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The dynamics of cerebral blood flow leading up to pre‐syncope in heat stressed humans
Author(s) -
Shibasaki Manabu,
Sato Kohei,
Crandall Craig,
Ogoh Shigehiko
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.528.6
Subject(s) - medicine , presyncope , anesthesia , cerebral blood flow , cerebral perfusion pressure , middle cerebral artery , heat stress , cardiology , perfusion , blood pressure , heart rate , ischemia , atmospheric sciences , geology
Whole‐body heat stress reduces tolerance to lower‐body negative pressure (LBNP). Lucas et al. (Am J Physiol, 2013) previously showed that elevating cerebral perfusion early in LBNP challenge (via breathing a hypercapnic gas mixture) did not restore LBNP tolerance. However, that study only evaluated blood velocity responses from the middle cerebral artery (MCA). Given regional differences in CO 2 responsiveness in the cerebral circulation, that work may not accurately reflect global cerebral perfusion responses to LBNP, as it did not account for perfusion from the anterior or posterior cerebral arteries. To address this deficit, seven healthy volunteers performed progressive LBNP to presyncope during passive heat stress, with or without breathing a hypercapnic gas mixture (5% CO 2 , 21% O 2 , balanced N 2 ) prior to the onset of LBNP; the order of the trials were randomized and performed on separate days. Internal carotid artery (ICA) and vertebral artery (VA) blood flows were measured throughout LBNP. External canal temperature increased by ~1.4 °C during heat stress (via water‐perfused suit) and was maintained during LBNP in both trials. Heat stress decreased end‐tidal CO 2 (P ET CO 2 ) by ~3mmHg. Administration of the hypercapnic gas increased P ET CO 2 to a level greater than pre‐heat stress values (43.0±2.4 to 49.3±3.6mmHg), and P ET CO 2 remained at or above pre‐heat stress baseline (43.7±3.6mmHg) at the end of LBNP. LBNP tolerance, evaluated by cumulative stress index, was similar between trials. Heat stress slightly decreased both ICA and VA blood flows, and subsequent inhalation of the hypercapnic gas increased both by 125±37% and133±33%, respectively, from pre‐heat stress baseline. Of note, during LBNP, both ICA and VA blood flows in the hypercapnic trial were greater relative to the respective blood flows during the control LBNP trial (all P<0.05). However, at the termination of LBNP, due to pre‐syncopal symptoms, ICA and VA blood flows decreased to similar levels between the hypercapnic and control LBNP trials. These findings suggested that hypercapnia‐induced cerebral vasodilation is insufficient to maintain cerebral blood flow, resulting in a failure to improvement in LBNP tolerance in heat stressed humans. Support or Funding Information 18H03166 JSPS KAKENHI Grant‐in‐Aid This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .