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 effects of topical application of 15-hydroperoxy-eicosatetraenoic acid (15-HPETE, 200 micrograms/ml) on cerebral arterioles were studied in anesthetized cats equipped with cranial windows. 15-HPETE induced arteriolar dilation during application, sustained dilation 1 h after washout, and reduced responsiveness to the vasoconstrictive effects of hypocapnia. Electron microscopy of cerebral arterioles disclosed discrete endothelial lesions and focal morphological abnormalities of the vascular smooth muscle. Topical application of superoxide dismutase or catalase or the combination of the two inhibited the functional and morphological abnormalities induced by 15-HPETE. The results show that the vascular effects of 15-HPETE are mediated by superoxide anion radical and hydrogen peroxide or by other radicals derived from them, such as the hydroxyl radical. The results, together with earlier findings, support the view that the oxygen radicals responsible for these cerebral vascular effects are generated via the prostaglandin hydroperoxidase reaction.
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PMID:Effects of 15-hydroperoxy-eicosatetraenoic acid (15-HPETE) on cerebral arterioles of cats. 643 43

In an experimental study the influences of beginning uremia were studied in nephrectomized rats. It was observed: (1) Though there was found a continuous decrease of extracellular pH due to accumulation of fixed acids there was a slight increase of intracellular pH resulting from concomitant hypocapnia. (2) There was found a constant loss of bicarbonate from the extra- and intracellular body compartment which was much more pronounced for the extracellular space. This loss of bicarbonate reflects the progressing metabolic acidosis and demonstrates that the intracellular compartment is more protected against an increase of hydrogen ion concentration than the extracellular space is. (3) The stability of the intracellular acid-base status during uremic metabolic acidosis arises the question whether our clinical practice with alkali substitution according to the Mellemgard-Astrup equation is still adequate in these cases. (4) Blood-gas analysis can only give information about the acid-base status of the extracellular body compartment. The large intracellular space which is the aim of our clinical therapy is excluded from these measurements. Simple reliance of blood-gas analysis may lead to wrong conclusions and mistakes in therapy.
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PMID:Influences of experimental uremia on the intra- and extracellular acid-base status of the rat. 644 28

Factors involved in blood oxygen transport were measured serially in the first, second and third trimester of pregnancy in 23 insulin-dependent diabetic women. Twenty-six non-pregnant diabetic patients served as a reference group. Diabetic pregnancy was associated with relative anemia, a significant increase in arterial pH, and hypocapnia. The concentration of red cell 2,3-diphosphoglycerate was significantly higher in the first trimester of diabetic pregnancy compared with non-pregnant diabetics (median value 16.4 vs. 15.0 mumol/g hemoglobin, p less than 0.02) and increased gradually from the first to the third trimester (16.4 to 17.2 mumol/g hemoglobin, p less than 0.01). The hemoglobin A1c concentration decreased simultaneously from 8.1% to 7.3% (p less than 0.01). The level of hemoglobin A1c in the first trimester was significantly lower than that in the non-pregnant diabetic patients (8.1 vs. 9.3%, p less than 0.01). In spite of the increase in red cell 2,3-diphosphoglycerate content and the decrease in hemoglobin A1c, factors known to reduce hemoglobin-oxygen affinity, the position of the oxyhemoglobin dissociation curve remained unchanged during diabetic pregnancy: P50 at actual pH in the first trimester, was 26.0 mmHg; in the second trimester, 26.9 mmHg, and in the third trimester, 26.8 mmHg (NS). These values of P50 at actual pH were identical with the value in the non-pregnant group (26.6 mmHg). Other factors influencing hemoglobin-oxygen affinity, such as hemoglobin concentration, hydrogen ion concentration and arterial oxygen saturation remained unchanged during diabetic pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Red cell 2,3-diphosphoglycerate and hemoglobin-oxygen affinity during diabetic pregnancy. 649 43

Acute respiratory alkalosis (blood pH, 7.60; arterial PCO2, 15 mmHg (1 mmHg = 133.322 Pa); plasma bicarbonate, 14 mM) was induced in nine anesthetized dogs by increasing their respiratory rate and depth. Renal glutamine extraction and ammonia production expressed per 100 mL of glomerular filtration rate did not change during acute hypocapnia, whereas arterial glutamine concentration decreased significantly from 0.47 to 0.36 mM. Hypocapnia did not change plasma potassium concentration and its urinary excretion. Acute hypocapnia increased lactate extraction and pyruvate production, whereas citrate extraction and glutamate and alanine production did not change. Citraturia remained minimal. Renal cortical glutamine concentration fell from 0.64 to 0.38 mM during hypocapnia while alpha-ketoglutarate, glutamate, malate, oxaloacetate, and citrate did not change. Lactate concentration rose from 1.1 to 2.0 mM. Glutamine concentration in the liver and muscle decreased following acute hypocapnia. Our data are compatible with the hypothesis that an acute respiratory alkalosis might not result in any change in the hydrogen ion concentration and (or) gradient between the mitochondrial matrix and the cytosol. Consequently, renal glutamine extraction and ammonia production are not reduced, renal cortical concentrations of relevant metabolites in the ammoniagenic pathway are not changed, and renal handling of citrate remains unaffected.
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PMID:Renal metabolism and ammoniagenesis during acute respiratory alkalosis in the dog. 649 24

Glomerular filtration rate (GFR) was altered by varying renal perfusion pressure in volume-expanded, anesthetized dogs infused with ethacrynic acid. Phosphate reabsorption varied linearly with GFR (r greater than 0.9), 0.83 of the increase in filtered load being reabsorbed. Phosphate reabsorption at comparable filtered loads was not significantly changed by raising plasma bicarbonate concentration from 30 to 55 mM and adjusting PCO2 to keep plasma pH constant. Plasma pH was altered by inducing hyper- and hypocapnia or infusing bicarbonate. Plasma phosphate concentration varied with plasma pH before phosphate infusion and was kept constant at 3.4 +/- 0.1 mM in intact and thyroparathyroidectomized dogs; some of which were also examined during hyperchloremic acidosis. At comparable GFR, phosphate and bicarbonate reabsorption correlated (r greater than 0.9), except during acidosis when the filtered load of bicarbonate became inadequate. In all experiments phosphate reabsorption and plasma pH correlated (r greater than 0.85). Compared with control values at plasma pH 7.4, phosphate reabsorption increased by about 40% during acidosis (pH 7.1) and decreased by about 50% during alkalosis (pH 7.8) both in intact and thyroparathyroidectomized dogs. We propose that net hydrogen ion secretion is the common determinant of phosphate and bicarbonate reabsorption.
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PMID:Glomerular filtration rate and plasma pH as determinants of phosphate reabsorption. 650 33

The arterial supply and venous drainage of the rabbit's brain were characterized by intravascular injection of casting material and intra-arterial administration of markers (crystal violet or dissolved hydrogen gas). The internal carotid artery supplies the homolateral cerebral cortex and subcortical structures except for the thalamus and the posterior portion of the nucleus caudatus; it also supplies the homolateral retina and optic nerve. No noncerebral structures are supplied by this artery. The dorsal sagittal sinus drains the dorsal and lateral parts of the frontal and parietal areas of the cerebral cortex, with no detectable extracerebral contamination. Electromagnetic measurement of flow in the internal carotid artery (ICBF), volumetric or H2-clearance measurement of flow in the dorsal sagittal sinus (SSBF), and H2-clearance determination in cerebral cortex yield comparable results on the cerebrovascular response to hyper- and hypocapnia. ICBF and SSBF are reliable and valid estimates of average blood flow through the homolateral cerebral hemisphere and the cerebral cortex, respectively.
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PMID:Cerebrovascular anatomy and blood flow measurements in the rabbit. 706 3

Patients with COPD usually are limited in their exercise tolerance by a limited ventilatory capacity. Lactic acidosis induced by exercise increases the stress on the ventilatory system due to CO2 generated by bicarbonate buffering and hydrogen ion stimulation. Patients with COPD are often observed to increase blood lactate levels at low levels of exercise. We wished to determine whether patients with COPD who experience lactic acidosis do so because of respiratory muscle production of lactate. Eight patients with moderate to severe COPD (FEV1 = 43.5 +/- 11.6% predicted) and 5 healthy subjects performed 10 min of moderate constant work rate exercise either breathing spontaneously or volitionally increasing their ventilation for 5 min to approximate the peak minute ventilation seen during incremental exercise. During volitional increased ventilation, 3% CO2 was added to the inspirate to prevent alkalosis and hypocapnia. In neither the healthy subjects nor the COPD group was the end-exercise lactate level significantly higher during volitional ventilation increase than during spontaneous ventilation. Further, in the COPD patients, the blood lactate levels during volitional ventilation increase were much lower than during maximal exercise (averaging 2.4 vs 5.3 mmol/L) despite similar ventilation levels (averaging 50 and 53 L/min). We conclude that it is unlikely that the respiratory muscles have an important influence on the blood lactate level elevation seen during maximal exercise in COPD patients.
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PMID:Contribution of the respiratory muscles to the lactic acidosis of heavy exercise in COPD. 758 24

The effects of halothane and sevoflurane on cat brain energy metabolism and regional cerebral blood flow (rCBF) were evaluated during normo- and hypocapnia. Brain energy status was evaluated with phosphorous nuclear magnetic resonance spectroscopy (31P-MRS) and rCBF was measured by the hydrogen clearance method. A high concentration of halothane (3 MAC) impaired brain energy metabolism, while even a higher concentration of sevoflurane (4 MAC) had no untoward effect on brain energy metabolism. At 3 MAC of halothane, there were measurable decreases in brain phosphocreatine (69% of the control) and increases in brain inorganic phosphate (about 250% of control Pi), even though CBF was about 70% of the control value. During hypocapnia, the phosphocreatine levels began to decrease at a Paco2 of 2.7 kPa with 2 MAC of sevoflurane (90% of the control), and at a Paco2 of 4.0 kPa with 2 MAC of halothane (92% of the control). rCBF had decreased to less than 50% of the control value when Paco2 was < or = 2.7 kPa with 2 MAC of sevoflurane and < or = 4.0 kPa with 2 MAC of halothane. Abnormal brain energy metabolism was only observed when rCBF was decreased to less than half of the control (non-anesthetized and normocapnic) value. Following administration of a vasopressor, metaraminol, the abnormal brain energy metabolism induced by 2 MAC of halothane at a Paco2 of 1.33 kPa was normalized in parallel with the improved rCBF values. We conclude that hyperventilation and fluctuating blood pressure contribute to the occurrence of abnormal brain energy metabolism during halothane and sevoflurane anesthesia. This is more pronounced with halothane than with sevoflurane. The hypocapnia-induced abnormality during exposure to 2 MAC of either agent was due to decreased CBF associated with low perfusion pressure, indicating that there was no direct effect of these anesthetics on cerebral energy metabolism.
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PMID:Brain energy metabolism and blood flow during sevoflurane and halothane anesthesia: effects of hypocapnia and blood pressure fluctuations. 827 58

The effects of halothane and sevoflurane on cat brain energy metabolism and regional cerebral blood flow (rCBF) were evaluated during normo- and hypocapnia. Brain energy status was evaluated with phosphorous nuclear magnetic resonance spectroscopy (31P-MRS) and rCBF was measured by the hydrogen clearance method. A high concentration of halothane (3 MAC) impaired brain energy metabolism, while even a higher concentration of sevoflurane (4 MAC) had no untoward effect on brain energy metabolism. At 3 MAC of halothane, there were measurable decreases in brain phosphocreatine (69% of the control) and increases in brain inorganic phosphate (about 250% of control Pi), even though CBF was about 70% of the control value. During hypocapnia, the phosphocreatine levels began to decrease at a PaCO2 of 2.7 kPa with 2 MAC of sevoflurane (90% of the control), and at a PaCO2 of 4.0 kPa with 2 MAC of halothane (92% of the control). rCBF had decreased to less than 50% of the control value when PaCO2 was < or = 2.7 kPa with 2 MAC of sevoflurane and < or = 4.0 kPa with 2 MAC of halothane. Abnormal brain energy metabolism was only observed when rCBF was decreased to less than half of the control (non-anesthetized and normocapnic) value. Following administration of a vasopressor, metaraminol, the abnormal brain energy metabolism induced by 2 MAC of halothane at a PaCO2 of 1.33 kPa was normalized in parallel with the improved rCBF values. We conclude that hyperventilation and fluctuating blood pressure contribute to the occurrence of abnormal brain energy metabolism during halothane and sevoflurane anesthesia. This is more pronounced with halothane than with sevoflurane.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Brain energy metabolism and blood flow during sevoflurane and halothane anesthesia: effects of hypocapnia and blood pressure fluctuations. 806 34

Acidosis has often been reported in inflamed tissues, and changes in strong relevant ions at the site of inflammation may provoke alterations in blood acid-base status. We measured changes in blood acid-base variables during carrageenan-induced inflammation in rats. We found a mixed acid-base disorder in rat blood during acute inflammation (12, 24, and 48 h). A metabolic acid contribution was found during the first 12 h and maintained further, as revealed by a decrease in plasma strong ion concentration difference ([SID]) and an increase in plasma weak acid concentration due to a rise in inorganic phosphate ([ATOT]P(i)). Plasma [SID] and [ATOT]P(i) changes were probably due to exchange of Na+ and P(i) between the inflammatory exudate and rat blood. A secondary respiratory compensation for the metabolic acid changes occurred in the blood of inflamed rats, resulting in significant hypocapnia. Furthermore, a progressive decrease in the total weak acid buffer concentration due to a decrease in plasma albumin ([ATOT]Alb) also counteracted the impact of changes in [SID] and P(i) to increase blood acidity. Therefore, despite the metabolic acid-base disorders induced by inflammatory processes, hydrogen ion (H+) homeostasis was maintained, and blood pH remained essentially unchanged in the inflamed rats.
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PMID:Blood acid-base changes during acute experimental inflammation in rats. 877 12


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