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

This study was designed to determine the effect of acute hyperventilation on distal nephron hydrogen ion secretion. The blood PCO2 declined and stabilized rapidly when bicarbonate loaded rats were hyperventilated. In contrast, the urine PCO2 declined slowly, resulting in an early increase in the urine minus blood (U-B) PCO2 which could not be obliterated by carbonic anhydrase infusion. Within approximately 50 min, the U-B PCO2 in the hyperventilated and carbonic anhydrase infused rats approached zero. Consequently, equilibrium between collecting duct urine and arterial blood PCO2 was then presumed to exist. This provided the basis for the subsequent studies on a series of rats. The U-B PCO2 decreased from a control of 22+/-1 mm Hg (mean+/-SEM) to 11+/-2 mm Hg (mean+/-SEM) with hypocapnia, and rose again to its control value when the blood PCO2 returned to prehyperventilation values. This decline in U-B PCO2 with acute hyperventilation could not be attributed to changes in urine flow, phosphate, or bicarbonate excretion, suggesting, therefore, a decrease in distal nephron (probably collecting duct) hydrogen ion secretion with acute hyperventilation. Possible pitfalls in the interpretation of the UB PCO2 are illustrated.
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PMID:The effect of hyperventilation on distal nephron hydrogen ion secretion. 0 92

The acid-base values of 13 patients with stable carbon dioxide tensions under controlled ventilation have been used to define the response to chronic hypocapnia in man. These patients had a respiratory paralysis and no apparent complicating disorders. Over a range of carbon dioxide tensions from 24 to 40 millimetres of mercury, the arterial blood hydrogen ion concentration decreased linearly by 0.32 nanomole per litre per millimetre of mercury decrement in carbon dioxide tension. Of primary interest was the finding that the slope of the regression line in chronic hypocapnia is close to that already reported for chronic hypercapnia. The physiological response to chronic hypocapnia in man is defined by a band that is approximately 10 nanomoles per litre (0.09 pH unit) wide for hydrogen ion concentration and 6 millimoles per litre wide for bicarbonate concentration. These significance bands may be used to differentiate additional acid-base disorders in patients with chronic hypocapnia over a clinically useful range of carbon dioxide tensions.
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PMID:Acid-base response to chronic hypocapnia in man. 2 Jan 87

It has generally been thought that homeostatic mechanisms of renal origin are responsible for minimizing the alkalemia produced by chronic hypocapnia. Recent observations from this laboratory have demonstrated, however, that the decrement in [HCO(-) (3)], which "protects" extracellular pH in normal dogs, is simply the by-product of a nonspecific effect of Paco(2) on renal hydrogen ion secretion; chronic primary hypocapnia produces virtually the same decrement in plasma [HCO(-) (3)] in dogs with chronic HCl acidosis as in normal dogs (Delta[HCO(-) (3)]/DeltaPaco(2) = 0.5), with the result that plasma [H(+)] in animals with severe acidosis rises rather than falls during superimposed forced hyperventilation. This observation raised the possibility that the secondary hypocapnia which normally accompanies metabolic acidosis, if persistent, might induce an analogous renal response and thereby contribute to the steady-state decrement in plasma [HCO(-) (3)] observed during HCl feeding. We reasoned that if sustained secondary hypocapnia provoked the kidney to depress renal bicarbonate reabsorption, the acute salutary effect of hypocapnia on plasma acidity might be seriously undermined. To isolate the possible effects of secondary hypocapnia from those of the hydrogen ion load, per se, animals were maintained in an atmosphere of 2.6% CO(2) during an initial 8-day period of acid feeding (7 mmol/kg per day); this maneuver allowed Paco(2) to be held constant at the control level of 36 mm Hg despite the hyperventilation induced by the acidemia. Steady-state bicarbonate concentration during the period of eucapnia fell from 20.8 to 16.0 meq/liter, while [H(+)] rose from 42 to 55 neq/liter. During the second phase of the study, acid feeding was continued but CO(2) was removed from the inspired air, permitting Paco(2) to fall by 6 mm Hg. In response to this secondary hypocapnia, bicarbonate concentration fell by an additional 3.0 meq/liter to a new steady-state level of 13.0 meq/liter. This reduction in bicarbonate was of sufficient magnitude to more than offset the acute salutary effect of the hypocapnia on plasma hydrogen ion concentration; in fact, steady-state [H(+)] rose as a function of the adaptive fall in Paco(2), Delta[H(+)]/Delta Paco(2) = -0.44. That the fall in bicarbonate observed in response to chronic secondary hypocapnia was the result of the change in Paco(2) was confirmed by the observation that plasma bicarbonate returned to its eucapnic level in a subgroup of animals re-exposed to 2.6% CO(2). These data indicate that the decrement in plasma [HCO(-) (3)] seen in chronic HCl acidosis is a composite function of (a) the acid load itself and (b) the renal response to the associated hyperventilation. We conclude that this renal response is maladaptive because it clearly diminishes the degree to which plasma acidity is protected by secondary hypocapnia acutely. Moreover, under some circumstances, this maladaptation actually results in more severe acidemia than would occur in the complete absence of secondary hypocapnia.
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PMID:The maladaptive renal response to secondary hypocapnia during chronic HCl acidosis in the dog. 2 Nov 98

Awake, intact dogs trained to wear a respiratory mask were studied in a hypobaric chamber at 140 m and at various stages of a 4-week exposure to 3,550 m. Resting ventilation, pulmonary gas exchanges, arterial blood gases and pH, acid-base status of the cisternal fluid (CSF) and ventilatory responses to transient O2 inhalation were measured. Attention is focussed on the time course of ventilatory acclimatization to altitude, characterized by hyperventilation with hypocapnia and a consequent increase of arterial Po2. (1) 75 percent of the increment in pulmonary ventilation due to hypoxia was achieved in 30 minutes; (2) the further increase, 25 percent of the total hyperventilation, was complete after 3 hr, with a corresponding Pco2 drop and pH increase in blood and CSF, and an increase in Pao2; (3) the secondary increase in ventilation, beyond the acute exposure period, was not related to return of [H+] in CSF towards control value; (4) the large transient decrease of ventilation following brief oxygen inhalation demonstrated a strong arterial chemoreflex drive in acclimatized animals. The extremely rapid ventilatory acclimatization to moderately high altitude in normal dogs appears to be mediated not by CSF hydrogen ion concentration but by a strong chemoreflex drive of ventilation.
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PMID:Blood and CSF acid-base changes, and rate of ventilatory acclimatization of awake dogs to 3,550 m. 24 Nov 5

A method for measuring regional myocardial blood flow with a polarographic hydrogen-clearance technique, and its experimental application in dogs, are described. Under pentobarbitone anaesthesia, flow to the superficial (3 mm) and deep (8 mm) layers of the left ventricle was not significantly different. Neither hypocapnia (PaCO2 = 24 mm Hg) nor halothane significantly altered differential distribution of blood flow to the superficial and deep layers of the myocardium. Hypocapnia was followed by a fall in myocardial blood flow (MBF) associated with increased myocardial vascular resistance (MVR). Administration of halothane 0.5 per cent at normal levels of PaCO2 led to a fall in MBF of approximately 20 per cent with no significant changes in MVR.
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PMID:A technique for measuring regional myocardial blood flow and its application in determining the effects of hyperventilation and halothane. 93 62

Changes in cerebrospinal fluid formation rate (VF) with hypocapnia were measured by the ventriculocisternal perfusion technique in 24 rhesus monkeys anesthetized with nitrous oxide. In addition cerebral blood flow (CBF) was measured by the hydrogen clearence methods, Vf in control animals declined at a mean rate of 2.3 mul/min each hour during the last 4.5 h of a 7-h perfusion although variables known to effect Vf remained stable. Three hours after perfusion began, Vf of normocapnic controls was 41.4 mul/min +/- 5.4; CBF, 59P ML/100 G PER MIN. When Pco(2) was reduced to half of control, Vf fell to 35.6 mul/min +/- 6.3 and CBF fell by 27%. When Pco(2) was doubled, Vf fell to 33.1 mul/min +/- 5.3 and CBF increased threefold. The difference in Vf id significant only for the hypercapnic group (p=0.01). When animals were used as their own controls, three were no significant differences in Vf with hypercapnia compared to normocapnia. These results indicated that in the monkey variations of Pco(2) within broad physiologic limits, which are sufficient to cause large changes in CBF, have little effect of Vf.
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PMID:PCO(2) and rate of formation of cerebrospinal fluid in the monkey. 96 50

The authors describe a method for Doppler ultrasound recording of flow velocity in the basilar artery of normal rabbits and rabbits with experimental subarachnoid hemorrhage (SAH). With this transcranial Doppler (TCD) model, clinical assumptions regarding flow velocity/cerebral blood flow (CBF) relationships, autoregulatory responses, and Doppler spectral waveform analysis can be tested under controlled conditions and compared with established methods of CBF measurement (hydrogen clearance). The time course of changes in flow velocity following SAH (cerebral vasospasm) is successfully demonstrated using the experimental TCD method. There are significant differences in the flow velocity and CBF responses to hypercapnia, hypocapnia, and trimethaphan-induced hypotension which indicate that TCD cannot be considered a simple alternative to CBF measurement for the study of cerebrovascular reactivity and cerebral autoregulation.
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PMID:Transcranial Doppler ultrasound studies of cerebral autoregulation and subarachnoid hemorrhage in the rabbit. 211 49

A 4 hr intravenous infusion of Escherichia coli endotoxin in a total dose of 100 mg/kg produced significant morphological and functional pulmonary alterations in pentobarbitone anesthetized rats. Lung vascular permeability index was increased from 2.11 +/- 0.34 in normal rats to 4.82 +/- 0.65 in untreated endotoxemic rats. Treatment of endotoxemic rats with recombinant human superoxide dismutase (r-HSOD) in doses of 0.1, 0.215, and 0.464 mg/kg.min i.v., infused concomitantly with endotoxin, dose-dependently reduced the permeability index to 3.28 +/- 0.96, 2.83 +/- 0.55 (P less than 0.05), and 2.16 +/- 0.65 (P less than 0.05). The wet lung weight was 523 +/- 15 and 664 +/- 46 mg/100 g bwt in normal and in untreated endotoxemic rats, respectively. r-HSOD dose-dependently inhibited the endotoxin-induced increase in wet lung weight to 617 +/- 40, 577 +/- 31, and 559 +/- 39 (P less than 0.05) mg/100 g bwt. r-HSOD (0.464 mg/kg.min) did not affect permeability index and wet lung weight in normal, nonintoxicated rats. Endotoxin infusion produced a significant increase in respiratory rate (max. +69%) and blood gas alterations, indicating a hyperventilatory hypocapnia in endotoxemic control rats. Infusion of r-HSOD (0.464 mg/kg.min) significantly inhibited the endotoxin-induced tachypnoe (max. +13%) and blunted the alterations in arterial hydrogen carbonate content and carbon dioxide tension. In conclusion, infusion of r-HSOD dose-dependently and significantly inhibited pulmonary edema formation and hyperventilatory dyspnoe in endotoxemic rats.
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PMID:Effects of recombinant human superoxide dismutase on increased lung vascular permeability and respiratory disorder in endotoxemic rats. 217 95

The change in blood pH during hypoxia was examined using rabbits. Rabbits were divided into 4 groups according to the test gases used (O2 5.1%: CO2 5.4%: N2 89.5%, O2 4.9%: N2 95.1%, O2 2.0%: CO2 5.6%: N2 92.4% and O2 1.9%: N2 98.1%). After an intravenous injection of urethane, the rabbit was fixed on its back on an operating table and the trachea was cannulated. Animals inhaled test gases through a cylindrical unidirectional valve box connected to the cannula. Blood samples were drawn from the catheterized femoral artery. The duration of exposure was 90 min. The animals in the CO2-added 5% O2 group survived the exposure, while only 2 animals survived in the CO2-free 5% O2 group. There was a difference of about 5 mmHg in the blood PO2 between both 5% O2 groups. There was also a marked difference in the time course of changes in the hydrogen ion [( H+]) concentrations between the groups. The [H+] in the CO2-free group began to increase after an initial fall and exceeded the value of the other group, reaching acidotic levels. The acidosis (metabolic) was considered to have been caused by the accumulation of lactic acid. Under the present experimental conditions the contribution of hypoxia to this acidosis was considered to be greater than that of hypocapnia. The animals in the 2% O2 groups died by the 11 min after the start of exposure. In the CO2-free group neither hypercapnia nor acidosis was observed during the exposure. The PO2 values at apnea were about 10 mmHg in both groups.
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PMID:The effect of carbon dioxide on the changes in blood pH during hypoxia. 250 70

The effects of halothane and isoflurane on regional cerebral blood flow (CBF) were studied in 18 New Zealand White rabbits anesthetized with nitrous oxide (N2O) and morphine sulfate (MS) at three different levels of PaCO2. CBF was measured using the hydrogen clearance technique. Monitored variables were intracranial pressure (ICP), central venous pressure, heart rate, mean arterial pressure, electroencephalogram, arterial blood gases, end-tidal (ET) volatile anesthetic, and ET CO2. Addition of 1 MAC halothane to the N2O/MS background anesthetic caused flow to increase significantly in all three regions studied (cortex, dorsal hippocampus, white matter) at all three levels of PaCO2 (low: 20-25 mmHg; normal: 35-40 mmHg; high: 50-55 mmHg). Addition of 1 MAC isoflurane to the background anesthetic caused CBF to decrease significantly in all regions during hypocapnia. During normocapnia, CBF was unchanged with the addition of 1 MAC isoflurane in all regions and during hypercapnia, CBF increased significantly only in the dorsal hippocampus following addition of 1 MAC isoflurane to the MS/N2O background anesthetic. Volatile anesthetic administration was associated with significant, although small, increases in ICP at all PaCO2 levels. We conclude that 1 MAC concentrations of halothane and isoflurane have opposite effects on CBF when added to a N2O/MS anesthetic during hypocapnia and that the effects of isoflurane on regional CBF are dependent on PaCO2 in rabbits under the anesthetic conditions of this experiment.
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PMID:Isoflurane, halothane, and regional cerebral blood flow at various levels of PaCO2 in rabbits. 308 28


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