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Diminished vasomotor component of systemic arterial pressure signals and baroreflex in brain death.

We compared the cardiovascular autonomic regulatory mechanisms between patients with brain death or under a persistent vegetative state and healthy volunteers, based on auto- and cross-spectral analysis of systolic blood pressure (SBP) and interpulse interval (PPI) signals. Brain-dead patients exhibited a significant reduction in the absolute and relative power of the low-frequency (LF; 0.04-0.15 Hz) component in both SBP and PPI spectra, along with appreciable decrease in the very low frequency (VLF; 0.004-0.04 Hz), LF, and high-frequency (HF; 0.15-0.4 Hz) power of the PPI signals. Patients in a persistent vegetative state exhibited a power of the VLF and LF component in the SBP spectrum that was comparable to that in healthy subjects, although a discernible reduction in the VLF, LF, and HF power of the PPI spectrum was manifested by the former group. Assessments with the magnitude of SBP-PPI transfer function and linear regression analysis of beat-to-beat fluctuations in SBP and PPI revealed a progressive decline in spontaneous baroreflex sensitivity from healthy subjects to patients in a persistent vegetative state or with brain death. We conclude that the vasomotor component of systemic arterial pressure signals and spontaneous baroreflex are highly correlated with the functional integrity of the brain stem.

Adult↗

P2 receptors in the central and peripheral nervous systems modulating sympathetic vasomotor tone.

Arterial pressure depends on the level of activity of sympathetic vasoconstrictor outflow to blood vessels. This activity is generated in the central nervous system, and involves inputs from a variety of brain regions projecting to sympathetic preganglionic neurones. Of especial interest are a group of neurones in the rostral ventrolateral medulla (RVLM), as they have been demonstrated to have a fundamental role in reflex regulation of the cardiovascular system, and in generation of tonic drive to sympathetic outflow. Sympathetic outflow to blood vessels is additionally modulated at sympathetic ganglia, and at the peripheral terminals of sympathetic nerves. This review considers the role of P2 purine receptors in this neural pathway. Ionotropic P2X receptors are expressed in the RVLM, in sympathetic ganglia, and at the sympathetic neuromuscular junction, and mediate fast excitatory neurotransmission, indicating a general role for ATP as a regulator of sympathetic vasomotor tone. P2Y receptors couple to G proteins and mediate slower signalling to ATP; they have been reported to inhibit prejunctionally neurotransmission at the peripheral terminals of sympathetic nerves, but little is known about their possible role in the central nervous system and in sympathetic ganglia.

Adenosine Triphosphate↗