Cerebral metabolism, oxidation and inflammation in severe passive hyperthermia with and without respiratory alkalosis
Bain AR, Hoiland RL, Donnelly J, Nowak-Flück D, Sekhon M, Tymko MM, Greiner JJ, DeSouza CA, Ainslie PN
The Journal of physiology · 21 citas
Etiquetas de revisión
Solo mecanismosDatos neutrales que nuestra revisión registró sobre cómo se hizo este estudio. Describen el método, nunca si nos gusta el resultado.
Cómo se estudió
- Diseño
- Ensayo clínico controlado (clasificado por nuestro filtro de IA)
- Estudiado en
- Personas
- Resultado principal
- Solo mecanismos
Quién lo pagó
- Financiación
- Financiación independiente
- Gobierno
- National Institutes of Health
- Gobierno
- NIH HHS
- Subvenciones
- National Institutes of Health (HL077450); National Institutes of Health (HL107715)
Según 2 financiadores declarados.
Publicación
- Publicado
- 2020-01-04 · J Physiol · vol. 598 · número 5 · págs. 943–954
- Editorial
- Wiley
- Citado
- 25 citas · más que el 83% de estudios similares · 1.6× el promedio de su campo
- Referencias
- 45 trabajos
- Acceso
- De pago
- Áreas de investigación
- Thermoregulation and physiological responses · Thermal Regulation in Medicine · Climate Change and Health Impacts
- Palabras clave
- Respiratory alkalosis, Inflammation, Hyperthermia, Respiratory system, Medicine, Alkalosis, Metabolism, Cardiology, Anesthesia, Internal medicine, Acidosis, Metabolic acidosis
- MeSH
- brain, humans, alkalosis, respiratory, inflammation, fever, cerebrovascular circulation, male, hyperthermia
9 autores
- Anthony Richard Bain🇨🇦 · autor de correspondenciaUniversity of Windsor
- Ryan L. Hoiland🇨🇦Interior Health; University of British Columbia; University of British Columbia, Okanagan Campus
- Joseph E. Donnelly🇬🇧University of Cambridge; Addenbrooke's Hospital
- Daniela Nowak‐Flück🇨🇦Interior Health; University of British Columbia; University of British Columbia, Okanagan Campus
- Mypinder S. Sekhon🇨🇦Interior Health; University of British Columbia; University of British Columbia, Okanagan Campus
- Michael M. Tymko🇨🇦Interior Health; University of British Columbia; University of British Columbia, Okanagan Campus
- Jared J. Greiner🇺🇸University of Colorado Boulder; Integrative Medicine Institute
- Christopher A. DeSouza🇺🇸University of Colorado Boulder; Integrative Medicine Institute
- Philip Neil Ainslie🇨🇦Interior Health; University of British Columbia; University of British Columbia, Okanagan Campus
Resumen
El texto original del estudio, en el idioma en que se publicó.
Key points
It was unknown whether respiratory alkalosis impacts the global cerebral metabolic response as well as the cerebral pro-oxidation and inflammatory response in passive hyperthermia. This study demonstrated that the cerebral metabolic rate was increased by ∼20% with passive hyperthermia of up to +2°C oesophageal temperature, and this response was unaffected by respiratory alkalosis. Additionally, the increase in cerebral metabolism did not significantly impact the net cerebral release of oxidative and inflammatory markers. These data indicate that passive heating of up to +2°C core temperature in healthy young men is not enough to confer a major oxidative and inflammatory burden on the brain, but it does markedly increase the cerebral metabolic rate, independently of PaCO2 .
Abstract
There is limited information concerning the impact of arterial PCO2 /pH on heat-induced alteration in cerebral metabolism, as well as on the cerebral oxidative/inflammatory burden of hyperthermia. Accordingly, we sought to address two hypotheses: (1) passive hyperthermia will increase the cerebral metabolic rate of oxygen (CMRO2 ) consistent with a combined influence of Q10 and respiratory alkalosis; and (2) the net cerebral release of pro-oxidative and pro-inflammatory markers will be elevated in hyperthermia, particularly in poikilocapnic hyperthermia. Healthy young men (n = 6) underwent passive heating until an oesophageal temperature of 2°C above resting was reached. At 0.5°C increments in core temperature, CMRO2 was calculated from the product of cerebral blood flow (ultrasound) and the radial artery-jugular venous oxygen content difference (cannulation). Net cerebral glucose/lactate exchange, and biomarkers of oxidative and inflammatory stress were also measured. At +2.0°C oesophageal temperature, arterial PCO2 was restored to normothermic values using end-tidal forcing. The primary findings were: (1) while CMRO2 was increased (P 2 , irrespective of arterial pH.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial.
Confianza de la comunidad
Cargando…
¿Cuánto confías en los hallazgos de este estudio?
Comentarios
¿Algo está mal aquí?
Señala este estudio si su información, etiquetas o financiación parecen incorrectas. Un editor revisa cada señalamiento.
Información educativa sobre investigación publicada. No es consejo médico ni una recomendación para empezar o dejar nada.