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 authors showed that 2,3-DPG red cell concentration (2,3-DPG) WAS SIGNIFICANTLY HIGHER DURING THE LAST WEEK Of the menstrual cycle of five women (1.08+/-0.09 mol-,p;Hb-1) (M +/- 1 SE) THAN DURING THE First part and the last but one week of the cycle (0.86+/-0.04 mol-molHb-1, p less than 0.01). PACO2 was significantly lower during the last week of the cycle (36.3+/-1.3 torr) than during the first part and the last but one week of the cycle(40.1+/-0.8 torr, p less than 0.001). This hypocapnia was due to transient hyperventilation in the second part of the menstrual cycle. 5 men were studied during 4 weeks to determinate control values. No change was observed. The 2,3-DGP mean value (1.10+/-0.01 mol-molGb-1) was not significantly different of the values observed in the women during the last week of the cycle. These results suggest that the 2,3-DPG increase during the last week of the menstrual cylce is problably due to a respiratory alkalosis induced by progesterone secretion.
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PMID:2,3-Diphosphoglycerate red cell concentration changes during the menstrual cycle in woman. 95 48

Hypophosphatemia revealed in patients with acute disorders of cerebral circulation was one of the causes of a decrease of the content of 2,3-DPG, ATP in red blood cells and of a reduction of Ca2(+)-ATPase activity in red blood cell membranes. In the given group of patients, hypophosphatemia was provoked by complete parenteral feeding, hypocapnia and by loss of phosphorus with urine and congestive gastrointestinal contents.
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PMID:[Causes, sequelae and possible ways of preventing hypophosphatemia in patients with cerebral ischemia]. 196 92

The first 5 days of treatment of 98 patients with acute disorders of the cerebral blood circulation revealed hypophosphatemia and related reduction of the level of 2, 3 DPG, ATP in the erythrocytes. The causes of hypophosphatemia in these patients were absence of entrance of phosphorus to the body, its loss with the urine and gastrointestinal contents and hypocapnia. The possible ways of correction of these disorders are discussed.
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PMID:[Characteristics of phosphorus metabolism in patients with acute disorders of cerebral circulation]. 262 71

To investigate the mechanisms underlying abnormal gas exchange in liver cirrhosis, 15 patients were studied while breathing room air, 11% O2, and 100% O2 in random sequence. Under basal conditions, patients showed mild reductions from normal in systemic and pulmonary vascular resistance, normal PaO2 (mean, 92.5 +/- 2.5 mm Hg), mild hypocapnia (mean, 34 +/- 0.7 mm Hg), and a slightly right-shifted oxyhemoglobin dissociation curve (P50, 27.2 +/- 0.4 mm Hg; 2,3-DPG, 13.1 +/- 0.6 mumol/g). Using the multiple insert gas elimination technique, we found mild to moderate ventilation-perfusion (VA/Q) inequality with a mean of 5% (range, 0 to 20%) of cardiac output (QT) perfusing low VA/Q ratio (less than 0.1) areas but no shunt. Breathing 11% O2, there were significant increases in QT, pulmonary artery pressure, and vascular resistance, whereas no changes occurred in VA/Q distribution, and there was no evidence for alveolar-endcapillary diffusion limitation for O2. In contrast, after 100% O2 shunt developed and VA/Q relationships worsened without significant hemodynamic changes. Furthermore, patients with cutaneous spider nevi (n = 8) showed more hepatocellular dysfunction (lower prothrombin values), lower systemic and pulmonary vascular resistance, less hypoxic pulmonary vasoconstriction (HPV), lower PaO2, and more VA/Q mismatch than did those without spiders. Our results confirm, therefore, that HPV is not fully abolished, as previously described, in hepatic cirrhosis. However, those patients with more advanced hepatic disease exhibit inadequate pulmonary vascular tone, which increases VA/Q inequality and lowers PaO2.
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PMID:Gas exchange and pulmonary vascular reactivity in patients with liver cirrhosis. 357 8

The concentration of red cell 2,3-diphosphoglycerate (2,3-DPG), hemoglobin-oxygen affinity and other oxygen transport variables were determined during first, second and third trimester of normal pregnancy as well as 3 months post partum in 18 healthy women. The median concentration of red cell 2,3-DPG increased significantly from the first to the third trimester (16.1 to 17.0 mumol/gHb, p less than 0.01), whereas 2,3-DPG decreased significantly post partum (p less than 0.01). Normal pregnancy was also associated with relative anemia, a significant increase in arterial pH, hypocapnia and hypophosphatemia. The difference in hemoglobin concentration from the first trimester to 3 months post partum was correlated inversely with the difference in red cell 2,3-DPG content (r = -0.52, p less than 0.05). In spite of the variations in red cell 2,3-DPG, hemoglobin-oxygen affinity expressed as P50 at actual pH remained unchanged during pregnancy and post partum. The study suggests that the increased level of 2,3-DPG during pregnancy may in part represent compensation for physiologic anemia and also compensate for a factor leading to increased hemoglobin-oxygen affinity during pregnancy.
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PMID:Red cell 2,3-diphosphoglycerate and hemoglobin--oxygen affinity during normal pregnancy. 649 42

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.
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PMID:The increased concentration of 2,3-diphosphoglycerate in red blood cells of spontaneously hypertensive rats. 944 32

The amount of O(2) available to tissues is essentially the product of cardiac output, [Hb], and O(2) saturation. Saturation depends on P(O2) and the O(2)Hb dissociation curve. With altitude, increased [2,3-DPG] shifts the dissociation curve rightward, but hypocapnia and alkalosis move it leftward. We determined both standard and in vivo P(50) in 5 fit subjects decompressed over 42 days in an altitude chamber to the equivalent of the Mt. Everest summit (Operation Everest II). Arterial and venous blood was sampled at five "altitudes " (P(B) = 760, 429, 347, 282, 253 mmHg), and P(O2), P(CO2), pH, O(2) saturation, [Hb] and [2,3-DPG] were measured. As reported previously, 2,3-DPG levels increased from 1.7 (P(B) = 760) to 3.8 mmol/L (P(B) = 282). Standard P(50) also increased (from 28.2 mmHg at sea level to 33.1 on the summit, p<0.001). Alone, this would have lowered saturation by 12 percentage points at a summit arterial P(O2) of approximately 30 mmHg. However, in vivo P(50) remained between 26 and 27 mmHg throughout due to progressive hypocapnia and alkalosis. Calculations suggest that the increase in standard P(50) did not affect summit V(O2 MAX)), alveolar, arterial and venous P(O2)'s, but reduced arterial and venous O(2) saturations by 8.4 and 17.4 points, respectively, and increased O(2) extraction by 7.9 percentage points. Reduced saturation was balanced by increased extraction, resulting in no significant overall O(2) transport benefit, thus leaving unanswered the question of the purpose of increased [2,3-DPG] concentrations at altitude.
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PMID:Hemoglobin P(50) during a simulated ascent of Mt. Everest, Operation Everest II. 1739 15