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)

A patient had the rare combination of central neurogenic hyperventilation (PaCO2 of 9 torr) and a normal level of consciousness for eight days. Morphine attenuated but never corrected the hyperventilation. Experimental effects of hypocapnia, which decreases both cerebral blood flow and metabolism in humans, are at odds with the normal mentation initially seen in this patient despite her marked and persistent hypocapnia. Death occurred after progressive brainstem dysfunction. Pathological study showed a well-differentiated astrocytoma involving primarily the medulla and pons, with scattered tumor foci throughout the entire neuraxis. Possible mechanisms for central neurogenic hyperventilation are discussed briefly in relation to the pathological findings and the observed response to morphine.
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PMID:Central neurogenic hyperventilation in an awake patient with brainstem astrocytoma. 681 Jul 46

The retrotrapezoid nucleus (RTN) contains chemically defined neurons (ccRTN neurons) that provide a pH-regulated excitatory drive to the central respiratory pattern generator. Here we test whether ccRTN neurons respond to stimulation of the perifornical hypothalamus (PeF), a region that regulates breathing during sleep, stress and exercise. PeF stimulation with gabazine increased blood pressure, phrenic nerve discharge (PND) and the firing rate of ccRTN neurons in isoflurane-anaesthetized rats. Gabazine produced an approximately parallel upward shift of the steady-state relationship between ccRTN neuron firing rate and end-tidal CO(2), and a similar shift of the relationship between PND and end-tidal CO(2). The central respiratory modulation of ccRTN neurons persisted after gabazine without a change in pattern. Morphine administration typically abolished PND and reduced the discharge rate of most ccRTN neurons (by 25% on average). After morphine administration, PeF stimulation activated the ccRTN neurons normally but PND activation and the central respiratory modulation of the ccRTN neurons were severely attenuated. In the same rat preparation, most (58%) ccRTN neurons expressed c-Fos after exposure to hypercapnic hyperoxia (6-7% end-tidal CO(2); 3.5 h; no hypothalamic stimulation) and 62% expressed c-Fos under hypocapnia (approximately 3% end-tidal CO(2)) after PeF stimulation. Under baseline conditions (approximately 3% end-tidal CO(2), hyperoxia, no PeF stimulation) few (11%) ccRTN neurons expressed c-Fos. In summary, most ccRTN neurons are excited by posterior hypothalamic stimulation while retaining their normal response to CNS acidification. ccRTN neurons probably contribute both to the chemical drive of breathing and to the feed-forward control of breathing associated with emotions and or locomotion.
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PMID:Activation of the retrotrapezoid nucleus by posterior hypothalamic stimulation. 1975 19