Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten patients with the Pickwickian syndrome, characterized by obesity, hypoxemia, hypercapnia, polycythemia, and cor pulmonale, underwent long-term treatment as outpatients with medroxyprogesterone acetate. Although there was no significant weight change in the group, PaO2 rose 12.6 +/- 2.7 mm Hg (SEM) from 49 +/- 2.6 mm Hg to 62 +/- 2.3 mm Hg (P less than 0.001), while PaCO2 fell 13 +/- 2.6 mm Hg from 51 +/- 1.9 mm Hg to 38 +/- 1.2 mm Hg (P less than 0.001). Hematocrit fell from 56 +/- 2.5% to 50 +/- 1.2%, a mean fall of 6% (P less than 0.01), during medroxyprogesterone acetate therapy. In the 2 patients who had cardiac catheterization before and during medroxyprogesterone acetate therapy, mean pulmonary arterial pressure fell 13 and 19 mm Hg. There were no recurrences of cor pulmonale during treatment. These effects on arterial blood gas values and clinical state were sustained during therapy. On withdrawal of medroxyprogesterone acetate during 1-month period, arterial oxygen and carbon dioxide tensions deteriorated to their previous pretreatment values. Reinstitution of medroxyprogesterone acetate caused improvement in both the oxygen and carbon dioxide tensions. We conclude that sublingual medroxyprogesterone acetate therapy is useful in the management of the Pickwickian syndrome.
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PMID:Progesterone for outpatient treatment of Pickwickian syndrome. 110 59

Hyperammonemia increases brain glutamine levels, causes astrocytic swelling, and depresses cerebral blood flow (CBF) responsivity to CO2. Methionine sulfoximine (MSO) inhibition of glutamine synthetase activity, known to be enriched in astrocytes, prevents ammonia-induced increases in brain glutamine and water content. We tested the hypothesis that inhibition of glutamine accumulation restores CBF responsivity to CO2 during acute hyperammonemia. Pentobarbital-anesthetized rats treated with either vehicle or MSO (150 mg/kg i.p.) received a 6-hour intravenous infusion of either sodium or ammonium acetate. With subsequent induction of hypercapnia, CBF increased from 113 +/- 14 (mean +/- SEM) to 194 +/- 9 ml/min per 100 g in control rats but was unchanged from 107 +/- 13 to 79 +/- 10 ml/min per 100 g in hyperammonemic rats. Treatment with MSO in hyperammonemic rats restored the CBF response to hypercapnia (from 73 +/- 8 to 141 +/- 14 ml/min per 100 g). With induction of hypocapnia, CBF decreased from 114 +/- 11 to 88 +/- 11 ml/min per 100 g in control rats but increased from 112 +/- 13 to 142 +/- 19 ml/min per 100 g in hyperammonemic rats. Treatment with MSO in hyperammonemic rats did not fully restore the response to hypocapnia but prevented the paradoxical increase in CBF (from 80 +/- 8 to 80 +/- 8 ml/min per 100 g). In control rats, MSO did not affect CO2 responsivity. Treatment with MSO prevented ammonia-induced increases in intracranial pressure. Hyposmotic-induced increases in brain water content and intracranial pressure attenuated the CBF response to hypercapnia but, unlike hyperammonemia, did not attenuate the response to hypocapnia. In contrast to hypercapnia, vasodilation in response to arterial hypotension was intact in hyperammonemic rats. We conclude that the grossly abnormal CBF responsivity to CO2 alterations during hyperammonemia is linked to glutamine accumulation rather than ammonia per se. Cerebral edema secondary to glutamine accumulation may contribute in part to abnormal CBF responses, although other aspects of astrocyte dysfunction are likely to be important.
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PMID:Restoration of cerebrovascular CO2 responsivity by glutamine synthesis inhibition in hyperammonemic rats. 139 82

In 20 patients with chronic renal failure on a hemodialysis with acetate-containing dialysing fluid gasometric, ventilation and breathing patterns disturbances were determined. The loss of CO2 in the dialysate is attributed the major cause of hypoxemia due to alveolar hypoventilation. Hemodialysis with bicarbonate-containing dialysate can be performed in the absence of any change in ventilation and PaO2 despite a systemic alkalosis. Hyperventilation during HD with high concentration of bicarbonate indicate that changes in CO2 tension in the pulmonary circulation can lead to a change in minute ventilation due to the presence of slowly adapting pulmonary chemoreceptors. In patients with low respiratory response, respiratory muscle weakness intensified additionally by hypercapnia may explain this phenomenon.
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PMID:[Effect of carbon dioxide (CO2) pressure on minute ventilation, parameters of gas exchange and blood gases during hemodialysis using fluid containing acetate and bicarbonate buffers]. 143 19

The effects of almitrine bismesylate and medroxyprogesterone acetate on oxygenation during wakefulness and sleep were compared in six patients with chronic obstructive lung disease and carbon dioxide retention. Patients received 1.5 mg/kg almitrine (a peripheral chemoreceptor stimulant), 100 mg of medroxyprogesterone (a central respiratory stimulant), or matched placebo daily for 15 days in random order in a crossover trial. When subjects were awake almitrine increased the ventilatory response to hypoxia and increased arterial oxygen tension (PaO2) to a greater extent than medroxyprogesterone, whereas medroxyprogesterone augmented the ventilatory response to hypercapnia and decreased arterial carbon dioxide tension (PaCO2) to a greater extent than almitrine. Neither drug influenced sleep architecture significantly, except that medroxyprogesterone increased the number of arousals. Almitrine had a more favourable effect than placebo on oxygenation as estimated from arterial oxygen saturation (SaO2) during the different stages of sleep, the number of episodes of hypoxaemia, and the amount of time that SaO2 was below 80%. The only change with medroxyprogesterone by comparison with placebo was a decrease in the number of hypoxaemic episodes. It is concluded that both active drugs improved blood gases during wakefulness, but that 1.5 mg/kg of almitrine is superior to 100 mg of medroxyprogesterone in improving SaO2 during sleep.
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PMID:Comparison of almitrine bismesylate and medroxyprogesterone acetate on oxygenation during wakefulness and sleep in patients with chronic obstructive lung disease. 214 54

Twelve patients with chronic obstructive pulmonary disease (COPD) were studied to determine the effect of ventilatory stimulation with chlormadinone acetate (CMA), a potent synthetic progesterone, on chemical and neuromechanical respiratory controls and pulmonary gas exchange. Using a randomized, double-blind, cross-over trial, 1 wk of CMA therapy caused a significant reduction in arterial CO2 tension (Paco2) by 4.6 +/- 0.6 (SE) mmHg. This Paco2 fall was associated with increased minute ventilation (Vl), tidal volume (VT), and mean inspiratory flow (VT/Tl). During CMA administration, occlusion pressure response to CO2 with and without inspiratory flow-resistive loading increased significantly (p less than 0.01) over that during placebo administration, whereas ventilatory response to CO2 did not. In addition, normocapnic ventilatory and occlusion pressure response to hypoxia were significantly elevated (p less than 0.01) during CMA therapy. Furthermore, the degree of load compensation, which was assessed by the ratio of the loaded to unloaded slope in the occlusion pressure response to CO2, increased in all subjects after CMA administration. These results indicate that CMA augments not only the respiratory neuromuscular response to hypercapnia and hypoxia, but also flow-resistive load compensation in patients with COPD, and it may provide support for the use of CMA in patients who are able to decrease their Paco2 with this agent.
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PMID:Effect of chlormadinone acetate on ventilatory control in patients with chronic obstructive pulmonary disease. 242 22

Plasma ADH, PA and PRA in patients with respiratory failure (RF) were studied. RF patients were divided into 4 groups, i.e. acute RF (ARF) and chronic RF (CRF), with or without hypercapnia. The levels of these hormones were significantly higher in RF than those in control subjects, moreover, they were markedly elevated in ARF than those in CRF. In multiple regression analysis, ADH correlated with PaO2, pH and PRA in RF patients, but correlated with serum osmolality in control subjects. It was considered that ADH in RF was affected by the direct effect of blood gases and circulatory disorder. The mechanism of elevated PA and PRA in RF probably was mediated through restriction of intake of water and Na, reduction of renal blood flow and decreased ACE often occurred in RF. Abnormally elevated hormones are more often recognized in edematous patients than in nonedematous patients. It was suggested that many patients with RF develop heart failure or edema due to hormonal abnormalities.
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PMID:[ADH (anti-diuretic hormone), aldosterone (PA) and renin activity (PRA) in patients with respiratory failure]. 269 88

We studied the effects of medroxyprogesterone acetate, a respiratory stimulant, on the incidence and duration of episodes of apnea and disordered breathing in 13 nonhypercapnic men with obstructive sleep apnea. Nocturnal polysomnography was done before and after four weeks of treatment with medroxyprogesterone acetate (60 mg/day) and one week after cessation of treatment. There were no significant (p less than 0.05) differences in the mean frequency of apneic episodes per hour of sleep before (31.3 +/- 5.7 [+/- SE]), during (26.8 +/- 6.6), or after (23.6 +/- 7.0) treatment, or in the mean number of disordered breathing episodes per hour of sleep before (19.4 +/- 5.6), during (21.4 +/- 5.8), or after (23.1 +/- 6.3) the period of treatment. Medroxyprogesterone did not alter significantly the total time of apnea or the total time for disordered breathing, expressed as percentages of total sleep time. Arterial oxygen desaturation during apnea and disordered breathing did not change with treatment. Medroxyprogesterone increased the minute ventilation and occlusion pressure responses to hypercapnia measured in the awake state; however, the results of this study demonstrate that medroxyprogesterone does not improve the breathing disorders during sleep in the nonhypercapnic patient with obstructive sleep apnea.
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PMID:Effects of medroxyprogesterone acetate in obstructive sleep apnea. 294 59

Previous studies have shown that some patients with chronic obstructive lung disease and hypercapnia will respond to medroxyprogesterone with improvement in arterial blood gases. The exact mechanism of this effect is unclear but it is presumed to be a result of ventilatory stimulation. To determine whether the ability to correct arterial blood gas abnormalities by voluntary hyperventilation would predict a subsequent favourable response to progesterone, we studied 11 subjects with chronic obstructive lung disease and chronic hypercapnia. Five subjects had chronic obstructive lung disease of moderate severity with mean (SE) FEV1 1.8 (0.34) 1 maximum voluntary ventilation (MVV) 40.4 (7.16) 1/min-1, arterial oxygen tension (Pao2) 53.8 (2.40 mm Hg, and arterial carbon dioxide tension Paco2) 49.6 (3.91) mm Hg, and were able to normalise their blood gas tensions during voluntary hyperventilation (Pao2 85.4 (8.01) mm Hg; Paco2 32.8 (3.43) mm Hg). Six subjects had severe chronic obstructive lung disease with FEV1 0.77 (0.12) 1, MVV 19 (3.09) 1/min-1, Pao2 60.0 (2.89) mm Hg and Paco2 50.5 (1.38) mm Hg, and they could not significantly alter their blood gases with voluntary hyperventilation (Pao2 62.5 (3.19) mm Hg, Paco2 49.7 (1.84) mm Hg). The groups were similar in age, height, weight, and resting Pao2 and Paco2. Each subject received one month of oral placebo and one month of medroxyprogesterone acetate (Provera). 20 mg orally thrice daily, given in a randomised, double blind fashion. The groups responded similarly with a significantly higher Pao2 and lower Paco2 while having medroxyprogesterone acetate than while having placebo. Two patients with polycythaemia showed a reduction in haemoglobin concentration while taking progesterone. It is concluded that the response to medroxyprogesterone is not predictable from spirometric or blood gas changes after voluntary hyperventilation.
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PMID:Oral progesterone treatment in chronic obstructive lung disease: failure of voluntary hyperventilation to predict response. 294 45

To further study the relationship between ventilatory response (VR) and exercise performance, and to investigate to what extent progesterone is responsible for ventilatory changes in the luteal phase of the menstrual cycle, we administered medroxyprogesterone acetate (MPA) to 10 normal males (20 mg three times a day for 5 doses) and compared results with those obtained in a similar study of females. With MPA, there was an increase in the resting VR to hypercapnia; the resting VR to hypoxia was not changed. There was a respiratory alkalosis at rest. During exercise, the PaCO2 remained lower but the pHa was not different because of a tendency toward lower bicarbonate concentration with MPA. Ventilation, when related to CO2 output, was increased at all exercise loads, indicating increased VR to endogenous CO2. However, ventilation was only minimally (3%) increased when related to oxygen uptake or workload. This apparent disparity is because of slightly lower CO2 output at a given oxygen uptake with MPA. As in females, maximal duration of exercise and maximal oxygen uptake were unchanged. Except for degree, MPA induced all the ventilatory changes seen in the menstrual cycle. Increased VR does not adversely affect exercise performance.
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PMID:Progesterone-induced changes in exercise performance and ventilatory response. 295 62

Studies of acutely induced hyperammonemia and chronic hyperammonemia associated with liver dysfunction suggest that cerebral blood flow (CBF) and O2 consumption (CMRO2) become uncoupled and that CMRo2 may depend on arterial CO2 tension (PaCO2). We examined CBF (radiolabeled microspheres) and CMRO2 during hypercapnia (PaCO2 congruent to 74 Torr) and hypocapnia (PaCO2 congruent to 21 Torr) both before and during intravenous ammonium acetate infusion in pentobarbital-anesthetized dogs. Continuous infusion over 120 min produced stable increases of arterial ammonia levels (1,400 mumol/l) by 30 min, whereas CBF, CMRO2, and O2 extraction (measured at sagittal sinus) remained unchanged when PaCO2 was held constant (congruent to 35 Torr). Acute hyperammonemia attenuated the increase in CBF during hypercapnia by 44% and abolished the decrease in CBF during hypercapnia. Regional blood flow to pons and midbrain increased under normocapnic conditions, and midbrain blood flow increased further during hypocapnia. Sodium acetate infusion did not affect CBF responses to CO2. Thus we failed to observe an uncoupling of global CBF and CMRO2 during normocapnic hyperammonemia, or an interaction of CO2 and ammonia on CMRO2, although the increased pons and midbrain blood flow may reflect regional effects of ammonia on reticular activating system metabolism. On the basis of the literature, we suggest that the attenuated hypercapnic CBF response may arise from impaired glial regulation of extracellular potassium and bicarbonate concentrations and that lactic acid production, enhanced by combined alkalosis and hyperammonemia, may contribute to the abolition of hypocapnic vasoconstriction.
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PMID:Interaction of CO2 and ammonia on cerebral blood flow and O2 consumption in dogs. 392 Sep 20


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