Vascular Neural Network in Subarachnoid Hemorrhage

Abstract

This perspective article uses a new concept named vascular neural network as an umbrella to redefine vascular pathophysiology for subarachnoid hemorrhage (SAH) induced vasospasm and early/delayed brain injury. Five vascular components are discussed including large artery moderate vasospasm which may not contribute to reduced cerebral blood flow (CBF) and poor outcomes after SAH. Even severe vasospasm alone with lumen diameter narrowing less than 75% of the normal diameter may not cause delayed brain injury, unless it is combined with peripheral and distal smaller artery dysfunctions. Vasospasm in smaller artery or arterioles contributes to the reduction of CBF and poor outcomes after SAH, because of limited or no collateral circulation reserves. Capillary or pre-capillary pear-string-type of contraction may block red blood cell flow and astrocyte edema compression may contribute to the loss of capillary density after SAH. Venules may be compressed by brain edema because venules have a thin wall of only one layer of endothelial cells with adventitia tissues. Deep cerebral vein vasospasm reduces venous flow and may cause venous infarction. When venous flow is obstructed, it is presumed that arterial dilatation may enhance brain edema and be harmful. Overall, all of these five vascular components in the vascular neural network are interrelated and more than one component or even all five components may be affected after SAH. All of these vascular components should be taken into consideration for patient care. Studying potential roles of venules and deep veins in the outcome of SAH patients and mechanisms of venule compression and vein spasm may be new aspects for future investigations.

Recombinant Osteopontin Stabilizes Smooth Muscle Cell Phenotype via Integrin Receptor/Integrin-Linked Kinase/Rac-1 Pathway After Subarachnoid Hemorrhage in Rats

“…A previous study indicated that MMP-9 was expressed in the vascular wall and the co-staining for vascular smooth muscle cells showed that the MMP-9 expression localized to the vascular smooth muscle cells after SAH 8 . The switch of vascular smooth muscle phenotype may not markedly affect the size or function of the large arteries in the previous study 1, 31 , but some studies reported that unbalanced contractile/synthetic vascular smooth muscle phenotype affected the size of the cerebral arteries and aggravated brain swelling and brain edema 29,30,32 . It is presumed that due to the limited two or three layers of smooth muscle cells in smaller arteries, vascular smooth muscle phenotype change causes the loss of small arteries vascular tone and affects BBB and autoregualtion.…”

“…The vascular neural network, which is an extended classical neurovascular unit, represents a new physiological unit to consider for therapeutic development in stroke 1, 3 . The vascular smooth muscle, as an important part of vascular neural network, might be an alternative therapy for early brain injury after SAH.…”

“…It is likely that neuroprotection will not occur without the proper control of blood circulation in the brain after subarachnoid hemorrhage (SAH) 1 . The cerebral vascular neural network which includes vascular smooth muscle cells are involved in the pathophysiology of SAH 2, 3 .…”

Delayed Docosahexaenoic Acid Treatment Combined with Dietary Supplementation of Omega-3 Fatty Acids Promotes Long-Term Neurovascular Restoration After Ischemic Stroke

“…Angiogenesis is an important endogenous repair mechanism after brain injury, which may improve tissue perfusion, support the activity of neurons and neural progenitor cells, and collectively, promote long-term functional improvement [40-44]. The potent effect of DHA and FO combined treatment in promoting post-stroke neurogenesis suggests the potential development of new blood vessels, which provided a vascular niche that is required during neurogenesis [7].…”

Temporal Lobe Epilepsy, Stroke, and Traumatic Brain Injury: Mechanisms of Hyperpolarized, Depolarized, and Flow-Through Ion Channels Utilized as Tri-Coordinate Biomarkers of Electrophysiologic Dysfunction

“…The anterior choroidal artery, which lies proximal to the MCA and the end artery structure of humans contrasted to the more collateral structure of mice may offer clues as science develops improved biotechnology to traverse these diverse pathways. In TBI, the most common vascular injury is subarachnoid haemorrhage [10] with secondary vascular issues from vasospasm or lumen narrowing of arteries from edema or increased intracranial pressure that further reduce brain perfusion [11]. Vertebrobasilar dissection is more common than anterior dissection in traumatic brain injury.…”