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

To examine the possible contribution of active H+ secretion mediated by brush border enzymes to proximal tubule HCO-3 absorption, paired reperfusions of surface proximal convoluted tubules were performed with the inhibitor dicyclohexylcarbodiimide (DCCD). In control studies using a solution devoid of HCO-3 but containing 5.5 mM glucose, 1 mM DCCD had no effect on glucose or fluid (Na+) absorption, suggesting that this inhibitor did not interfere with sodium entry at the brush border or mitochondrial energy production (ATP synthesis). In experiments using a perfusion solution containing 18-25 mM HCO-3, DCCD caused a fall in absolute CO2 absorption of approximately 15% under eucapneic conditions and 30% during acute hypercapnia. One millimole per liter amiloride (an inhibitor of the passive Na+-H+ exchanger) caused a 15% inhibition of CO2 absorption during acute hypercapnia and a disproportionately large reduction in fluid (Na+) absorption. The latter was not due to cell poisoning, since 1 mM amiloride had no inhibitory effect on fluid or glucose absorption when a HCO-3-free perfusion solution was used. Addition of 1 mM DCCD to a perfusion solution containing either 10(-3) M amiloride or 10(-4) M acetazolamide caused a significant inhibition of CO2 absorption compared with amiloride or acetazolamide alone. The observations are consistent with the view that in addition to passive Na+-H+ exchange, active transport mediated by either a H+-ATPase or a redox-driven H+ pump in the brush border contributes significantly to HCO-3 absorption in the proximal tubule.
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PMID:Evidence for a DCCD-sensitive component of proximal bicarbonate reabsorption. 406 52

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

1. Unit activity was recorded with steel micro-electrodes from 486 hypothalamic neurones in rat diencephalic island preparations.2. The histograms of firing frequencies for populations of hypothalamic units from unanaesthetized preparations and from those under urethane anaesthesia were not significantly different. The firing rates of both were significantly faster than those observed in intact brains under urethane.3. The mean distance between stable units in unanaesthetized island preparations did not differ significantly from that in preparations anaesthetized with urethane.4. The response of individual neurones to intravenous injections of urethane was variable, and apparently not associated with the onset or maintenance of anaesthesia. Some showed transient acceleration, some deceleration and some no change in rate or pattern of discharge.5. All neurones tested were slowed or stopped by intravenous injections of subanaesthetic doses of sodium methohexitone (Brietal). The responses were highly reproducible and dose-dependent.6. Brietal also produced a fall in arterial pressure and depressed respiration. Inhalation of amyl nitrite evoked larger hypotensive responses but did not affect unit activity; nor did inhalation of CO(2) (hypercapnia) or N(2)O (hypoxia).7. It is concluded that urethane anaesthesia is not associated with any direct action on hypothalamic neurones. The depression of firing rate in hypothalamic neurones induced by Brietal may represent an important forebrain mechanism in anaesthesia by this agent.
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PMID:Unit activity in rat diencephalic islands--the effect of anaesthetics. 554 21

The pulmonary vasopressor response to acidemia was studied in intact dogs in a hemodynamically separated lobe which was pump perfused with systemic arterial or venous blood at a fixed rate. The magnitudes of the lobar vasopressor responses to perfusion with blood rendered acidic by infusions of hydrochloric lactic, and acetic acids, and by hypercapnia (membrane oxygenator) were significantly different. Although the PH of the perfusing blood in each group fell to similar extents (pH 7.1-7.0), the lobar pressor response was greatest with hydrochloric acid (HCl), smaller with lactic and acetic acids, and absent with hypercapnia. A lobar vasopressor response also occurred during lobar perfusion with blood which had been extracorporeally acidified with HCl or acetic acid, but then returned to control pH by infusions of sodium bicarbonate and Tris before reaching the lung. A lobar vasopressor response also resulted from pump perfusion of the lobar artery with femoral venous blood during perfusion of the isolated ipsilateral femoral artery with similarly treated aortic blood. However, no lobar vasopressor response resulted from pump perfusion of the lobar artery with blood removed transseptally from a right pulmonary vein during acidification (HCl) of the right pulmonary artery (to pH 7.0).The data indicate that, in this experimental preparation involving closed-chest dogs spontaneously breathing air or 35% oxygen, the lobar vasopressor response to infusions of acidifying agents is not directly related to the pH of blood actually perfusing the lobar vessels. Additionally, the vasopressor response is prevented by prior perfusion of the acidified blood through a pulmonary vascular bed but not by prior perfusion through the femoral vascular bed. Although these experiments do not establish the mediation of the lobar vasopressor response, activation of vasoactive agents in blood at or near the acidification site is suggested. In these experiments, the acidemia was produced under conditions which are not like the usual ones of developing metabolic acidosis or alveolar hypercapnia, in that strong acids were directly infused into blood which perfused only one lung lobe. The mediation of the present pressor responses and of those found in the more usual forms of experimental and clinical acidosis may therefore be dissimilar.
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PMID:The pulmonary vasopressor response to decreases in blood pH in intact dogs. 555 5

Patients with pulmonary dysfunction and CO2 retention have renal hemodynamic abnormalities accompanied by increased plasma renin activity. To determine if hypercapnia impairs renal function, particularly through the renin-angiotensin system, the effects of acute hypercapnic acidosis (HC), using 8.5% CO2, were measured in five unanesthetized dogs during (a) the intact state; (b) renin-angiotensin antagonism using either 1-sarcosine, 8-glycine angiotensin II ( [Sar1, Gly8] AII) or SQ 14,225; and (c) exogenous angiotensin II infusion. As partial arterial carbon dioxide pressure (PaCO2) increased (p less than 0.05) from control (C) of 35 +/- 1 (SEM) to 48 +/- 1 mm Hg during HC, arterial pH fell (p less than 0.05) from 7.36 +/- 0.01 to 7.24 +/- 0.005. Renal function was uncompromised with HC, and glomerular filtration rate (GFR) and urinary sodium excretion increased (p less than 0.05) despite a fourfold rise in plasma renin activity from C of 0.6 +/- 0.3 to 2.2 +/- 0.8 ng AI ml-1 h-1 during HC. Administration of [Sar1, Gly8] AII during HC did not consistently alter systemic or renal hemodynamic responses, and effects of SQ 14,225 during HC were also observed during normocapnia. Although systemic vascular responses to exogenous AII infusion were similar, the renal vasoconstrictor response was antagonized during HC with unchanged GFR and renal blood flow. These findings indicate that despite activation of the renin-angiotensin system, acute hypercapnic acidosis is unassociated with impairment of renal function in unanesthetized dogs. This may be related to diminished renal vascular AII responsiveness during hypercapnia.
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PMID:Renal and cardiovascular responses to acute hypercapnic acidosis in conscious dogs: role of renin--angiotensin. 618 44

The present studies evaluate the effect of acute hypercapnia on distal nephron H+ secretion (DNH+S) in vivo by means of the urine-blood PCO2 difference (U-B PCO2) in alkaline urine. Bicarbonaturia was induced by either a sodium bicarbonate infusion or L-lysine administration. Our results demonstrate that the U-B PCO2, as a function of the urinary bicarbonate concentration, was significantly lower during acute respiratory acidosis; this effect was not dependent on changes in glomerular filtration rate and/or fractional excretion of sodium, potassium, and chloride. Infusion of the sodium salts of sulfate, a nonreabsorbable anion, did not correct the diminished U-B PCO2. Amiloride caused the U-B PCO2 to fall in normocapnic dogs but not in hypercapnic dogs. When hypercapnia was superimposed in dogs with extracellular fluid volume contraction, there were no changes in the U-B PCO2. This study indicates that acute hypercapnia in the intact dog decreases DNH+S and is compatible with an effect of hypercapnia on the voltage-dependent component of urine acidification. The mechanism appears to be direct rather than secondary to factors that influence the rate of sodium delivery to the distal nephron.
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PMID:Decreased distal acidification in acute hypercapnia in the dog. 629 83

The effects of hyperlactatemia on cerebral glucose metabolism of normoglycemic 20-day-old rats were studied in animals breathing air or 20% CO2:21% O2:59% N2. Sodium lactate or sodium bicarbonate were given intraperitoneally, together with a mixture of [3H]deoxyglucose and [2-14C]glucose. Animals were sacrificed in a freeze-blowing apparatus at intervals of 2-15 min after injection. Blood lactate levels in the lactate-injected rats were 4-6 mM. Hyperlactatemia caused a gradual decline in the brain rate of glucose utilization in air-breathing animals to 50-70% of control rates. Results with both tracers were similar. Concentrations of Krebs cycle intermediates and glutamate did not decrease. These findings indicate that lactate can partially replace glucose as an oxidative fuel for developing rat brain. Hypercapnia depressed the rate of glucose utilization by developing brain and rates were 30-40% lower still in lactate-injected hypercapnic rats. Decreases in levels of Krebs cycle intermediates and glutamate were similar in both groups. Thus, lactate and CO2 are additive in their depressant effects on brain glucose utilization. The observation that lactate did not prevent the decreases in Krebs cycle intermediates and glutamate caused by hypercapnic acidosis suggests an inhibition of flux through pyruvate dehydrogenase during hypercapnia. The data from this study, coupled with data on lactate transport across the blood-brain barrier, indicate that the direction of movement of lactate and its rate of utilization by developing brain are functions of its concentration on blood relative to brain. Physiological and pathological conditions which elevate blood lactate levels above those in brain will, then, have a sparing effect upon brain glucose utilization.
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PMID:Effects of lactate on glucose metabolism of developing rat brain. 632 76

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

By using adult rabbits in which the lung surfactant had been reduced by repeated whole-lung lavage, we examined the effects of surfactant supplement and positive end-expiratory pressure (PEEP). The rabbits were anesthetized with pentobarbital sodium and mechanically ventilated with pure O2. Surfactant that was extracted from pigs' lungs was supplemented to the rabbits through the trachea. The PEEP was set at 4 cmH2O. The seven rabbits that were ventilated without the supplement and without the PEEP all died of hypoxia, hypercapnia, and reduction of lung compliance within 2 h. The 18 rabbits that were ventilated with either the supplement or the PEEP showed some elevations of arterial O2 tension, but 9 of them died within 4 h. After application of both the surfactant supplement and the PEEP, six out of the eight rabbits survived for more than 11 h with nearly normal values of blood gases and compliance. We concluded that the combination of the transtracheal surfactant supplement and ventilation with PEEP has favorable therapeutic effects on surfactant deficiency.
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PMID:Effects of surfactant supplement and end-expiratory pressure in lung-lavaged rabbits. 638 55

This study examined urinary acidification shortly after recovery from chronic hypocapnia induced by hypoxemia. Distal acidification was evaluated by measuring the urinary PCO2 and urine-blood PCO2 difference (U-B PCO2) when blood PCO2 had returned to normal. In posthypocapnic rats, maximal alkalinization of the urine by acute sodium bicarbonate loading failed to increase urine PCO2 and U-B PCO2 to the level of posthypoxemic control rats and normal control rats with comparable blood pH and urine bicarbonate concentration. To test the hypothesis that decreased distal hydrogen ion secretion in posthypocapnic rats resulted from intracellular alkalosis secondary to protracted hypocarbia, posthypocapnic rats were exposed to hypercapnia of brief duration (30 min) and prolonged duration (120 min) in an attempt to restore distal acidification to normal. In posthypocapnic rats, hypercapnia of brief duration was associated with a significant increase in urine PCO2 and a fall in urine pH. Prolonged hypercapnia resulted in a marked increase in urine PCO2 and a further fall in urine pH. At any urinary bicarbonate concentration, however, the urine PCO2 and U-B PCO2 posthypocapnic rats exposed to hypercapnia were still significantly lower than in normal control rats identically subjected to prolonged hypercapnia and with comparable blood PCO2 and blood pH. Our findings indicate that distal acidification after abrupt recovery from chronic hypocapnia is decreased as if the kidneys were still under the influence of sustained hypocapnia. These findings could not be ascribed to extracellular alkalemia but could be explained by postulating that decreased urinary acidification resulted from persistence of cell alkalinity secondary to the accumulation of non-CO2 buffers generated during protracted hypocarbia. Alternatively, factors other than cell pH could mediate the adaptive decrease in distal hydrogen ion secretion of posthypocapnic rats.
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PMID:Suppression of distal urinary acidification after recovery from chronic hypocapnia. 641 9


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