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 Table of Contents    
ORIGINAL ARTICLE
Year : 2023  |  Volume : 16  |  Issue : 1  |  Page : 35-38  

Effects of head posture on intraocular pressure and heart rate of human beings


Department of Ophthalmology, Regional Institute of Ophthalmology, Banaras Hindu University, Varanasi, Uttar Pradesh, India

Date of Submission20-May-2022
Date of Decision08-Jun-2022
Date of Acceptance17-Dec-2022
Date of Web Publication21-Feb-2023

Correspondence Address:
Tanmay Srivastav
Assistant Professor, Department of Ophthalmology, Maa Vindhyavasini Autonomous State Medical College, Mirzapur, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ojo.ojo_147_22

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   Abstract 


BACKGROUND: The study analyzed the association of head posture on intraocular pressure (IOP). The study aimed to evaluate and measure the changes in IOP and heart rate (HR) of human beings on head-down posture. The study included 105 patients at the department of ophthalmology of a tertiary care center in India.
SUBJECTS AND METHODS: Patients underwent applanation tonometry and HR variability (HRV) analysis before and after 20 min of head-down posture (approximately 20°). The IOP and HRV were measured.
STATISTICAL ANALYSIS USED: The statistical methods of Paired t-test and linear regression analysis were applied. P < 0.05 was defined as statistically significant.
RESULTS: After 20 min of the 20° head-down position, an increase in IOP was significant from 15.0 ± 2.0 mmHg to 18.0 ± 2.3 mmHg (P < 0.001). A decrease in HR was also significant from 78 ± 10.48 bpm to 72 ± 10.52 bpm after the head-down position for 20 min (P < 0.05).
CONCLUSIONS: These outcomes presented the first evidence of the activation of the parasympathetic nervous system in the head-down position which might cause decreased HR and the collapse of Schlemm's canal lumen, which in turn leads to the increased IOP.

Keywords: Aqueous humor, autonomic nervous system, glaucoma, intraocular pressure, Schlemm's canal


How to cite this article:
Kumar A, Srivastav T. Effects of head posture on intraocular pressure and heart rate of human beings. Oman J Ophthalmol 2023;16:35-8

How to cite this URL:
Kumar A, Srivastav T. Effects of head posture on intraocular pressure and heart rate of human beings. Oman J Ophthalmol [serial online] 2023 [cited 2023 Mar 26];16:35-8. Available from: https://www.ojoonline.org/text.asp?2023/16/1/35/370034




   Introduction Top


People going in space experience ocular changes during long-duration spaceflight, including choroidal folds, edema of the optic disc, retinal nerve fiber layer thickening, increased intraocular pressure (IOP), and decreased visual acuity.[1] During a 6-month duration onboard the International Space Station (ISS), more than half of the astronauts presented with abnormal ophthalmic findings termed visual impairment and intracranial pressure syndrome.[2]

The increase in the IOP of astronauts is an important finding in the microgravity environment.[3],[4],[5] The leading hypothesis suggests that the increase of episcleral venous pressure (EVP) contributes to ocular changes.[6] However, Wenreib et al. demonstrated that only 1 mmHg change in IOP was associated with a 0.83 mmHg change in EVP during the microgravity analog environment, which suggests another possible explanation besides EVP.[7] The exact etiology of the IOP changes in astronauts on spaceflight is still unknown.

Head-down posture leads to the headward shift of fluid similar to which occurs during spaceflight, head-down posture has been used for a long on Earth to simulate the effects of microgravity on the human body and to evaluate possible countermeasures.[8] Prolonged head-down bed test also produces similar changes as those occurring in microgravity, such as bone demineralization, muscle loss, reduced metabolic needs, and decreased sensory stimulation.[9] Since the head-down bed test is designed to simulate the effects of microgravity on the human body, it is hypothesized that microgravity-induced ophthalmological changes found in long-duration spaceflight might occur in head-down bed test subjects. Therefore, the purpose of our study was to evaluate the ocular outcomes and to elucidate the possible mechanisms underlying IOP change following the head-down posture.


   Subjects and Methods Top


The study protocols were approved by the institutional ethics committee. Written informed consent was obtained before the enrollment from all participants under the tenets outlined in the Declaration of Helsinki.

A total of 105 healthy patients visiting our outpatient department for routine eye checkups at the department of ophthalmology, were recruited in our study from July 2019 to September 2020. Ophthalmic examination of all participants was done. Either of the eyes was randomly selected in our study.

Inclusion criteria were as follows: (1) IOP <20 mmHg and normal ophthalmoscopic appearance of the optic nerve (cup-to-disc ratio <0.4 in both eyes, cup-to-disc ratio asymmetry <0.2, absence of hemorrhage, and localized or diffuse rim thinning). (2) Age >18 years old, should not have received any medicines affecting the circulatory system.

Exclusion criteria were as follows: (1) Best-corrected visual acuity (BCVA) <0.5 (to ensure that the participants had good fixation). (2) Refractive error (RE) ≤−3.0 D and RE ≥+3.0 D. (3) Cataract and other ocular diseases that hamper imaging of optical coherence tomography. (4) The presence of other eye diseases such as age-related macular degeneration and retinal detachment.

Measurement of intraocular pressure, blood pressure, and heart rate

All participants were asked to maintain an upright position for 10 min followed by a head-down posture (20° head-down position) for 20 min. The IOP was measured before and after the head-down position using a Goldmann applanation tonometer in the upright posture. Heart rate (HR), systolic blood pressure (SBP), and diastolic blood pressure (DBP) were recorded using an automatic sphygmomanometer. The mean arterial pressure (MAP) and mean ocular perfusion pressure (MOPP) were calculated using the equation below: MAP = ([2 × DBP] +SBP)/3; MOPP = MAP-ΔPf-ΔPh-IOP. ΔPf is the pressure difference because of the flow resistance of the vessels between the heart and the eye (assumed by the author of Bill to be 5 cm H2O, approximately 4 mmHg). ΔPh is the static pressure difference of a water column with a height equal to the distance between the heart and the eye. Applying this formula in our manuscript, in the 20° head-down position, the eyes were approximately 6 cm above the level of the heart, and the ΔPh was 4 mmHg.

Statistical analysis

All statistical analyses were performed using the SPSS software package (Version 16.0, SPSS Inc., Chicago, IL, USA). The data are presented as the mean values (Mean ± Standard Deviation). One sample Kolmogorov–Smirnov test and the test of homogeneity of variance were adopted. A paired samples t-test was adopted to compare the differences of the parameters during the head-down position. Statistical significance was defined as a P < 0.05.


   Results Top


A total of 105 participants were enrolled in this study, i.e., 40 (38.09%) males and 65 (61.91%) females. The mean age was 31.23 ± 3.0 years (range 22–41, years), mean BCVA was 0.96 ± 0.05 (range 0.8–1.0), and mean RE was 2.29 ± 1.89 diopter (range – 2.91–1.17, diopter). All data met the law of normal distribution and homoscedasticity.

IOP increased significantly after the 20° head-down position from 15.0 ± 2.0 mmHg to 18.0 ± 2.3 mmHg [P < 0.001]. HR decreased significantly from 78 ± 10.48 bpm to 72 ± 10.52 bpm after the head-down position for 20 min. However, there are no significant differences between MAP and MOPP [Table 1].
Table 1: Physiological parameters following head-down test for 20 min

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Participants were instructed to maintain the 20° head-down position for 20 min. Both IOP and HR changed significantly (P < 0.05), as evaluated by the Paired Samples t-test (data consistency with normally distributed).


   Discussion Top


On Earth, the hydrostatic pressure increases gradually from head to toe due to gravity. The pressure was higher at the lower extremities than the upper extremities involving the eye during the upright posture. In space with absent or low gravity, the hydrostatic pressure of the tissues gets altered due to the lack of gravitational gradient. The fluid shift during the weightlessness in spaceflight was thought as the main reason for increased IOP.[10] As the head-down position causes a headward fluid shift similar to that which occurs during spaceflight, the head-down posture test is designed to simulate the effects of microgravity on the human body.[8] The same result was found in our study that IOP increased significantly after the acute head-down position for 20 min.

During the 8-day manned German Spacelab mission, IOP increased by ~ 5 mmHg after 25 min of weightlessness,[11] and IOP was similarly found 4–7 mmHg increased during the 1st day on 6 Space Shuttle missions.[12] However, IOP was normalized after the 4th day of spaceflight.[12] During the long-duration spaceflight of the German-Russian MIR 10-day Spacelab D2 mission, IOP was also found similar to preflight throughout the mission.[13] It was found that chronically elevated IOP was not observed in astronauts. The stable IOP during long spaceflight appears to occur despite a sustained cephalad venous fluid shift. Huang AS mentioned in his study that a compensatory mechanism normalizes IOP during spaceflight.[14]

The autonomic nervous system maintains the balance of numerous body processes, such as blood pressure, heartbeat, breathing, and digestion.[15] The influence of the autonomic nervous system on IOP has been the subject of great interest since 1727.[16] Previous studies have shown that excision of the superior cervical sympathetic ganglion lowered and that electrical stimulation of the sympathetic nerve trunk raised IOP and[17] decreased parasympathetic innervation reduce IOP.[15] From the above, the autonomic nervous system is involved in the regulation of IOP.

A study done by Diedrich et al., which included a short-term head-down tilt of 6°, caused an acute activation of the parasympathetic nerve traffic and decreased HR.[18] In our result, HR was also found significantly lowered. Above all, the IOP fluctuation during acute head-down positioning might be explained by the activation of the parasympathetic nervous system. The pathophysiological mechanism of IOP increase induced by parasympathetic nerve need be further elaborated.

Schlemm's canal was first identified by the German anatomist, Friedrich Schlemm in 1830, which maintains aqueous humor homeostasis and stability of IOP.[19] Allingham et al. found that the collapse of Schlemm's canal accounts for approximately half of the decrease in the outflow facility of aqueous humor.[20] Hann et al. also found that abnormal pressure in the Schlemm's canal is a contributing factor to outflow facility in primary open-angle glaucoma (POAG) eyes.[21] Above all, the anatomic change of Schlemm's canal plays a critical role in the modulation of the outflow facility.[22],[23] In our preliminary study, the inner wall of the Schlemm's canal containing vasoactive intestinal peptide was validated, this indicates that vagus nerves might be involved in Schlemm's canal regulation.[24] After 20 min of head-down position, we found that there was a significant decrease in HR and an increase in IOP.

The outflow resistance of the aqueous humor in the traditional pathway was involved in the regulation of IOP.[20],[21],[22],[23] Yuan et al. found that Schlemm's canal dilation by Micro-stent implanting operation significantly increased the outflow facility and reduced IOP.[25] Genaidy et al. found that canaloplasty (SC dilatation program) successfully decreased the IOP after 12 months in eyes with POAG.[26] In our study, the IOP peak after 20 min of head-down position might be explained by the collapse of the SC lumen of increased parasympathetic nervous activity.

Overall, the collapse of the Schlemm's canal could be explained by the activation of the peripheral parasympathetic nervous system after the 20 min short-term head-down posture, which might be involved in the regulation of IOP.


   Conclusions Top


Our study not only offers some interesting insights into ocular physiology but also has some limitations which warrant discussion. First, results might be compared to those in nonnormal or developmental glaucoma populations in future studies. Second, there is no significant correlation between IOP, with a decreased HR.

In the future, studies can be done with a larger sample size to correlate parasympathetic activation on head-down posture which leads to increased IOP.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Zhang LF, Hargens AR. Intraocular/Intracranial pressure mismatch hypothesis for visual impairment syndrome in space. Aviat Space Environ Med 2014;85:78-80.  Back to cited text no. 1
    
2.
Mader TH, Gibson CR, Pass AF, Kramer LA, Lee AG, Fogarty J, et al. Optic disc Edema, Globe flattening, choroidal folds, and hyperopic shifts observed in astronauts after long-duration space flight. Ophthalmology 2011;118:2058-69.  Back to cited text no. 2
    
3.
Marshall-Goebel K, Mulder E, Bershad E, Laing C, Eklund A, Malm J, et al. Intracranial and intraocular pressure during various degrees of head-down tilt. Aerosp Med Hum Perform 2017;88:10-6.  Back to cited text no. 3
    
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Anderson AP, Butterfield JS, Subramanian PS, Clark TK. Intraocular pressure and cardiovascular alterations investigated in artificial gravity as a countermeasure to spaceflight associated neuro-ocular syndrome. J Appl Physiol (1985) 2018;125:567-76.  Back to cited text no. 4
    
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Taibbi G, Cromwell RL, Zanello SB, Yarbough PO, Ploutz-Snyder RJ, Godley BF, et al. Ocular outcomes evaluation in a 14-day head-down bed rest study. Aviat Space Environ Med 2014;85:983-92.  Back to cited text no. 5
    
6.
Lavery WJ, Kiel JW. Effects of head down tilt on episcleral venous pressure in a rabbit model. Exp Eye Res 2013;111:88-94.  Back to cited text no. 6
    
7.
Aihara M, Lindsey JD, Weinreb RN. Episcleral venous pressure of mouse eye and effect of body position. Curr Eye Res 2003;27:355-62.  Back to cited text no. 7
    
8.
Pavy-Le Traon A, Heer M, Narici MV, Rittweger J, Vernikos J. From space to Earth: Advances in human physiology from 20 years of bed rest studies (1986-2006). Eur J Appl Physiol 2007;101:143-94.  Back to cited text no. 8
    
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Taibbi G, Cromwell RL, Zanello SB, Yarbough PO, Ploutz-Snyder RJ, Godley BF, et al. Ocular outcomes comparison between 14- and 70-day head-down-tilt bed rest. Invest Ophthalmol Vis Sci 2016;57:495-501.  Back to cited text no. 9
    
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Nelson ES, Mulugeta L, Myers JG. Microgravity-induced fluid shift and ophthalmic changes. Life (Basel) 2014;4:621-65.  Back to cited text no. 10
    
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12.
StengerMB, TarverWJ, BrunstetterT, GibsonCR, LaurieSS, Lee SM, et al. Risk of Spaceflight Associated Neuro-Ocular Syndrome (SANS). NASA Human Research Program Human Health Countermeasures Element. NASA Johnson Space Center; 2017. Available from: https://humanresearch roadmap.nasa.gov/evidence/reports/SANS.pdf. [Last accessed on 2023 Jan 04].  Back to cited text no. 12
    
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Draeger J, Schwartz R, Groenhoff S, Stern C. Self tonometry during the German 1993 Spacelab D2 mission. Ophthalmologe 1994;91:697-9.  Back to cited text no. 13
    
14.
Huang AS, Stenger MB, Macias BR. Gravitational influence on intraocular pressure: Implications for spaceflight and disease. J Glaucoma 2019;28:756-64.  Back to cited text no. 14
    
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Gherezghiher T, Hey JA, Koss MC. Parasympathetic nervous control of intraocular pressure. Exp Eye Res 1990;50:457-62.  Back to cited text no. 15
    
16.
Feibel RM. Sympathectomy for glaucoma: Its rise and fall (1898-1910). Surv Ophthalmol 2015;60:500-7.  Back to cited text no. 16
    
17.
Gallar J, Liu JH. Stimulation of the cervical sympathetic nerves increases intraocular pressure. Invest Ophthalmol Vis Sci 1993;34:596-605.  Back to cited text no. 17
    
18.
Diedrich A, Drescher J, Nalishitj V, Kirchner F. Acute effects of simulated microgravity on heart rate variability. J Gravit Physiol 1994;1:P35-6.  Back to cited text no. 18
    
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Karpinich NO, Caron KM. Schlemm's canal: More than meets the eye, lymphatics in disguise. J Clin Invest 2014;124:3701-3.  Back to cited text no. 19
    
20.
Allingham RR, de Kater AW, Ethier CR. Schlemm's canal and primary open angle glaucoma: Correlation between Schlemm's canal dimensions and outflow facility. Exp Eye Res 1996;62:101-9.  Back to cited text no. 20
    
21.
Hann CR, Vercnocke AJ, Bentley MD, Jorgensen SM, Fautsch MP. Anatomic changes in Schlemm's canal and collector channels in normal and primary open-angle glaucoma eyes using low and high perfusion pressures. Invest Ophthalmol Vis Sci 2014;55:5834-41.  Back to cited text no. 21
    
22.
Allingham RR, de Kater AW, Ethier CR, Anderson PJ, Hertzmark E, Epstein DL. The relationship between pore density and outflow facility in human eyes. Invest Ophthalmol Vis Sci 1992;33:1661-9.  Back to cited text no. 22
    
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Johnson M, Chan D, Read AT, Christensen C, Sit A, Ethier CR. The pore density in the inner wall endothelium of Schlemm's canal of glaucomatous eyes. Invest Ophthalmol Vis Sci 2002;43:2950-5.  Back to cited text no. 23
    
24.
Ji P, Chen L, Gong J, Yuan Y, Li M, Zhao Y, et al. Co-expression of vasoactive intestinal peptide and protein gene product 9.5 surrounding the lumen of human Schlemm's canal. Exp Eye Res 2018;170:1-7.  Back to cited text no. 24
    
25.
Yuan F, Schieber AT, Camras LJ, Harasymowycz PJ, Herndon LW, Allingham RR. Mathematical modeling of outflow facility increase with trabecular meshwork bypass and Schlemm canal dilation. J Glaucoma 2015;25:1-10.  Back to cited text no. 25
    
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