria were evident in 10 of 22 (45%) of the antemortem CSF samples and bacteria were isolated from slightly more than half (11/19) of the specimens subjected to microbial culturing. Escherichia coli was the agent most frequently isolated from the CSF. Two of the 9 E coli isolates were resistant to trimethoprim potentiated sulfonamide drugs and all (4/4) of the CSF E coli isolates tested for susceptibility to triple-sulfonamide drugs were resistant. Twenty-seven of the 32 calves died or were euthanatized within 2.43 days after hospitalization.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Meningitis in neonatal calves: 32 cases (1983-1990). 164 35

Gamma-aminobutyric acid (GABA) is a putative central neurotransmitter that depresses respiratory neurons and has a metabolism in the brain that is tied to CO2 fixation and H+ metabolism. Therefore, the effect of 3 concentrations of GABA (10, 30, and 50 mM) in different groups of pentobarbital-anesthetized dogs was investigated by ventriculocisternal perfusion for 15 to 45 min. During multiple perfusion sequences, tidal volume (VT) and respiratory frequency were recorded continuously, whereas heart rate (HR), mean systemic arterial pressure (Psa), cardiac output, mean pulmonary arterial pressure, and pulmonary capillary wedge pressure were monitored periodically. Minute ventilation decreased by a reduction in VT. The mean VT (+/- SEM) decreased after 15 min of GABA perfusion from 365.9 +/- 19.5 to 151.0 +/- 15.0 ml with 50 mM GABA in mock CSF, from 272.8 +/- 25.1 to 110.6 +/- 7.4 with 30 mM GABA, and from 223.6 +/- 22.3 to 155.3 +/- 21.8 with 10 mM GABA. A decrease in mean inspiratory flow was associated with the reduction in VT. The decrease in ventilation was associated with respiratory acidosis. At each GABA concentration, mean Psa decreased, whereas HR fell only with 50 mM. Other cardiovascular parameters did not change. Perfusion with mock CSF alone restored cardiorespiratory depression caused by GABA. Mean Psa fell with GABA whether ventilation was kept constant mechanically or not. These results support the hypothesis of a GABA-sensitive mechanism via a population of receptors that affect respiratory and cardiovascular function and are accessible by ventriculocisternal perfusion.
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PMID:Reversible depression of ventilation and cardiovascular function by ventriculocisternal perfusion with gamma-aminobutyric acid in dogs. 371 57


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