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

Hypocapnia is known to have an antiphosphaturic effect that overcomes the phosphaturic effect of hypoxia. The objective of this study was to examine whether conscious rats exposed to acute hypoxia show a decrease in phosphate excretion due to the concomitant hypocapnia. Wistar rats weighing 200 g were exposed to hypoxia (inspired oxygen fraction = 0.10) or normoxia (inspired oxygen fraction = 0.21) for 6 h; and rats were alternately exposed to hypoxia or normoxia every 12 h for a total 36 h. Renal clearance and hormone studies were performed. Rats exposed to 6 h of hypoxia (n = 11) showed significant hypophosphaturia and decreases in absolute and fractional excretion of phosphate (0.38 +/- 0.10 microgram min-1, mean +/- SE, P < 0.0001 and 0.59 +/- 0.15%, P < 0.0001) as compared with normoxic rats (n = 11, 3.91 +/- 0.68 micrograms min-1 and 5.62 +/- 0.85%). In addition, nephrogenous adenosine 3',5'-cyclic monophosphate level per glomerular filtrate was significantly decreased (-0.87 +/- 0.64 nmol dL GF-1, P < 0.05) and plasma parathyroid hormone level was unchanged (45.2 +/- 9.5 pg mL-1) after 6 h of hypoxia as compared with normoxic rats (4.03 +/- 1.83 nmol dL GF-1 and 54.3 +/- 10.4 pg mL-1). A parallel increase in urinary noradrenaline and a decrease in dopamine excretion was observed in rats after 6 h of hypoxia. The decreased phosphate and adenosine 3',5'-cyclic monophosphate excretion during acute hypoxia were restored to normoxic levels by reoxygenation with 21% oxygen in the study of 12-h intermittent hypoxia. In summary, (1) hypoxia produced by inhalation of 10% oxygen for 12 h or less causes reduced phosphate and adenosine 3',5'-cyclic monophosphate (cAMP) excretion by spontaneously breathing rats; (2) these effects are reversed by reoxygenation and (3) hypoxia elicits a parallel increase in noradrenaline excretion and a decrease in dopamine excretion. These data suggest that renal adrenergic and dopaminergic systems play important roles in hypophosphaturia during acute hypoxia in conscious rats.
Acta Physiol Scand 1996 Dec
PMID:Phosphate and cyclic AMP excretion decreases during less than 12 hours of hypoxia in conscious rats. 897 Dec 52

It has been recognised that high haemoglobin oxygen capacity is essential for the development of high blood pressure in spontaneously hypertensive rats. In the present study we have found increased concentration of 2,3 diphosphoglycerate (2,3-DPG) in red blood cells of spontaneously hypertensive rats (SHR) of Okamoto-Aoki strain. As 2,3-DPG is the major factor decreasing haemoglobin affinity to oxygen, our finding suggests that at given value of pO2 oxygen delivery to the tissue of SHR would be increased. Therefore increased concentration of 2,3-DPG in red blood cells of SHR would be of the pathophysiological meaning by promoting autoregulatory increase in total vascular resistance in this strain of rats. The mechanism responsible for enhanced synthesis of 2,3-DPG in SHR remains unclear. Intracellular alkalosis due to either hypocapnia and/or an enhanced activity of Na+/H+ antiporter occurring in SHR are the most plausible explanations for the above finding.
J Physiol Pharmacol 1997 Dec
PMID:The increased concentration of 2,3-diphosphoglycerate in red blood cells of spontaneously hypertensive rats. 944 32

Central sleep apnoea (CSA) in congestive heart failure is sleep state dependent and occurs typically in stages I and II of non-REM sleep. The pre-requisites are hypocapnia and some prolongation of the circulation time. It is not certain whether abnormalities in after-discharge activity in the brainstem are also important. The presence of CSA in patients with left ventricular dysfunction is a poor prognostic sign and associated with a higher mortality in that group compared to age, sex and ejection fraction matched patients with congestive cardiac failure alone. It is reasonable to speculate that the CSA causes an increase in sympathetic nervous system activity which would maintain afterload at a high level or tend to increase it with time. The application of a high afterload to an impaired left ventricle leads over time to a further reduction in ejection fraction. From other studies, particularly ACE inhibitor studies, it is known that ejection fraction and prognosis are almost linearly related. It could therefore be said that once CSA has developed it may lead to a vicious circle of increasing afterload and further reduction in ejection fraction, causing worsening CSA and further increases in afterload. A number of treatments have been shown to be of benefit: supplemental nocturnal oxygen therapy, acetazolamide and nasal CPAP therapy have all been shown to reduce CSA. In addition nasal continuous positive airways pressure (CPAP) has been shown by two groups in Canada to also improve ejection fraction. The beneficial effects on ejection fraction in particular, persist after the treatment has been withdrawn, which suggests either remodelling of the left ventricular musculature or a resetting of the baseline sympathetic nervous system activity. The impressive increase in ejection fraction due to three months nasal CPAP therapy in one study (an average 35% increase) is both dramatic and exciting for the future. It is reasonable to expect improvement in prognosis for patients with CCF whose ejection fraction rises with CPAP treatment. Finally, only a limited number of studies have been published. Unfortunately the impressive results from Canada have not yet been reproduced in other centres around the world.
Respirology 1997 Dec
PMID:Central sleep apnoea and heart failure (Part I). 952 93

Bright-field and dark-field illumination techniques for in vivo measurements of reduced pyridine nucleotide fluorescence were compared in 15 rats during periods of normocapnia, hypocapnia, hypercapnia, and anoxia. Parameters investigated included fluorescence, cortical reflectance, cortical blood flow, and electroencephalograms. In normal brain, with preserved autoregulation, reduced pyridine nucleotide fluorescence was constant through a wide range in Pa(CO2), cortical blood flow, and cerebral blood volume in animals studied using vertical illumination (bright-field) techniques. There was a marked increase in reduced pyridine nucleotide fluorescence at death from anoxia. Artifacts were reduced by monochromators for excitation, emission, and reflected light; low-intensity vertical excitation energy and high-sensitivity recording instrumentation; and a small avascular (123 microns) field. Potential sources of error include photodecomposition, hemoglobin interference from absorption and reflectance, and light scattering. Vertical excitation techniques using a small field appeared to give more reliable and reproducible results than circumferential techniques using a larger field of observation.
Anal Biochem 1978 Dec
PMID:Comparison of dark-field and bright-field incident illumination for in vivo measurements of reduced pyridine nucleotides. 976 36

Hypocapnia produces cerebral vasoconstriction. The mechanisms involved in hypocapnia-induced elevation of vascular smooth muscle tone remain unclear. We addressed the hypothesis that, in cerebrovascular smooth muscle, increases in extracellular pH (pHo) cause increases in Ins(1,4,5)P3 and cytosolic calcium ([Ca2+]c). Superfused primary cultures of piglet cerebral microvascular smooth muscle cells were exposed to artificial CSF (aCSF) of control (pHo 7. 4, PCO2 36 mm Hg), metabolic alkalosis (pHo 7.7, PCO2 36 mm Hg), or respiratory alkalosis (pHo 7.7, PCO2 19 mm Hg). Intracellular pH (pHi) and [Ca2+]c were measured, using BCECF and fura-2, respectively, with dual wavelength spectroscopy. Ins(1,4,5)P3 was determined by a protein binding assay. Both metabolic and respiratory acidosis treatments increased pHi from the control value of about 7.2 to 7.35. Metabolic and respiratory alkalosis increased Ins(1,4,5)P3, as we showed previously. Metabolic and respiratory alkalosis increased [Ca2+]c about 80% and 110%, respectively. Neither Ins(1,4,5)P3 nor [Ca2+]c increased in cells treated with aCSF that produced control pHo with increased pHi (7.3). In contrast, when pHo increased (7.7), but pHi was maintained at control (7.2), Ins(1,4,5)P3 increased from 123 pmol/well to 307 pmol/well and [Ca2+]c increased 46%. However, the increase of [Ca2+]c was less than with either respiratory or metabolic alkalosis. Thus, hypocapnia-induced cerebral vasoconstriction could involve production of Ins(1,4,5)P3 with resultant elevation in [Ca2+]c. While the Ins(1,4,5)P3 signal appears to be dependent on an increase in extracellular pH, a role for intracellular pH cannot be completely excluded.
Proc Soc Exp Biol Med 1998 Dec
PMID:pHo, pHi, and PCO2 in stimulation of IP3 and [Ca2+]c in piglet cerebrovascular smooth muscle. 982 45

To determine whether nonchemical inhibition of respiratory activity occurs during inspiratory pressure support (IPS) ventilation (IPSV), respiratory motor output (in 9 subjects), obtained by calculating transdiaphragmatic pressure-time products, and central respiratory output (in 5 subjects), obtained by integrating the electromyographic activity of the diaphragm (EMGdi) during mechanical inspiratory time, EMGdi per minute, and electrical inspiratory time, as determined from onset to peak EMGdi, were compared during spontaneous ventilation (control) and IPSV with (IPS+CO2) and without (IPS) correction of hypocapnia. Both IPS and IPS+CO2 induced significant decreases in transdiaphragmatic pressure-time products (46 +/- 31 and 53 +/- 23%, respectively), EMGdi during mechanical inspiratory time (49 +/- 12 and 57 +/- 14%, respectively), EMGdi per minute (65 +/- 22 and 69 +/- 15%, respectively), and electrical inspiratory time (73 +/- 8 and 65 +/- 6%, respectively). Because correction of hypocapnia failed to eliminate the marked inhibition of both respiratory and central motor output seen with IPS, we conclude that nonchemical inhibition of respiratory activity occurs during IPSV.
J Appl Physiol (1985) 1998 Dec
PMID:Nonchemical influence of inspiratory pressure support on inspiratory activity in humans. 984 40

In this article, we review how the knowledge of the pathophysiology of panic disorder has expanded, with special emphasis on laboratory models using lactate and carbon dioxide challenges. Experiments in the late 1960s revealed that lactate infusion can induce panic attacks. A prominent feature of these attacks is hyperventilation. Because lactate infusion induces a metabolic alkalosis, one would rather expect a compensatory hypoventilation. For years hyperventilation was thought to be causally linked to panic, but it has since been proven to be a symptom rather than a cause of panic attacks. Similarly, it is not hypocapnia but hypercapnia that has proven to be capable of provoking panic attacks. Carbon dioxide challenges are comparable to lactate infusion in the degree to which they meet the criteria for an ideal model of panic disorder. Experiments with carbon dioxide in first-degree relatives of panic disorder patients and in monozygotic twins support the idea of a constitutional predisposition to panic disorder. Of the various other agents that have been used to trigger panic attacks, cholecystokinin seems particularly promising as a valid laboratory model of panic disorder and may provide valuable data regarding the mechanism of panic attacks. The false suffocation alarm theory, proposed by Klein, is an integrative hypothesis that may account for a large number of the laboratory as well as clinical observations.
J Psychosom Res 1998 Dec
PMID:Experimental pathophysiology of panic. 985 52

To quantify any mechanical inhibitory effect of nasal intermittent positive pressure ventilation (IPPV) on inspiratory activity of the diaphragm we ventilated five conscious relaxed subjects on two occasions at respiratory rates similar to quiet breathing (QB) and at three levels of applied pressure (Pappl)--6, 9 and 12 cmH2O, each during hypocapnia (P(CO2) allowed to decrease) and eucapnia (CO2 added to inspired gas). Diaphragm activity was assessed from transdiaphragmatic pressure (esophageal and gastric balloons) and diaphragm EMG (surface electrodes) both integrated with time (integral(Pdi x dt) and integral(EMGdi x dt), respectively). Neural inspiratory time (Tin) was measured as onset to peak of the integral(EMGdi x dt) signal. Relative to QB, integral(Pdi x dt) was 50-69% less during eucapnic IPPV 6-12 cmH2O (P < 0.005) and 67-85% less during hypocapnic IPPV (P < 0.005). Tin decreased (P < 0.05) with IPPV and, on ceasing IPPV, there was apnoea (prolonged expiratory time) on 23 of 27 occasions; these changes were independent of P(CO2). Integral(EMGdi x dt) decreased (P < 0.05) at Pappl 12 cmH2O during eucapnia and at all Pappl during hypocapnia. The repeatability of integral(EMGdi x dt) was substantially less than integral(Pdi x dt) (F = 42, P << 0.01). We conclude that, during non-invasive IPPV in awake healthy subjects mechanical factors are of major importance in inhibiting inspiratory activity of the diaphragm.
Respir Physiol 1999 Dec 01
PMID:Diaphragm inhibition with positive pressure ventilation: quantification of mechanical effects. 1064 59

Hyperoxia can improve oxygen delivery in patients exposed to hypocapnia for neurosurgical procedures but this effect may be modified by regional differences in the degree of hypocapnic vasoconstriction. Using functional magnet resonance imaging (fMRI), we have investigated the influence of hyperoxia on blood flow and blood oxygenation in the primary visual cortex in hypocapnic volunteers. Consecutive fMRI measurements were performed in 10 awake, male volunteers during hypocapnia (mean PE'CO2 3.3 (SD 0.1) kPa) and normocapnia (PE'CO2 5.3 (0.1) kPa) at FIO2 values of 0.21 and 1.0, respectively. Hypocapnia significantly reduced the pixel count in the primary visual cortex (median 169 (quartiles 34-246) vs 21 (0-40) pixels at an FIO2 of 0.21). Additional hyperoxia had no influence on this reduction in pixel count (16 (0-28) pixels at FIO2 1.0 vs 21 (0-40) pixels at FIO2 0.21). Hyperoxia did not influence hypocapnic vasoconstriction in the primary visual cortex. These data suggest that in the primary visual cortex, administration of oxygen alone may not be sufficient to improve oxygen delivery under hypocapnic conditions.
Br J Anaesth 1999 Dec
PMID:Effects of hyperoxia and hypocapnia on regional venous oxygen saturation in the primary visual cortex in conscious humans. 1070 Jul 78

Hyperventilation with dry air increases airway surface fluid (ASF) osmolality and causes acute mucosal injury, leukocyte infiltration, and delayed airway obstruction and hyperreactivity in canine peripheral airways. The purpose of this study was to determine whether ASF hypertonicity per se can account for these hyperventilation-associated effects. We first measured ASF osmolality before and after normal (NSC) and hypertonic (HSC) saline aerosol challenges to document the magnitude of hypertonicity produced by these stimuli. We then measured canine peripheral airway resistance and reactivity to hypocapnia and aerosolized histamine before and after NSC and HSC. Cells and eicosanoid mediators recovered in bronchoalveolar lavage fluid at 5 and 24 h after NSC and HSC were examined. We found that HSC but not NSC caused acute ASF hyperosmolality, increased mediator release, and delayed airway hyperreactivity in the absence of mucosal injury and leukocyte infiltration. These observations suggest that ASF hyperosmolality contributes to the development of the late-phase response to hyperventilation and further suggest that hyperventilation-induced mucosal injury independently initiates leukocyte infiltration and late-phase airway obstruction.
J Appl Physiol (1985) 2000 Dec
PMID:Hypertonic saline aerosol increases airway reactivity in the canine lung periphery. 1109 May 60


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