Cerebrovascular Compliance in Humans

Pulsatile blood flow consists of two components: steady flow and oscillatory flow. Steady blood flow is primarily regulated by vascular resistance while vascular compliance represents a key mediator of oscillatory blood flow. However, most studies investigating the regulation of cerebral blood flow in humans have focused on vascular resistance. Recently, emerging evidence has implicated vascular compliance as an important contributor to the regulation of cerebral perfusion. Therefore, the research contained herein aimed to i) quantify cerebrovascular compliance responses to blood pressure alterations and ii) explore mechanisms regulating cerebrovascular compliance in humans. The studies employed a Windkessel modelling approach to calculate cerebrovascular compliance using blood pressure waveforms measured at the brachial artery and middle cerebral artery blood velocity waveforms. Study One evaluated the nature of the cerebrovascular compliance response to transient reductions in blood pressure induced by standing upright. The findings demonstrate rapid and large increases in cerebrovascular compliance that contribute to the preservation of systolic blood velocity during the hypotensive phase of standing. Study Two investigated the impact of cerebral vasodilation on cerebrovascular compliance. Two vasodilatory stimuli, hypercapnia acting primarily through endothelial pathways and sodium nitroglycerin acting through non-endothelial pathways, produced reductions in cerebrovascular compliance. Hypercapnia dilates the entire cerebral vascular bed while sodium nitroglycerin dilates only the large cerebral arteries. Nonetheless, similar reductions in cerebrovascular compliance were observed. Study Three examined the role of sympathetic innervation, cholinergic innervation, and myogenic mechanisms in regulating cerebrovascular compliance. Distinct blockade of -adrenergic receptors (phentolamine), endothelial muscarinic receptors (glycopyrrolate), and calcium channels (nicardipine), produced large increases in cerebrovascular compliance. Similar changes in cerebrovascular compliance were observed under baseline conditions and during oscillatory lower body negative pressure to induce blood pressure fluctuations. Overall, these studies provide support for the role of cerebrovascular compliance in regulating cerebral perfusion. Additionally, these studies generated new knowledge regarding neural, endothelial, and myogenic mechanisms governing human cerebrovascular compliance