The recent study by Ficarrotta and Passglia (Journal of Physiology, 2020), particularly their theory of a, as yet undetermined, neural feedback loop regulating intraocular pressure (IOP), provides an exciting new perspective in explaining the aetiology of Spaceflight Associated Neuro-ocular Syndrome (SANS). Ficarrotta and Passaglia (Journal of Physiology, 2020) demonstrate quite elegantly that intracranial pressure is the afferent arm of a central neural feedback mechanism, which provides an efferent signal modulating the outflow facility (aqueous humor), thus regulating IOP. As they point out, IOP has a much greater influence on the biomechanics of the optic nerve head than ICP, and thus principal aim of IOP regulation is the maintenance of the translaminal pressure (TLP) across the lamina cribrosa. The focus of research to explain the aetiology of SANS has been on the effects of microgravity on ICP, but it would appear that increased IOP, particularly by factors influencing ocular haemodynamics, is the prime cause for the impaired vision observed in astronauts.
COBISS.SI-ID: 33296679
The present study assessed the effect of 6° head down (establishing the cephalad displacement noted in astronauts in microgravity) prone (simulating the effect on the eye) tilt during rest and exercise (simulating exercise performed by astronauts to mitigate the sarcopenia induced by unloading of weight-bearing limbs), in normocapnic and hypercapnic conditions (the latter simulating conditions on the International Space Station) on IOP. Volunteers (average age = 57.8 ± 6 yrs.; N=10) participated in two experimental sessions, each comprising: i) 10-min rest, ii) 3-min handgrip dynamometry (30% max), and iii) 2-min recovery, inspiring either room air (NCAP), or a hypercapnic mixture (1% CO2, HCAP). We measured IOP in the right eye, cardiac output (CO), stroke volume (SV), heart rate (HR) and mean arterial pressure (MAP) at regular intervals. Baseline IOP in the upright seated position while breathing room air was 14.1 ± 2.9 mmHg. Prone 6° HDT significantly (p ( 0.01) elevated IOP in all three phases of the NCAP (rest: 27.9 ± 3.7 mmHg; exercise: 32.3 ± 4.9 mmHg; recovery: 29.1 ± 5.8 mmHg) and HCAP (rest: 27.3 ± 4.3 mmHg; exercise: 34.2 ± 6.0 mmHg; recovery: 29.1) trials, with hypercapnia augmenting the exercise-induced elevation in IOP (p ( 0.01). CO, SV, HR and MAP were significantly increased during handgrip dynamometry, but there was no effect of hypercapnia. The observed IOP measured during prone 6°HDT in all phases of the NCAP and HCAP trials exceeded the threshold pressure defining ocular hypertension. The exercise-induced increase in IOP is exacerbated by hypercapnia.
COBISS.SI-ID: 33184551