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Cerebrovascular Regulation During an Insulin‐Glucose Challenge: Contribution of Nitric Oxide
Author(s) -
Ward Aaron T.,
Carter Katrina J.,
Sauder Christina J.,
Kellawan J. Mikhail,
Weiben Oliver,
Schrage William G.
Publication year - 2018
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.2018.32.1_supplement.712.16
Subject(s) - insulin , medicine , saline , cerebral blood flow , hemodynamics , nitric oxide , anesthesia , endocrinology , blood flow
While it is known that cerebral blood flow (CBF) is regulated by various chemical factors, such as arterial CO 2 , the role of nitric oxide (NO) in this regulation is unclear. NO production can be increased via numerous stimuli, including insulin. However, the CBF response to an insulin surge has yet to be fully examined. Additionally, the potential contribution of NO to an insulin surge remains poorly understood. Therefore, we tested the hypotheses that a) an insulin‐glucose challenge will increase CBF, and b) these effects will be attenuated by NO synthase inhibition (L‐NMMA). Four healthy adults (2 male, 2 female; age 21±1 yrs, height: 175±7 cm, weight: 61±4 kg) completed two visits (saline control vs. L‐NMMA) under fasted conditions (>10 hours) in a single‐blind placebo‐controlled study. CBF was measured via 4D MRI utilizing phase‐contrast vastly‐undersampled isotropic projection reconstruction (PC VIPR) at baseline and 60 mins following ingestion of a 75g Oral Glucose Tolerance Test (OGTT). L‐NMMA was infused at 36 mg/kg/hr for 5 min prior to baseline measurements with subsequent infusion at 1 mg/kg/hr for 60 min. Saline infusion was matched to L‐NMMA infusion rates. CBF was quantified as the sum of flow from both internal carotid arteries and the basilar artery. Hemodynamics (HR, MAP, ETCO 2 ) and glucose were monitored. Cerebrovascular conductance (CVC) was calculated as CBF÷MAP. HR, MAP, and ETCO 2 were similar between conditions and between time points (all p>0.05). Plasma glucose increased significantly from baseline to 60 mins (p<0.05) and did not differ between groups (p>0.05). CBF (saline 782±120 mL/min vs. L‐NMMA 700±106 mL/min) and CVC (saline 8.7±1.4 mL/min/mmHg vs. LNMMA 8.2±1.0 mL/min/mmHg), a difference of ~11% and ~7%, respectively, did not differ at baseline (p>0.05). During OGTT, CBF (saline 723±146 mL/min vs. L‐NMMA 694±138 mL/min) and CVC (saline 8.6±1.7 mL/min/mmHg vs. LNMMA 8.0±1.6 mL/min/mmHg) were similar between conditions (p>0.05) and did not change over time (p>0.05). L‐NMMA trended to reduce CBF (p=0.087) and CVC (p=0.057) overall. These data suggest that CBF does not significantly increase following an insulin‐glucose challenge. However, NO may mediate basal CBF regulation in healthy adults, suggesting additional endothelial‐mediated regulation of the cerebrovasculature. Support or Funding Information ADA 1‐16‐ICTS‐099 This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .