Twenty normal male subjects with brisk hypoxic ventilatory responses were recruited and ventilatory responses to sustained isocapnic hypoxia (SaO2 80.4 (SD 1.3)% for 20 min) were studied on separate days under four conditions: hypoxia alone, with or without domperidone, and 0.1 MAC of end-tidal isoflurane, with or without domperidone. Ventilatory variables were subjected to analysis of variance with estimation of the effects of isoflurane and domperidone, and their interaction. Isoflurane reduced the initial increase in ventilation significantly by 3.12 (95% confidence limits 1.69, 4.55) litre min-1 (P < 0.05) and domperidone increased the initial increase in ventilation by 1.78 (0.35, 3.21) litre min-1 (P < 0.05). Neither isoflurane nor domperidone affected the subsequent ventilatory decline. No interaction was found between these agents. These results confirm that 0.1 MAC of isoflurane suppressed the initial hypoxic ventilatory response but not the subsequent ventilatory decline when hypoxia was sustained. Domperidone offset the suppressive effect of isoflurane on the hypoxic ventilatory response but no interaction was detected.
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http://dx.doi.org/10.1093/bja/74.2.134 | DOI Listing |
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue
December 2024
Department of Critical Care Medicine, Qingdao Municipal Hospital, Qingdao 266001, Shandong, China.
Objective: To explore the quantitative analysis results of different patterns of chest computed tomography (CT) in patients with coronavirus infection and its relationship with viral load and pathophysiological status.
Methods: A retrospective clinical cohort study was conducted. Patients with coronavirus infection admitted to Qingdao Municipal Hospital from June 9 to 15, 2023 (all patients underwent chest CT examination within 24 hours after diagnosis) were enrolled.
Am J Physiol Lung Cell Mol Physiol
January 2025
Instituto de Ciencias Biomédicas, Universidad Autónoma de Chile, Santiago, Chile.
Chronic intermittent hypoxia (CIH), the main feature of obstructive sleep apnea, heightened chemosensory discharges of the carotid body (CB), which contributes to potentiate the ventilatory hypoxic response and elicits hypertension. We aimed to determine: 1) whether the persistence of cardiorespiratory alterations found in long-term CIH depend on the inputs from the CB and, 2) in what extension the activation of glial cells and neuroinflammation in the caudal region of the nucleus of the Solitary Tract (NTS) requires functional CB chemosensory activity. To evaluate these hypotheses, we exposed male mice to CIH for 60 days.
View Article and Find Full Text PDFJ Appl Physiol (1985)
January 2025
School of Sport, Exercise and Rehabilitation Sciences College of Life and Environmental Sciences University of Birmingham Edgbaston, Birmingham, UK.
The respiratory control system exhibits neural plasticity, adjusting future ventilatory responses based on experience. We tested the hypothesis that ventilatory long-term facilitation induced by hypercapnic acute intermittent hypoxia (AIH) at rest enhances subsequent ventilatory responses to steady-state exercise. Fourteen healthy adults (age = 27 ± 5 years; 7 males) participated in the study.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Geosciences, Princeton University, Princeton, NJ, 08540, USA.
Hypoxia tolerance and its variation with temperature, activity, and body mass, are critical ecophysiological traits through which climate impacts marine ectotherms. To date, experimental determination of these traits is limited to a small subset of modern species. We leverage the close coupling of carbon and oxygen in animal metabolism to mechanistically relate these traits to the carbon isotopes in fish otoliths (δC).
View Article and Find Full Text PDFRespir Physiol Neurobiol
December 2024
Department of Biology, Bates College, Lewiston, ME 04240, USA.
Chronic hyperoxia during early postnatal development depresses breathing when neonatal rats are returned to room air and causes long-lasting attenuation of the hypoxic ventilatory response (HVR). In contrast, little is known about the control of breathing of juvenile or adult mammals after chronic exposure to moderate hyperoxia later in life. Therefore, Sprague-Dawley rats were exposed to 60 % O for 7 days (juveniles) or for 4 and 14 days (adults) and ventilation was measured by whole-body plethysmography immediately after the exposure or following a longer period of recovery in room air.
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