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

The influence of hypoxemia on the brain content of several organic acids and NH+4, AND ITS RELATIONship to the accompanying hypocapnia was studied in unanesthetized rats subjected to hypoxemia for periods ranging between 2 hours and 7 days. Under acute conditions, 'mild' hypoxemia (FO2 = 6--7%), these increases were greater and accompanied by increased gamma-aminobutyric acid (GABA) and decreased glutamic and aspartic acid levels; glutamine and NH+4 remained normal. When hypocapnia was prevented, 'severe' hypoxemia induced only a rise in GABA and slight elevations in lactic and alpha-ketoglutaric acid. During prolonged severe hypoxemia, the effects on the brain amino acids were maintained throughout, indicating that they are independent from the intracerebral pH which should progressively normalize. The effect on lactic acid gradually disappeared. The results show that during hypocapnic hypoxemia the rise in brain GABA is hypoxemia dependent, the decrease in glutamic and aspartic acid is hypocapnia dependent and the increase in lactic acid is in a large way alkalosis dependent.
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PMID:Brain amino acids in conscious rats in chronic normocapnic and hypocapnic hypoxemia. 92

In humans, hyperventilation (HV) has various effects on systemic physiology and, in particular, on neuronal excitability and synaptic transmission. However, it is far from clear how the effects of HV are mediated at the cortical level. In this study we investigated the effects of HV-induced hypocapnia on primary motor (M1) and visual cortex (V1) excitability. We used 1) motor threshold (MT) and phosphene threshold (PT) and 2) stimulus-response (S-R) curves (i.e., recruitment curves) as measures of excitability. In the motor cortex, we additionally investigated 3) the intrinsic inhibitory and facilitatory neuronal circuits using a short-interval paired-pulse paradigm. Measurements were performed before, during, and after 10 min of HV (resulting in a minimum end-tidal Pco(2) of 15 Torr). HV significantly increased motor-evoked potential (MEP) amplitudes, particularly at lower transcranial magnetic stimulation (TMS) intensities. Paired-pulse stimulation indicated that HV decreases intracortical inhibition (ICI) without changing intracortical facilitation. The results suggestthat low Pco(2) levels modulate, in particular, the intrinsic neuronal circuits of ICI, which are largely mediated by neurons containing gamma-aminobutyric acid. Modulation of MT probably resulted from alterations of Na(+) channel conductances. A significant decrease of PT, together with higher intensity of phosphenes at low stimulus intensities, furthermore suggested that HV acts on the excitability of M1 and V1 in a comparable fashion. This finding implies that HV also affects other brain structures besides the corticospinal motor system. The further exploration of these physiological mechanisms may contribute to the understanding of the various HV-related clinical phenomenona.
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PMID:Excitability of human motor and visual cortex before, during, and after hyperventilation. 1699 May 3