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)

The purpose of this study was to investigate the pulmonary effects of hyperventilation in anesthetized, mechanically ventilated guinea pigs. Airway resistance (Raw), dynamic lung compliance (CDyn), blood pressure (BP), heart rate (HR), arterial blood gases (PaO2, PaCO2), pH and arterial plasma HCO3- were measured before and after a 10-min period of hyperventilation produced by increasing the respiratory rate from 60 to 120 breaths/min while maintaining tidal volume at 4 ml. There was a significant increase in Raw and decrease in CDyn lasting up to 20 min after hyperventilation was stopped with no change in BP and HR. PaO2 was reduced from 109 +/- 3 mm Hg before to 53 +/- 7 mm Hg at 5 min after hyperventilation. The Raw and CDyn changes were prevented and reversed with the bronchodilators salbutamol and aminophylline indicating that reversible bronchospasms are induced in guinea pigs following a period of hyperventilation. Additional studies demonstrated that the pulmonary mechanical responses to hyperventilation were not changed by vagotomy, ventilation with high CO2 or by pretreatment with chlorpheniramine, methysergide, atropine, indomethacin, FPL 55712 or calcium-influx blockers. These results indicate that neither vagal reflexes, airway hypocapnia, receptors of histamine, serotonin, acetylcholine nor the products of arachidonic acid metabolism were involved in hyperventilation-induced bronchospasm in guinea pigs.
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PMID:Hyperventilation-induced bronchoconstriction in guinea pigs. 393 Apr 9

The relative importance of pCO2 versus pH in regulating myocardial blood-flow (MBF) is not settled. Therefore, the influence of hypocapnia, hypercapnia and sodium carbonate infusion, on MBF and myocardial metabolism, has been investigated in 10 closed-chest pentobarbital anaesthetized dogs. The animals were hyperventilated, and CO2 was added to the inspiratory gas to induce normocapnia and hypercapnia. A mass spectrograph continuously measured the ventilatory gas components, and MBF was measured by the hydrogen desaturation technique with a catheter positioned in the coronary sinus. During the experiments, there were no significant alterations in heart rate, mean aortic blood-pressure, myocardial oxygen consumption or uptake of glucose and free fatty acids. During hypocapnia MBF was insignificantly reduced, while myocardial oxygen extraction increased significantly. During hypercapnia, however, MBF increased more than 40%. This increase in MBF was abolished following an infusion of sodium carbonate. Thus, in the present study, increased MBF, observed during hypercapnia, was due to the reduction in pH and not to the increase in pCO2.
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PMID:Effects of carbon dioxide and pH on myocardial blood-flow and metabolism in the dog. 393 53

1. The effects of high ambient temperatures on blood acid base status were studied in four breeds of fowl. 2. All breeds efficiently regulated body temperature below ambient temperature at 45 degrees C (Tb = 38.521 + 0.110Ta, at 25-45 degrees C). 3. A slight hypocapnia was partly compensated for by a decreased HCO3 concentration. This resulted in only a slight respiratory alkalosis at extreme temperatures (+0.021 and +0.042 pH units at 42 and 45 degrees C, respectively). 4. Changes in Paco2 were negatively correlated with tidal volume: Paco2 (torr) = 33.10390 - 1.17493 VT(ml); r = -0.925, P much less than 0.001. 5. The present findings are consistent with an hypothesis that modulation of tidal volume during thermal panting might play a major role in acid-base regulation.
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PMID:Acid-base regulation during thermal panting in the fowl (Gallus domesticus): comparison between breeds. 613 Aug 75

We hypothesized that part of the newborn tolerance of asphyxia involves strong ion changes that minimize the cerebral acidosis and hasten its correction in recovery. After exposure of newborn puppies to 15 or 30 min experimental asphyxia (inhalation of gas with fractional concentration of CO2 and of O2 in inspired gas = 0.07-0.08 and 0.02-0.03, respectively), blood lactate increased to 13.2 and 23.4 mmol/l, respectively, brain tissue lactate increased to 14.4 and 19.7 mmol/kg, and cerebrospinal fluid (CSF) lactate increased to 7.6 and 14.4 mmol/l. We presume that the tissue lactate increase reflects increases in brain cell and extracellular fluid lactate concentration. The lactate increase, a change that will decrease the strong ion difference (SID), [HCO3-], and pH, was accompanied by increases in Na+ (plasma, CSF, brain), K+ (plasma, CSF), and osmolality without change in Cl-. After 60-min recovery, plasma and brain lactate decreased significantly, but CSF lactate remained unchanged. [H+] recovery was more complete than that of the strong ions due to hyperventilation-induced hypocapnia. We conclude that during asphyxia-induced lactic acidosis, changes in strong ions occur that lessen the decrease in SID and minimize the acidosis in plasma and CSF. To the extent that the increase in brain tissue sodium reflects increases in intra-and extracellular fluid sodium concentration, the decrease in SID will be less in these compartments as well. In recovery, CSF ionic values change little; plasma and brain tissue lactate decrease with a similar time course, and the [H+] is rapidly returned toward normal by hypocapnia even while the SID is below normal.
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PMID:Newborn puppy cerebral acid-base regulation in experimental asphyxia and recovery. 632 80

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

Menstruating women exhibit a light but sustained hypocapnia during the luteal phase. To elucidate whether the hypocapnia results primarily from a respiratory or renal mechanism, we measured the rate of urinary excretion of acid at intervals during the menstrual cycle in five subjects. The acid-base composition of arterial blood in three subjects and end-tidal PCO2 in the remaining two subjects were also determined. During the follicular phase, the acid-base composition of blood and the rate of net acid excretion remained virtually constant. After ovulation, significant decreases in PaCO2 (3.5 mmHg), [HCO3]p (2 meq/liter), and net acid excretion (2 meq/h) occurred in the first 4-6 days of the luteal phase (14 days long). Following this, net acid excretion returned to the preovulatory level. PaCO2 and [HCO3]p, however, remained decreased for 3 more days. At the end of the luteal phase, restoration of PaCO2 proceeded faster than that of [HCO3]p. The acid-base changes in blood and urine observed during the luteal phase were comparable to those occurring during adaptation and recovery from sustained hypocapnia, suggesting that hypocapnia during the luteal phase is primarily respiratory in origin.
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PMID:Renal contribution to acid-base regulation during the menstrual cycle. 640 38

The intracellular pH (pHi) and bicarbonate concentration ([HCO3-]icw) of cardiac and skeletal muscles were monitored during respiratory alkalosis in order to further elucidate the homeostatic processes which operate in these tissues to ameliorate deviations from normal acid-base status. Rats were mechanically hyperventilated to induce hypocapnia, pHi was determined by the DMO method, and [HCO-3]icw was calculated from the Henderson-Hasselbalch equation using pHi and the partial pressure of carbon dioxide of vena caval blood. A significant intracellular alkalosis occurred in both cardiac and skeletal muscles during hypocapnia, but the changes in pHi were less in the heart than in skeletal muscle. The decreases in cardiac [HCO-3]icw were greater than those attributable to the physicochemical buffering of the heart. These data are consistent with an intramyocardial source of protons other than physicochemical buffering during respiratory alkalosis. The decreases in skeletal muscle [HCO-3]icw were less than those due to physicochemical buffering. These data are consistent with a net extrusion from skeletal muscles cells of the protons derived from physicochemical buffering during respiratory alkalosis.
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PMID:The effects of hypocapnia on intracellular pH and bicarbonate. 642 99

Early superficial (SF) and juxtamedullary (JM) proximal convolutions of the rabbit kidney were perfused in vitro to determine the effects of carbonic anhydrase inhibition (10(-4) M acetazolamide) and acute changes in PCO2 (decreases to approximately equal to 15 and increases to approximately equal to 74 mmHg) on potential differences (PD in mV), volume reabsorption (Jv in nl x mm-1 x min-1), and bicarbonate reabsorption (JCO2 in pmol x mm-1 x min-1). At PCO2 37 mmHg early JM exhibited a more lumen-negative PD (-7.5 vs. -5.3), greater Jv (1.13 vs. 0.82), and greater JCO2 (86.7 vs. 44.4) than early Sf. Sf and JM had similar responses to acetazolamide: PD became more negative (-5.2 to -5.9 in SF; -8.8 to -10.1 in JM), Jv decreased (0.92 to 0.68 in SF; 1.11 to 0.76 in JM), and JCO2 decreased (35.7 to 7.7 in SF; 99.2 to 27.4 in JM). Increasing PCO2 to approximately equal to 74 mmHg decreased lumen-negative PD, increased Jv, and increased JCO2 in SF and JM (-5.5 to -4.8, 0.72 to 0.95, and 47.6 to 80.4 in SF; -6.6 to -5.7, 1.19 to 1.47, and 78.0 to 111.3 in JM). Decreasing PCO2 to approximately equal to 15 mmHg increased lumen-negative PD, decreased JCO2, but had no effect on Jv in both segments (-4.9 to -5.8, 51.3 to 6.3, and 0.80 to 0.79 in SF; -7.0 to -7.9, 75.3 to 19.6, and 1.34 to 1.41 in JM). It is concluded that 1) early SF and JM display quantitative heterogeneity, 2) PCO2 changes within the physiologic range produce large changes in HCO3 absorption in early proximal tubules and 3) large changes in HCO3- reabsorption are dissociated from changes in volume reabsorption during hypocapnia.
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PMID:Effects of CO2 and acetazolamide on bicarbonate and fluid transport in rabbit proximal tubules. 677 38

Interregional differences in intracellular pH (pHi) in brain tissue, and its regulation following 1 and 5 h of respiratory alkalosis (with and without hypoxemia) were determined in N2O anesthetized dogs. Two techniques for pHi estimation were used (TCO2 and 14C-DMO) and included corrections for measured extracellular fluid (35SO4(2-)) space (ECS). Cortical pHi by the two techniques agreed closely in control and in 3 of the 4 experimental conditions, suggesting: (a) our estimation of extracellular fluid (ECF) [HCO3-] from measured CSF [HCO3-] was a valid assumption; and (b) our method had sufficient resolution to determine the magnitude of brain pHi regulation during respiratory acid-base disturbances. When moderate normoxic respiratory alkalosis (PaCO2 approximately 25 mm Hg) was imposed for 5 h, pHi (in most brain regions) was well regulated and always exceeded the incomplete regulation noted in bulk CSF. When moderate hypoxemia (PaO2 approximately 45 mm Hg) accompanied hypocapnia, pHi was more closely regulated during the early phase (1 h) of respiratory alkalosis. Increased levels of metabolic acids (especially lactic acid) were critical to brain pHi regulation during the initial hour of respiratory alkalosis and accounted for much of the independent effect of hypoxemia on pHi regulation. However, these metabolic acids remained unchanged as pHi was more completely regulated between 1 and 5 h of continued hypocapnia or hypoxic hypocapnia. This time-dependent regulation of pHi may involve some regulatory role for changed transmembrane fluxes of H+ and/or HCO3-. Significant interregional differences were observed in both pHi and in ECS; with tendencies toward more alkaline pHi and lower ECS in brain stem and white matter. With respiratory alkalosis ECS fell and intracellular fluid increased in both cortex and caudate nucleus, possibly reflecting an osmotic effect of increased metabolic acid levels or reduction in cell membrane ion pumping.
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PMID:Interregional differences in brain intracellular pH and water compartmentation during acute normoxic and hypoxic hypocapnia in the anesthetized dog. 678 4

On day 16 of the chick embryo, a catheter was implanted in the allantoic vein carrying arterialized blood, and a syringe was attached to the blunt end of the shell connecting to the air cell. This technique allowed for repetitive sampling and analysis of air cell gas and arterialized blood when these eggs were exposed to a He-O2 or SF6-O2 atmosphere. Exposure to He-O2 reduced the arterial CO2 tension(PaCO2) from 36 to 17 Torr and increased pH by 0.17 units; exposure to SF6-O2 increased PaCO2 from 37 to 62 Torr and reduced the pH by 0.14 units. These responses were brought about by changes in the gas conductance of the shell, resulting in a diffusive hypocapnia and respiratory alkalosis in He-O2 and a diffusive hypercapnia and respiratory acidosis in SF6-O2. During a 4-h exposure to these foreign gases the observed pH changes were smaller than predicted because of marked shifts of HCO3- into the blood (SF6-O2) or out of the blood (He-O2).
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PMID:Changes in acid-base balance of chick embryos exposed to a He or SF6 atmosphere. 679 Apr 88


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