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Global Cerebrovascular Dysfunction in the Metabolic Syndrome Following Ischemic Stroke
Author(s) -
Branyan Kayla,
Brooks Steve,
DeVallance Evan,
Asano Shinichi,
Frisbee Jefferson,
Chantler Paul
Publication year - 2016
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.30.1_supplement.948.5
Subject(s) - medicine , stroke (engine) , middle cerebral artery , microvessel , endothelial dysfunction , cerebral blood flow , cerebral arteries , cardiology , insulin resistance , insulin , anesthesia , ischemia , mechanical engineering , immunohistochemistry , engineering
Insulin resistance is suggested to impact endothelial function by attenuating nitric oxide (NO) synthase activity, which is important for blood flow control. This reduction in insulin sensitivity and decrease in endothelial function leads to an increased risk for poor cardiovascular outcomes such as stroke. Many studies have examined the ipsilateral middle cerebral artery (MCA) to determine the effect of stroke on the cerebral microvasculature. Neither the contralateral MCA, nor the posterior cerebral arteries (PCA) have been thoroughly scrutinized to determine the more global impact of stroke on cerebrovascular function. Obese Zucker rats (OZRs) are used as a representative model of insulin resistance, where their lean counterparts (LZRs) are considered healthy controls. To look at the possible effect of decreased NO bioavailability on the ipsilateral and contralateral hemispheres of the brain, OZRs and LZRs were induced with stroke by transient middle cerebral artery occlusion (tMCAO) for 60 minutes. The purpose of this study was to compare the reactivity of both the ipsilateral and contralateral MCAs and PCAs at 24 hours post‐stroke to determine if stroke impacted the cerebral hemispheres differently. OZRs and LZRs were separated into sham and tMCAO groups. The ipsilateral and contralateral MCA and PCA were isolated and hung in a pressurized microvessel myobath. To assess endothelial function, the MCAs and PCAs were exposed to increasing doses of acetylcholine. A DAF‐FM diacetate assay was used to detect the amount of NO production in the aorta as a representative measure of NO synthesis within the vasculature. After 24 hours, LZR tMCAOs had lower NO production than the sham animals (p<0.05) but OZR tMCAOs did not have a significant decrease in NO release. LZR and OZR tMCAOs had similar NO production values after 24 hours. Both groups had decreases in their MCA and PCA reactivity 24 hours post‐stroke (p<0.05). In the MCAs, ipsilateral reactivity was lower in OZRs than in LZRs. This effect was not seen in the PCA, where both the contralateral and ipsilateral had similar decreases in reactivity in LZRs. OZR ipsilateral PCA reactivity was further attenuated from the contralateral (p<0.05). OZR MCA reactivity was improved by incubation with TEMPOL but not LZRs. This same effect was not seen in PCAs where TEMPOL did not improve dilation in either group. The results from this study suggest that NO bioavailability is important for endothelial function after an ischemic stroke. It also suggests that both hemispheres of the brain are affected by stroke, although not to the same degree. Likewise, vessels such as the PCA are also impaired by occlusion of the MCA suggesting a more global effect on the cerebral microvasculature. Support or Funding Information AHA NIH