Cerebrovascular and corticomotor function during progressive passive hyperthermia in humans
Ross EZ, Cotter JD, Wilson L, Fan JL, Lucas SJ, Ainslie PN
Journal of applied physiology (Bethesda, Md. : 1985) · 57 citas
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Cómo se estudió
- Diseño
- Ensayo clínico controlado (clasificado por nuestro filtro de IA)
- Estudiado en
- Personas
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiación no declarada
Publicación
- Publicado
- 2011-12-03 · J Appl Physiol (1985) · vol. 112 · número 5 · págs. 748–758
- Editorial
- American Physiological Society
- Citado
- 73 citas · más que el 91% de estudios similares · 2.7× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 42 trabajos
- Acceso
- De pago
- Áreas de investigación
- Heart Rate Variability and Autonomic Control · Thermoregulation and physiological responses · Thermal Regulation in Medicine
- Palabras clave
- Transcranial magnetic stimulation, Anesthesia, Medicine, Middle cerebral artery, Hyperthermia, Cerebral blood flow, Ventilation (architecture), Cardiology, Stimulation, Femoral artery, Perfusion, Internal medicine, Ischemia
- MeSH
- muscle, skeletal, knee joint, middle cerebral artery, motor cortex, femoral nerve, humans, hyperventilation, fever, hypocapnia, carbon dioxide, blood flow velocity, electromyography, body temperature, blood pressure, cerebrovascular circulation, respiration, adult, female, male, transcranial magnetic stimulation
6 autores
- EMMA Z. ROSS🇬🇧 · autor de correspondenciaBrunel University of London; University of Brighton
- James David Cotter
- Luke C. Wilson🇳🇿University of Otago
- Jui‐Lin Fan🇨🇭University of Geneva
- Samuel J. E. Lucas🇳🇿University of Otago
- Philip Neil Ainslie🇨🇦University of British Columbia; University of British Columbia, Okanagan Campus
Resumen
El texto original del estudio, en el idioma en que se publicó.
The present study examined the integrative effects of passive heating on cerebral perfusion and alterations in central motor drive. Eight participants underwent passive hyperthermia [0.5°C increments in core temperature (Tc) from normothermia (37 ± 0.3°C) to their limit of thermal tolerance (T-LIM; 39.0 ± 0.4°C)]. Blood flow velocity in the middle cerebral artery (CBFv) and respiratory responses were measured continuously. Arterial blood gases and blood pressure were obtained intermittently. At baseline and each Tc level, supramaximal femoral nerve stimulation and transcranial magnetic stimulation (TMS) were performed to assess neuromuscular and cortical function, respectively. At T-LIM, measures were (in a randomized order) also made during a period of breathing 5% CO(2) gas to restore eucapnia (+5% CO(2)). Mean heating time was 179 ± 51 min, with each 0.5°C increment in Tc taking 40 ± 10 min. CBFv was reduced by ∼20% below baseline from +0.5°C until T-LIM. Maximal voluntary contraction (MVC) of the knee extensors was decreased at T-LIM (-9 ± 10%; P < 0.05), and cortical voluntary activation (VA), assessed by TMS, was decreased at +1.5°C and T-LIM by 11 ± 8 and 22 ± 23%, respectively (P < 0.05). Corticospinal excitability (measured as the EMG response produced by TMS) was unaltered. Reductions in cortical VA were related to changes in ventilation (Ve; R(2) = 0.76; P < 0.05) and partial pressure of end-tidal CO(2) (Pet(CO(2)); R(2) = 0.63; P < 0.05) and to changes in CBFv (R(2) = 0.61; P = 0.067). Interestingly, although CBFv was not fully restored, MVC and cortical VA were restored towards baseline values during inhalation of 5% CO(2). These results indicate that descending voluntary drive becomes progressively impaired as Tc is increased, presumably due, in part, to reductions in CBFv and to hyperthermia-induced hyperventilation and subsequent hypocapnia.
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