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)

To understand the interplay between microcirculatory control and carotid body (CB) function, we simultaneously measured carotid body microvascular PO2 (CBM PO2) and chemosensory activity in the cat in vivo under several experimental conditions. Cats were anesthetized with pentobarbital sodium, paralyzed, and artificially ventilated. CBs were exposed, and steady-state CBM PO2 was measured by the O2-dependent quenching of the phosphorescence of Pd-meso-tetra-(4-carboxyphenyl)porphine, which was administered intravenously. A few fibers of the carotid sinus nerve were used to record chemosensory discharges. At arterial PO2 (PaO2) of 103.4 +/- 4.1 Torr, CBM PO2 was 52.5 +/- 3.6 Torr (n = 9). Graded lowering of PaO2 from 160 to 50 Torr resulted in nearly proportional decreases in CBM PO2, but at lower PaO2 the decrease in CBM PO2 became more substantial. As PaO2 decreased, chemosensory discharge increased in parallel with CBM PO2. Hypercapnia and hypocapnia did not significantly change the relationship between PaO2 and CBM PO2, although the chemosensory discharge responded significantly. CBM PO2 and chemosensory discharge were not affected by hemorrhagic hypotension until arterial blood pressure fell below approximately 50 Torr and then CBM PO2 decreased and chemosensory discharge increased. The lack of a significant effect of hemorrhagic hypotension indicated that O2 delivery to CB was almost independent of the systemic blood pressure. Taken together, the observations suggest that CB microcirculation and PO2 are subject to control by intrinsic mechanisms and that CBM PO2 is compatible with oxidative metabolism playing a role in O2 chemoreception during hypoxia.
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PMID:Contribution of in vivo microvascular PO2 in the cat carotid body chemotransduction. 822 9

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.
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PMID:Central sleep apnoea and heart failure (Part I). 952 93

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.
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PMID:Central sleep apnoea and heart failure (part II). 965 53

Ammonia intoxication, which results in astrocytic edema and glutamine accumulation, blocks cerebral vasodilation during hypercapnia but not during hypoxia. Ammonia's effect on blood flow during hypocapnia is unclear, with some brain regions showing a paradoxical increase in flow. Here, we studied the responses to hypocapnia of pial arterioles not surrounded by astrocytic end feet to avoid mechanical compression by local edema. Blood flow was measured by microspheres in pentobarbital sodium-anesthetized rats equipped with closed cranial windows that permitted intravital microscopy. The normal pial arterial constriction in hypocapnia (12 +/- 1%; mean +/- SE) was blocked (2 +/- 1%) during a 6-h intravenous infusion of ammonium acetate, with some regions (cerebrum, midbrain) showing increased flow during hypocapnia. After pretreatment with methionine sulfoximine (MSO), which inhibits glutamine synthesis, the normal hypocapnic constrictor response was retained in pial arterioles (11 +/- 2%) during hyperammonemia. The increase in the calculated cerebrovascular resistance also was retained. An analog of MSO that does not block glutamine synthesis (buthionine sulfoximine) was ineffective in maintaining hypocapnic reactivity. In a sodium acetate-treated control group, MSO did not alter the pial arteriolar response. Normal vasoconstrictive ability was shown during ammonium infusion in response to U-46619, a thromboxane analog. We conclude that the inhibition of hypocapnic responsivity induced by ammonium is not due to paralysis of the pial arteriolar smooth muscle or to vascular compression by swollen astrocytes but is in some way due to glutamine metabolically produced from the ammonium.
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PMID:Preserved hypocapnic pial arteriolar constriction during hyperammonemia by glutamine synthetase inhibition. 995 Aug 45

We describe a 74-year-old patient with dyspnoea and tachypnoea induced by chlorpromadinone acetate, a synthetic progesterone used to treat prostatic hyperplasia. The dyspnoea, tachypnoea and hypocapnia improved after discontinuing the chlorpromadinone acetate. It is important to recognize that synthetic progesterones can cause dyspnoea and hyperventilation.
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PMID:Dyspnoea and hyperventilation induced by synthetic progesterone chlorpromadinone acetate for the treatment of prostatic hypertrophy. 1155 87

This investigation was designed to determine if suppression of testosterone alters the ventilatory response to carbon dioxide in the presence of high and low levels of oxygen. Eleven healthy male subjects completed a series of rebreathing trials during wakefulness, before and after treatment with a long-acting gonadotropin-releasing hormone agonist. Five subjects also completed studies during non-rapid eye movement (NREM) sleep. During wakefulness, subjects initially hyperventilated to reduce the partial pressure of carbon dioxide (P(ET,CO2)) below 25 Torr. Subjects then rebreathed from a bag containing a normocapnic (42 Torr), low (50 Torr) or high oxygen (140 Torr) gas mixture. During each trial P(ET,CO2) increased while oxygen was maintained at a constant level. The threshold of the ventilatory response to carbon dioxide was considered to be the point at which minute ventilation began to rise in a linear fashion as P(ET,CO2) increased. The slope of the ventilatory response above the threshold was used as a measure of sensitivity to carbon dioxide. During NREM sleep, hypocapnia was induced via nasal mechanical ventilation. Several trials were completed until the cessation of mechanical ventilation resulted in a central apnoea which demarcated the threshold of the ventilatory response to carbon dioxide. In response to treatment with leuprolide acetate, the threshold measured in wakefulness decreased during carbon dioxide rebreathing in the presence of low (41.05 +/- 0.77 versus 39.40 +/- 0.83 Torr; P = 0.01) and high (46.32 +/- 0.56 versus 44.78 +/- 0.83 Torr; P = 0.01) oxygen levels. An increase in sensitivity (4.82 +/- 0.61 versus 7.17 +/- 1.20 l min(-1) Torr(-1); P = 0.02) was also observed during rebreathing in the presence of high but not low oxygen levels. The increase in sensitivity was accompanied by an increase in carbon dioxide production. The findings observed during NREM sleep were similar to those observed during wakefulness, since the P(ET,CO2) that demarcated the threshold was decreased after leuprolide treatment (42.1 +/- 0.6 versus 39.6 +/- 0.6 Torr; P = 0.002). Additionally, the decrease in P(ET,CO2) required to induce an apnoea was greater after treatment with leuprolide (2.56 +/- 0.25 versus 4.06 +/- 0.29 Torr; P = 0.004). We conclude that suppression of testosterone decreases the threshold of the ventilatory response to carbon dioxide during both wakefulness and sleep.
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PMID:Treatment with leuprolide acetate decreases the threshold of the ventilatory response to carbon dioxide in healthy males. 1548 11

Severe, short-term decreases in alveolar Pco2 acutely lower intraocular pressure (IOP). We wondered if less severe, physiologically relevant Pco2 reductions would also lower ocular tension and if this effect would persist in the longer term. To investigate the acute influence of small Pco2 changes on IOP, 11 healthy persons hyperventilated to reduce end-tidal Pco2 by first 10% (5 min) and then 20% (5 min). IOP fell when Pco2 fell 20% (14.5 +/- 2.1 mm Hg vs, 16.8 +/- 1.0 in a matched control series; p < 0.05) and remained depressed 20 min after Pco2 had returned to baseline levels. To investigate the persistence over time of this hypocapnia-associated IOP reduction, nine healthy persons hyperventilated to reduce end-tidal Pco2 by 15% for 1 h. IOP was substantially reduced by 30 min (11.7 +/- 0.5 vs. 14.8 +/- 0.6 mm Hg; p < 0.05) and at 60 min (11.2 +/- 0.7 vs. 14.2 +/- 0.6 mm Hg; p < 0.05) of sustained hypocapnia. In contrast, when the effects of acute hypocapnia were compared with standard nonselective beta-adrenergic blockade (levobunolol HC1, 1 drop 0.5% solution instilled 12 and 2 h before study; N = 7 normals), a 20% Pco2 reduction was less effective in lowering IOP than was drug treatment, and induction of hypocapnia failed to alter IOP after drug treatment [baseline IOP 14.4 +/- 1.3 mm Hg vs. 10.0 +/- 1.6 mm Hg after levobunolol (p < 0.05) and 10.7 +/- 1.9 mm Hg after hypocapnia and levobunolol were combined]. In addition, 3 days' treatment with the ventilatory stimulant drug medroxyprogesterone acetate (150 mg/day in 10 men, initial IOP </= 18 mm Hg) significantly elevated ventilation and lowered Pco2 but failed to change IOP. We conclude that although IOP is clearly linked to Pco2 in the short term, manipulation of Pco2, either alone or in combination with drug therapy, may not be an effective means for long-term IOP reduction.
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PMID:Ocular hypotension during short- and long-term hypocapnia. 1992 Jun 1

This study sought to test the hypothesis that orthostasis-induced cerebral hypoperfusion would be less severe in physically active elderly humans (ACT group) than in sedentary elderly humans (SED group). The peak O(2) uptake of 10 SED (67.1 +/- 1.4 yr) and 9 ACT (68.0 +/- 1.1 yr) volunteers was determined by a graded cycling exercise test (22.1 +/- 1.2 vs 35.8 +/- 1.3 ml.min(-1).kg(-1), P < 0.01). Baseline mean arterial pressure (MAP; tonometry) and middle cerebral arterial blood flow velocity (V(MCA); transcranial Doppler) were similar between the groups (SED vs. ACT group: 91 +/- 3 vs. 87 +/- 3 mmHg and 54.9 +/- 2.3 vs. 57.8 +/- 3.2 cm/s, respectively), whereas heart rate was higher and stroke volume (bioimpedance) was smaller in the SED group than in the ACT group. Central hypovolemia during graded lower body negative pressure (LBNP) was larger (P < 0.01) in the ACT group than in the SED group. However, the slope of V(MCA)/LBNP was smaller (P < 0.05) in the ACT group (0.159 +/- 0.016 cm/s/Torr) than in the SED group (0.211 +/- 0.008 cm/s/Torr). During LBNP, the SED group had a greater augmentation of cerebral vasomotor tone (P < 0.05) and hypocapnia (P < 0.001) compared with the ACT group. Baseline MAP variability and V(MCA) variability were significantly smaller in the SED group than in the ACT group, i.e., 0.49 +/- 0.07 vs. 1.04 +/- 0.16 (mmHg)(2) and 1.06 +/- 0.19 vs. 4.24 +/- 1.59 (cm/s)(2), respectively. However, transfer function gain, coherence, and phase between MAP and V(MCA) signals (Welch spectral estimator) from 0.08-0.18 Hz were not different between SED (1.41 +/- 0.18 cm.s(-1).mmHg(-1), 0.63 +/- 0.06 units, and 38.03 +/- 6.57 degrees ) and ACT (1.65 +/- 0.44 cm.s(-1).mmHg(-1), 0.56 +/- 0.05 units, and 48.55 +/- 11.84 degrees ) groups. We conclude that a physically active lifestyle improves the intrinsic mechanism of cerebral autoregulation and helps mitigate cerebral hypoperfusion during central hypovolemia in healthy elderly adults.
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PMID:Chronic physical activity mitigates cerebral hypoperfusion during central hypovolemia in elderly humans. 2004 43


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