The effects of reduced end-tidal carbon dioxide tension on cerebral blood flow during heat stress

摘要

Passive heat stress reduces arterial carbon dioxide partial pressure (P_aco_2) as reflected by 3 to 5 Torr reductions in end-tidal carbon dioxide tension (Petco2)- Heat stress also reduces cerebrovascular conductance (CBVC) by up to 30%. While P_aCo_2 is a strong regulator of CBVC, it is unlikely that the relatively small change in Petco2 during heating is solely responsible for the reductions in CBVC. This study tested the hypothesis that P_aco_2> referenced by P_etco_2> is not the sole mechanism for reductions in CBVC during heat stress. Mean arterial blood pressure (MAP), P_Etco_2> middle cerebral artery blood velocity (MCA V_meam), and calculated CBVC (MCA V_mean/MAP) were assessed in seven healthy individuals, during three separate conditions performed sequentially: (1) normothemia, (2) control passive heat stress and (3) passive heat stress with Petco2 clamped at the normothermic level (using a computer-controlled sequential gas delivery breathing circuit). MAP was similar in the three thermal conditions (P = 0.55). Control heat stress increased internal temperature ~ 1.3 deg C, which resulted in decreases in P_etco_2 , MCA Vmean and calculated CBVC (P < 0.001 for all variables). During heat stress + clamp conditions internal temperature remained similar to that during the control heat stress condition (P = 0.31). Heat stress + clamp successfully restored P_etco_2 to the normothermic level (P = 0.99) and increased MCA V_mean (P= 0.002) and CBVC (P = 0.008) relative to control heat stress. Despite restoration of P-Etco_2> MCA V_mem (P = 0.005) and CBVC (P = 0.03) remained reduced relative to normothermia. These results indicate that heat stress-induced reductions in P_aco_2> as referenced by Petco_2> contribute to the decrease in MCA V_mean and CBVC; however, other factors (e.g. perhaps elevated sympathetic nerve activity) are also involved in mediating this response.