ArticleThe Journal of physiology1999
Effects of somatostatin on the control of breathing in humans.
Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 14 citations in OpenAlex.
- The retrotrapezoid nucleus and the neuromodulation of breathing.Journal of neurophysiology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
1. Somatostatin depresses the ventilatory response to hypoxia (AHVR). This study sought to determine whether somatostatin also reduced the peripheral chemoreflex sensitivity to hypercapnia, and if so, whether this was related to the reduction in AHVR. 2. Nine subjects completed the study. AHVR and the ventilatory responses to hypercapnia under both hyperoxic and hypoxic conditions were assessed both without and with an infusion of somatostatin (0.5 BsBs5mgBs5 h-1). Peripheral (fast) and central (slow) responses to hypercapnia were distingushed by use of a multi-frequency binary sequence input in end-tidal PCO2 (PET,CO2) that included 13 steps into and out of hypercapnia. 3. The acute ventilatory response to a reduction in end-tidal PO2 (PET,O2) from 100 to 50 Torr (at a PET, CO2 of +1.5-2.0 Torr above normal) was reduced from (mean +/- s.e.m. ) 16.4 +/- 3.3 to 9.5 +/- 3.2 l min-1 (P < 0.005, Student's t test) by somatostatin. The magnitude of the ensuing hypoxic ventilatory decline was unaltered (8.8 +/- 2.7 l min-1 in control vs. 8.0 +/- 2. 9 l min-1 with somatostatin). 4. The peripheral chemoreflex sensitivity to CO2 in hypoxia was reduced from 2.42 +/- 0.36 to 1.18 +/- 0.20 l min-1 Torr-1 (P < 0.005) with somatostatin. The reduction under hyperoxic conditions from 0.75 +/- 0.34 to 0.49 +/- 0.09 l min-1 Torr-1 did not reach significance. Central chemoreflex sensitivity to CO2 was unchanged. Changes in peripheral chemoreflex sensitivity to CO2 in hypoxia correlated with changes in AHVR. 5. We conclude that peripheral chemoreflex sensitivity to CO2 is reduced by somatostatin, probably via the same mechanism as that by which somatostatin exerts its effects on AHVR.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.