Background: Neurological injury, the leading cause of death after cardiac arrest resuscitation, has been shown to worsen progressively in the post-cardiac arrest period. This deterioration may be due to impaired cerebral autoregulation, leading to harmful alterations in cerebral perfusion. We aimed to investigate the myogenic response, a key component of cerebral autoregulation, in the post-cardiac arrest period. Method: Rats were anesthetized, intubated, catheterized, and randomized into a sham group or cardiac arrest group. Cardiac arrest rats underwent 7 minutes of cardiac arrest. Subsequently, groups were observed for 4 hours. Middle cerebral arteries (MCAs) were examined utilizing pressure myography and confocal microscopy. qPCR was performed on the posterior communicating arteries. Results: The myogenic response to increasing levels of intraluminal pressure was significantly reduced in MCAs from cardiac arrest rats compared with sham (p=0.02, mixed model for repeated measures). The MCAs demonstrated comparable contraction to increasing concentrations of U46619, but a high K + solution yielded significantly lower vasoconstriction in cardiac arrest MCAs compared with sham (sham: 152±5 µm and cardiac arrest: 166±3 µm, p=0.03). qPCR showed reduced gene expression of cytoplasmic tyrosine kinase ABL1, rho-associated protein kinase 1, and endothelial NO synthase in cerebral arteries from cardiac arrest rats compared with sham. Confocal microscopy revealed no significant differences in nitrotyrosine or F-actin expression between groups in MCAs. Conclusion: In rat MCAs, the myogenic response, myogenic tone, and the maximum contraction are significantly reduced 4 hours after cardiac arrest. Our results suggest impaired calcium-sensitizing mechanisms in cerebral myogenic vasoconstriction after cardiac arrest.
Hansen et al. (Mon,) studied this question.