Attenuated myogenic response and contractility in middle cerebral arteries after cardiac arrest: a randomized experimental rat study

Neurological injury, the leading cause of death after cardiac arrest resuscitation, has been shown to worsen progressively in the postcardiac 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 postcardiac arrest period. Rats were anesthetized, intubated, catheterized, and randomized into a sham group or cardiac arrest group. Cardiac arrest rats underwent 7 min of cardiac arrest. Subsequently, groups were observed for 4 h. Middle cerebral arteries (MCAs) were examined using pressure myography and confocal microscopy. qPCR was performed on the posterior communicating arteries. The myogenic response to increasing levels of intraluminal pressure was significantly reduced in MCAs from cardiac arrest rats compared with sham (<i>P</i> = 0.02, mixed model for repeated measures). The MCAs demonstrated comparable contraction with 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, <i>P</i> = 0.03). qPCR showed reduced gene expression of cytoplasmic tyrosine kinase ABL1, rho-associated protein kinase 1, and endothelial nitric oxide 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. In rat MCAs, the myogenic response, myogenic tone, and the maximum contraction are significantly reduced 4 h after cardiac arrest. Our results suggest impaired calcium-sensitizing mechanisms in cerebral myogenic vasoconstriction after cardiac arrest.<b>NEW & NOTEWORTHY</b> Cerebral autoregulation is impaired in the postcardiac arrest period, potentially altering cerebral blood flow and exacerbating neurological injury after resuscitation. To our knowledge, the current study is the first to demonstrate that cerebral arteries exhibit reduced myogenic response, tone, and contractility in an animal model following resuscitation from cardiac arrest. These alterations in vasoreactivity appear to result, at least in part, from decreased calcium sensitivity in cerebral vascular smooth muscle cells.