Subarachnoid haemorrhage-induced cerebral vasospasm: a subcellular perspective on the control of tension

Abstract

Vasospasm occurs in many human pathologies often resulting in tissue infarction and increasing morbidity and mortality. Cerebral vasospasm following subarachnoid haemorrhage, whilst a relatively rare condition, has a well described time course with clear neurological end-points and remains largely unresponsive to current therapies. The mechanisms underlying cerebral vasospasm have been investigated but are still poorly understood. The relationship between oxidative metabolism and force generation has not been extensively investigated, with much of the work done dependent upon force measurements to investigate the vascular changes. We propose that the relationship between force generation, relaxation, intracellular signalling and control of the contractile apparatus via protein phosphatases may be an important mechanism of disease and a therapeutic target. This is a potential new therapeutic avenue applicable to cerebral vasospasm and vasospasm affecting other organs.