Abstract
Neurovascular coupling, also termed functional hyperemia, is one of the physiological key mechanisms to adjust blood flow in a neural tissue in response to functional activity. In the retina, increased neural activity, such as that induced by visual stimulation, leads to the dilatation of retinal arterioles, which is accompanied by an immediate increase in retinal and optic nerve head blood flow. According to the current scientific view, functional hyperemia ensures the adequate supply of nutrients and metabolites in response to the increased metabolic demand of the neural tissue. Although the molecular mechanisms behind neurovascular coupling are not yet fully elucidated, there is compelling evidence that this regulation is impaired in a wide variety of neurodegenerative and vascular diseases. In particular, it has been shown that the breakdown of the functional hyperemic response is an early event in patients with diabetes. There is compelling evidence that alterations in neurovascular coupling precede visible signs of diabetic retinopathy. Based on these observations, it has been hypothesized that a breakdown of functional hyperemia may contribute to the retinal complications of diabetes such as diabetic retinopathy or macular edema. The present review summarizes the current evidence of impaired neurovascular coupling in patients with diabetes. In this context, the molecular mechanisms of functional hyperemia in health and disease will be covered. Finally, we will also discuss how neurovascular coupling may in future be used to monitor disease progression or risk stratification.
Highlights
Diabetes is a complex systemic disease, frequently accompanied by serious long-term microvascular and macrovascular complications [1]
The current review focuses on retinal functional hyperemia in patients with diabetes
Using dual-beam bidirectional Doppler Fourier Domain optical coherence tomography (OCT) (D-OCT), it has been shown that total retinal blood flow increases by approximately 50% in response to flicker light stimulation, which is in line with results obtained using other methods [101]
Summary
Diabetes is a complex systemic disease, frequently accompanied by serious long-term microvascular and macrovascular complications [1]. Tissues with high neural activity such as the retina show an intrinsic mechanism to adapt blood flow to increased metabolic demands caused by firing neurons. This regulatory response, which is called functional hyperemia or neurovascular coupling, is a key element that ensures the supply of the retinal tissue with oxygen and other nutrients to changing local metabolic requirements due to changing neural activity [12]. We will discuss the role of neurovascular coupling as an intrinsic mechanism to adapt perfusion to changes in metabolic demand and how an impairment of this regulation process may contribute to the pathogenesis of diabetic complications in the eye. We will describe how neurovascular coupling may in the future be used to monitor disease progression or risk stratification
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