Increased cerebral endothelium-dependent vasodilation in rats in the postcardiac arrest period

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Cardiovascular lability is common after cardiac arrest. We investigated whether altered endothelial function is present in cerebral and mesenteric arteries 2 and 4 h after resuscitation. Male Sprague-Dawley rats were anesthetized, intubated, ventilated, and intravascularly catheterized whereupon rats were randomized into four groups. Following 7 min of asphyxial cardiac arrest and subsequent resuscitation, cardiac arrest and sham rats were observed for either 2 or 4 h. Neuron-specific enolase levels were measured in blood samples. Middle cerebral artery segments and small mesenteric arteries were isolated and examined in microvascular myographs. qPCR and immunofluorescence analysis were performed on cerebral arteries. In cerebral arteries, bradykinin- induced vasodilation was inhibited in the presence of either calcium-activated K+ channel blockers (UCL1684 and senicapoc) or the nitric oxide (NO) synthase inhibitor, Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME), whereas the combination abolished bradykinin-induced vasodilation across groups. Neuron-specific enolase levels were significantly increased in cardiac arrest rats. Cerebral vasodilation was comparable between the 2-h groups, but markedly enhanced in response to bradykinin, NS309 (an opener of small and intermediate calcium-activated K+ channels), and sodium nitroprusside 4 h after cardiac arrest. Endothelial NO synthase and guanylyl cyclase subunit a-1 mRNA expression was unaltered after 2 h, but significantly decreased 4 h after resuscitation. In mesenteric arteries, the endothelium-dependent vasodilation was comparable between corresponding groups at both 2 and 4 h. Our findings show enhanced cerebral endothelium-dependent vasodilation 4 h after cardiac arrest mediated by potentiated endothelial-derived hyperpolarization and NO pathways. Altered cerebral endotheliumdependent vasodilation may contribute to disturbed cerebral perfusion after cardiac arrest.

OriginalsprogEngelsk
TidsskriftJournal of Applied Physiology
Vol/bind131
Nummer4
Sider (fra-til)1311-1327
Antal sider17
ISSN8750-7587
DOI
StatusUdgivet - okt. 2021

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