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Kiel JW. The Ocular Circulation. San Rafael (CA): Morgan & Claypool Life Sciences; 2010.

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The Ocular Circulation.

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Chapter 5Ocular blood flow effects on IOP

Two conceptual models serve as the basis for understanding IOP (Fig 5.1). One model treats the IOP in terms of the ocular pressure-volume relation, which is an exponential function of the total ocular volume and the elasticity of the corneoscleral coat. This model is the theoretical basis for indentation tonometry and tonography18,19. The other model treats the steady-state IOP as a function of aqueous flow and outflow resistance20. This model is the theoretical basis for understanding ocular hypertension and hypotony as well as current drug and surgical treatment of ocular hypertension (i.e., elevated IOP). Both models provide insight into IOP physiology.

Figure 5.1. Schematic of IOP generation.

Figure 5.1

Schematic of IOP generation. (Pin: extraocular arterial pressure; Pa: intraocular arterial pressure; Pc: intraocular capillary pressure; Pv: intraocular venous pressure; Pout: extraocular venous pressure; Ra; arterial resistance; Rv: venous resistance; (more...)

If the corneoscleral elastance is constant, changes in IOP must involve changes in ocular volume. The main contributors to the total ocular volume are the vitreous, lens, aqueous and blood. The volumes of the vitreous and lens are relatively stable and do not typically have an acute influence on IOP. The volumes of blood and aqueous are more labile and cause most variations in IOP. Changes in the volume of aqueous occur with transient imbalances in aqueous production and outflow. Similarly, ocular blood volume changes happen during transient imbalances in the flow of blood into and out of the eye. Most of the ocular blood volume is in the choroid, the highly vascularized tissue between the retina and sclera.

Because most IOP measurement techniques are discontinuous, the effect of blood flow (or more specifically, blood volume) on IOP generally goes unnoticed. However, continuous IOP measurement by direct cannulation shows that ocular blood volume contributes to IOP (Fig 5.2, top). For example, blood pressure synchronous changes in IOP are clearly evident. The IOP pulse is caused by pulsatile arterial inflow and steady venous outflow giving rise to fluctuations in ocular blood volume (Fig 5.2, bottom). This IOP pulse is used to estimate the pulsatile component of ocular blood flow22.

Figure 5.2. Top: Blood pressure and IOP recorded by direct cannulation of the central ear artery and vitreous compartment in an anesthetized rabbit.

Figure 5.2

Top: Blood pressure and IOP recorded by direct cannulation of the central ear artery and vitreous compartment in an anesthetized rabbit. Bottom: Computer simulation showing cardiac synchronous IOP pulsations due to fluctuations in blood volume caused (more...)

Another example of the blood volume contribution to IOP is seen at death (Fig 5.3). If the heart is stopped quickly, the arterial pressure falls toward the mean circulatory filling pressure23, blood flow into the eye stops and the residual blood volume drains out of the eye, resulting in a rapid net decrease in blood volume and an equally rapid fall in IOP. In anesthetized rabbits under control conditions, the IOP immediately before and after death are typically 15 mmHg and 7 mmHg, respectively. This occurs in seconds, which is too fast for aqueous dynamics to play a role in the IOP decrease.

Figure 5.3. Drop in IOP occurs immediately upon cardiac arrest induced with an overdose of pentobarbital (100 mg/kg, i.

Figure 5.3

Drop in IOP occurs immediately upon cardiac arrest induced with an overdose of pentobarbital (100 mg/kg, i.v.) in a deeply anesthetized rabbit. Continued venous outflow without corresponding arterial inflow results in the net loss of blood volume responsible (more...)

In contrast to death, ocular blood volume is normally relatively well regulated during changes in arterial pressure24. As shown in Fig 5.4 (left), an acute increase in arterial pressure induced by occluding the aorta causes only a small increase in IOP due to choroidal vasoconstriction under control conditions. Both autoregulatory myogenic24 and autonomic neural mechanisms25 have been proposed to explain this response (see below). However, what is important to note is that when this choroidal regulation is abolished with a systemic vasodilator, a similar acute elevation of arterial pressure can elicit a significantly larger increase in IOP (Fig 5.4 right). Here again, it is clear that ocular blood volume contributes to total ocular volume and so influences the IOP.

Figure 5.4. IOP responses to acute increases in arterial pressure in an anesthetized rabbit.

Figure 5.4

IOP responses to acute increases in arterial pressure in an anesthetized rabbit. Raising arterial pressure to 110 mmHg elicits a modest increase in IOP under control conditions (left) and a much larger increase when choroidal regulation is impaired by (more...)

A sustained pressure-induced increase in ocular blood volume does not produce a sustained increase in IOP as shown in Figure 5.5. Instead, the elevated IOP increases the pressure gradient for aqueous outflow, which causes a compensatory decrease of aqueous volume so that IOP gradually returns to baseline24. If the increase in blood volume is small, the compensation is relatively quick, whereas compensation for a larger increase in blood volume, as occurs when choroidal regulation is impaired, takes longer. In either situation, IOP falls below baseline when the arterial pressure-induced distention of the vasculature is abruptly ended, reflecting the compensatory loss of aqueous volume, which is gradually restored by continued aqueous production, which returns IOP to baseline. Such compensatory volume shifts were noted by Duke-Elder, who observed a marked shallowing of the anterior chamber and rise of IOP to 80 – 90 mmHg upon ligation of the vortex veins in anesthetized dogs, the most extreme method to cause choroidal engorgement26.

Figure 5.5. IOP responses to sustained increases in arterial pressure under control and vasodilated conditions in anesthetized rabbits.

Figure 5.5

IOP responses to sustained increases in arterial pressure under control and vasodilated conditions in anesthetized rabbits. Raising arterial pressure mechanically to 110 mmHg under control conditions elicits a relatively small increase in IOP that returns (more...)

The effect of blood volume on IOP is also apparent in the ocular pressure-volume relationship. In anesthetized rabbits, cumulative intraocular saline injections give different pressure-volume relationships when arterial pressure is held at different levels, which are all different from that obtained post mortem (Fig 5.6)27. The original Friedenwald tables used in tonometry and tonography were based on enucleated eyes re-inflated with saline to achieve a normal IOP19,28. This procedure eliminated any blood volume buffering of the IOP response to additional saline injections. However, as Figure 5.6 shows, the pressure volume relationship and the ocular rigidity coefficient (an index of corneoscleral elastance) are both dependant on the arterial pressure distending the ocular vessels.

Figure 5.6. Effect of mean arterial pressure (MAP) on the intraocular pressure-volume relationship and ocular rigidity in anesthetized rabbits.

Figure 5.6

Effect of mean arterial pressure (MAP) on the intraocular pressure-volume relationship and ocular rigidity in anesthetized rabbits. Reproduced with permission from Experimental Eye Research, Elsevier.

Copyright © 2010 by Morgan & Claypool Life Sciences.
Bookshelf ID: NBK53324
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