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Anesth Analg 1999;88:781
© 1999 International Anesthesia Research Society

NEUROSURGICAL ANESTHESIA

Trabecular Outflow Facility and Formation Rate of Aqueous Humor During Anesthesia with Sevoflurane-Nitrous Oxide or Sevoflurane-Remifentanil in Rabbits

Alan A. Artru, MD*, and Yoshihiro Momota, DDS{dagger}

*Department of Anesthesiology, University of Washington School of Medicine, Seattle, Washington; and {dagger}Department of Anesthesiology, Osaka Dental University, Osaka, Japan

Address correspondence and reprint requests to Alan A. Artru, MD, Department of Anesthesiology, Box 356540, University of Washington School of Medicine, Seattle, WA 98195-6540. Address e-mail to artruaa{at}u.washington.edu


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Appendix 1
 References
 
In the present study, we examined the effect of sevoflurane and remifentanil on intraocular pressure (IOP) and fluid dynamics. Twenty-eight rabbits were anesthetized with halothane, and IOP was measured via a 25-gauge needle in the anterior chamber. Rabbits were then assigned to one of four groups, and halothane was replaced with sevoflurane 1% (n = 7), 2% (n = 7), 3% (n = 7), or 1% + remifentanil 0.65 µg · kg-1 · min-1 IV (n = 7). In all groups, a series of intraocular infusions was made into the anterior chamber, and IOP, trabecular outflow facility, the rate of aqueous humor formation, and intraocular compliance were determined. With sevoflurane only, intraocular compliance decreased (55 ± 14, 39 ± 22, 31 ± 17 nL/mm Hg; P < 0.05) as the concentration of sevoflurane increased. With sevoflurane 1% + remifentanil, intraocular compliance was significantly increased (100.1 ± 30.5 nL/mm Hg; P < 0.05) compared with sevoflurane 1%, 2%, or 3%. Trabecular outflow facility, rate of aqueous humor formation, and IOP did not differ among groups, and IOP was similar to values obtained during halothane anesthesia.

Implications: The dose-related effects of sevoflurane on intraocular compliance did not produce significant intraocular pressure differences. Adding remifentanil to sevoflurane increased intraocular compliance. Sevoflurane or sevoflurane + remifentanil causes a decrease in intraocular pressure compared with the average of previously reported values in awake rabbits, and the magnitude of the decrease is similar to that previously reported in rabbits anesthetized with ethyl urethane, pentobarbital, or halothane alone or in combination with propofol, cocaine, or lidocaine.


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Appendix 1
 References
 
Preventing intraocular pressure (IOP) increases during anesthesia and ophthalmological surgery may help to avoid impairment of ocular and visual function postoperatively. Limited information is available regarding the effects of sevoflurane and remifentanil on IOP and intraocular fluid dynamics. In adults, sevoflurane decreases IOP by 40% compared with preoperative values (1). In children, IOP during sevoflurane maintenance anesthesia was not significantly different from the IOP value measured just after anesthesia induction (2). Although there are no reports of the effects of remifentanil on IOP, alfentanil (another short-duration opioid) decreases the IOP response to succinylcholine and endotracheal intubation when combined with propofol (3).

IOP is determined by ocular volume (intraocular fluid [IOF] volume, choroidal blood volume, vitreous volume) and ocular compliance (scleral rigidity and extraocular muscle tone) (4,5). IOF volume, in turn, is determined by aqueous humor formation rate and the facility of outflow of aqueous humor (6,7). There are no reports of the effects of sevoflurane or remifentanil on aqueous humor formation rate or outflow facility or intraocular compliance. Accordingly, we used a previously reported rabbit model to examine the effects of sevoflurane and remifentanil on aqueous humor formation rate and outflow facility and intraocular compliance, as well as on IOP.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Appendix 1
 References
 
This study was approved by the Animal Care Committee of the University of Washington. Twenty-eight unmedicated New Zealand White rabbits (weight 3.1–4.0 kg) were studied. Anesthesia was induced with halothane (>1.5% inspired concentration) and nitrous oxide (66%) in oxygen. IOP during halothane served as the baseline value with which subsequent IOP values during sevoflurane or sevoflurane + remifentanil anesthesia were compared (see below). The trachea was intubated, and the lungs were mechanically ventilated. The percent inspired oxygen was adjusted to maintain PaO2 at 120–200 mm Hg. Expired CO2 was continuously monitored, and ventilation was regulated by a servo-controller to maintain expired CO2 at values representing normocapnia for rabbits (PaCO2 28–32 mm Hg) (8). The right femoral artery was cannulated to permit arterial blood sampling for blood gas analysis and continuous monitoring of systemic arterial blood pressure. Mean arterial blood pressure (MAP) was determined by electronic integration of the systemic arterial blood pressure trace. Needle electrodes were inserted at both shoulders and both thighs to monitor the electrocardiogram and heart rate. A urinary catheter was inserted, and the right femoral vein was cannulated for saline and drug administration. An IV infusion of pancuronium 0.5–1.0 mg/h maintained neuromuscular blockade, thereby minimizing the contribution of extraocular muscle tone to ocular compliance. Depletion of vascular volume was minimized by a continuous infusion of saline at 4–6 mL · kg-1 · h-1. Temperature was monitored by a rectal thermistor probe and was maintained by servo-controlled heat lamps at 38.0 ± 0.5°C (8).

The animal was then turned to the prone position, and the head was slightly elevated and fixed in a stereotaxic frame. A 25-gauge needle was inserted at the medial corneal-scleral junction and advanced horizontally into the anterior chamber. Care was taken to place the needle so that no aqueous humor was lost from the anterior chamber and the normal curvature of the cornea was maintained (9). Needle placement was considered satisfactory if variability of IOP with ventilation [previously reported with both invasive (10) and noninvasive (11,12) measurement of IOP] was observed. A T-connector was attached to the intraocular needle to permit measurement of both aqueous humor pressure in the anterior chamber and the pressure of the intraocular infusions. Aqueous humor pressure was measured by connecting one arm of the T-connector to a strain-gauge transducer via a short length of fine nylon tubing. The transducer was placed at eye level, and the mid-ocular line was used as the zero reference. The second arm of the T-connector was attached to a variable-speed syringe pump (Model 600–900 V; Harvard Apparatus Co., Inc., Dover, MA) to permit intraocular infusions. Drying of the cornea and sclera was minimized by continuous infusion of a saline solution onto the surface of the eye at 7 mL/h using a syringe pump. Wound edges were infiltrated with bupivacaine (0.25%), and the concentration of halothane was decreased to 0.8%–1.0% inspired to maintain MAP at 60–100 mm Hg.

After stabilization of aqueous humor pressure and systemic values (at least 30 min later), baseline IOP was recorded. Rabbits were then randomly assigned to one of four groups. Halothane was replaced in Group 1 (n = 7) by sevoflurane 1.0% expired, in Group 2 (n = 7) by sevoflurane 2.0%, in Group 3 (n = 7) by sevoflurane 3.0%, and in Group 4 (n = 7) by sevoflurane 1.0% combined with a continuous IV infusion of remifentanil at 0.65 µg · kg-1 · min-1. In all four groups, IOP was again recorded after stabilization of IOP and systemic values (at least 60 min later). A series of intraocular infusions was then begun, and the IOP response to each infusion was determined. The intraocular infusion rates were determined based on the IOP responses and included rates of 1.4, 1.7, 2.2, 3.2, 4.6, 9.2, and 13.5 µL/min (13,14). The infusion fluid was saline labeled with fluorescein 0.1%. Fluorescein was used as a tracer to detect leakage at the site of insertion of the 25-gauge needle into the anterior chamber. If leakage was detected, no measurements were taken from that eye, and a new 25-gauge needle was inserted into the contralateral eye.

The aqueous humor pressure response to each infusion determined the duration of the infusion. When pressure increased slowly and it seemed that pressure would stabilize at <35 mm Hg, infusions were continued for 8–15 min until steady aqueous humor pressure was achieved. When pressure increased rapidly with no indication of stabilizing at <35 mm Hg, infusions were discontinued after 2–5 min. Three or four of the lower infusion rates from each set produced stable aqueous humor pressure at <35 mm Hg, and one or two of the higher infusion rates in each set produced rapidly increasing aqueous humor pressure (Fig. 1). At the conclusion of each infusion, the infusion syringe was set to withdraw fluid from the anterior chamber until aqueous humor pressure returned to baseline levels. We allowed 15–20 min between infusions to permit complete restabilization of aqueous humor pressure at preinfusion values.



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  		Figure 1. An example of intraocular pressure (IOP) responses to intraocular infusion. Although the pattern of IOP response for each animal was similar to this illustration, the value at which IOP stabilized for each infusion rate varied from animal to animal. Each of four successive infusions in this illustration was begun at baseline IOP. The rate of intraocular fluid infusion was increased with each successive infusion. With Infusions 1–3, IOP stabilized at <35 mm Hg. With Infusion 4, IOP increased with no sign of stabilization at <35 mm Hg.

 
The conventional determination of IOF dynamics is based on the relationship that, in the steady state, the rate of anterior chamber aqueous formation equals the sum of outflow across the trabecular meshwork (pressure-dependent flow) and outflow into the anterior face of the ciliary body (termed uveoscleral outflow, pressure-independent flow) (6,7). The rate of anterior chamber aqueous formation is the component measurable by the fluid infusion method we used and is equal to the product of trabecular outflow facility and the hydrostatic pressure driving force (the difference between IOP and the hydrostatic pressure of the canal of the Schlemm or episcleral venous pressure). The conventional determination of IOF dynamics assumes that when IOP is changed by {Delta}IOP, trabecular outflow facility and hydrostatic pressure of the canal of Schlemm remain constant and outflow across the trabecular meshwork changes such that trabecular outflow facility = change in outflow across the trabecular meshwork/{Delta}IOP (6,7). Thus, in the present study, the IOP responses to the series of fluid infusions yielding steady-state IOPs were used to calculate trabecular outflow facility using the above equation. Outflow across the trabecular meshwork was calculated from trabecular outflow facility using the equation: outflow across the trabecular meshwork = the product of trabecular outflow facility and the hydrostatic pressure driving force, assuming hydrostatic pressure of the canal of Schlemm is 64.5% of baseline IOP (6,7,15). Rate of anterior chamber aqueous formation was calculated assuming outflow across the trabecular meshwork represents 87% of rate of anterior chamber aqueous formation (16).

Resistance to trabecular outflow was calculated as the inverse of trabecular outflow facility (7). Intraocular compliance was calculated from the rapid, linear increases of aqueous humor pressure that did not stabilize at <35 mm Hg. Using this technique, it is assumed that when the high-flow curves are linear, a negligible fraction of the infused volumes leaves the fluid-containing space and the system acts as an integrator (17). Therefore, in the present study, intraocular compliance was calculated as the infusion rate/({Delta}IOP/{Delta}t) where {Delta}IOP/{Delta}t is the slope of the linear increase of IOP (14).

Statistical comparisons among and within groups were made using two-way analysis of variance with rejection of the null hypothesis at the 0.05 probability level. For systemic values, comparisons within groups were made using repeated-measures analysis of variance. Values are expressed as mean ± SD. The best line of fit for the entire set of flow-pressure data pairs for each group was calculated. The y-intercept from the best line of fit indicates the fraction of outflow across the trabecular meshwork that occurred independently of IOP.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Appendix 1
 References
 
The IOPs in the groups receiving sevoflurane 1%, 2%, 3%, and 1% combined with remifentanil were 13 ± 3, 14 ± 4, 13 ± 3, and 15 ± 2 mm Hg, respectively (Table 1). These IOPs did not differ among groups and also did not differ from the pre-sevoflurane IOP (i.e., IOP during halothane anesthesia) of 13 ± 2 mm Hg. Accordingly, hydrostatic pressure of the canal of Schlemm was estimated as 8, 9, 8, and 10 mm Hg for sevoflurane 1%, 2%, 3%, and 1% combined with remifentanil. Trabecular outflow facility for the four groups was 0.24 ± 0.13, 0.33 ± 0.17, 0.27 ± 0.14, and 0.30 ± 0.17 µL · min-1 · mm Hg-1, respectively. The best line of fit for the entire set of flow-pressure data pairs for all the groups was a linear equation. The y-intercept for the data obtained during sevoflurane 1%, 2%, and 3%, and 1% + remifentanil was 1.5, 1.3, 1.0, and 1.4 µL/mL, respectively (Fig. 2). Outflow across the trabecular meshwork calculated from trabecular outflow facility, estimated hydrostatic pressure of the canal of Schlemm, and IOP during infusions was 3.5 ± 0.9, 3.6 ± 1.1, 4.2 ± 0.9, and 3.8 ± 1.2 µL/min, respectively. Rate of anterior chamber aqueous formation calculated from outflow across the trabecular meshwork was 4.0 ± 1.0, 4.1 ± 1.3, 4.8 ± 1.0, and 4.4 ± 1.4 µL/min, respectively.


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  		Table 1. Intraocular Fluid Dynamics
 


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  		Figure 2. A set of flow-pressure data pairs from one of the experimental groups is shown. Flow-pressure data pairs were taken from the stabilization intraocular pressures produced by intraocular infusion of fluorescein-labeled saline. The best line of fit for the entire set of data pairs was a linear equation. Each point represents one flow-pressure data pair. Three flow-pressure data pairs were generated for each animal (corresponding to the three intraocular infusions producing an intraocular pressures stabilizing at <35 mm Hg, as illustrated in Figure 1).

 
Resistance to trabecular outflow calculated as the inverse of trabecular outflow facility was 4.2 ± 2.7, 3.0 ± 1.5, 3.7 ± 1.3, and 3.3 ± 1.8 mm Hg · µL-1 · min-1, respectively. Intraocular compliance calculated from the high infusion rates was 55 ± 14, 39 ± 22, 31 ± 17, and 100 ± 31 (P < 0.05) nL/mm Hg, respectively. There was a significant interaction of sevoflurane concentration with intraocular compliance. Intraocular compliance with sevoflurane + remifentanil was significantly increased compared with that in the other groups.

Within each group, systemic values were not significantly different among conditions (i.e., intraocular infusion rates). Mean values calculated from the four to six experimental conditions within each group are shown in Table 2.


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  		Table 2. Systemic Values
 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Appendix 1
 References
 
In the present study, the principal findings were a decrease of intraocular compliance as the concentration of sevoflurane increased and an increase of intraocular compliance with sevoflurane 1% + remifentanil compared with sevoflurane 1%, 2%, or 3%. In contrast, trabecular outflow facility, rate of aqueous humor formation, and IOP did not differ among the groups. These results should be interpreted in relation to previously reported values in rabbits.

The reported value for trabecular outflow facility in unanesthetized rabbits is 0.24 ± 0.01 µL · min-1 · mm Hg-1 (18). Values in anesthetized rabbits range from 0.077 ± 0.040 to 0.33 ± 0.03 µL · min-1 · mm Hg-1 (13,14,17,18). In the present study, values for trabecular outflow facility during sevoflurane 1%, 2%, and 3% were similar to those previously reported in anesthetized rabbits. The interpretation of the y-intercept values from the entire set of flow-pressure data pairs for each experimental group as a measure of IOP-dependent versus IOP-independent trabecular outflow is unproven. It may be that, in the present study, positive y-intercept values consistently occurred simply because the linear regression only approximates the ideal relationship between flow and pressure. In previous studies, the y-intercept has been used to estimate the fraction of outflow across the trabecular meshwork occurring independently of IOP. The larger fraction of outflow across the trabecular meshwork is pressure-dependent and is proportional to the slope of the set of flow-pressure data pairs. A smaller fraction of outflow across the trabecular meshwork seems to be pressure-independent, as indicated by the y-intercept of the equation describing the flow-pressure data pairs. Y-intercept values from previous studies in anesthetized rabbits range from 0.2 to 0.6 µL/min (14,17). That y-intercept values were smaller than the mean rates of anterior chamber aqueous humor formation in the present study reemphasizes the small contribution made by pressure-independent flow to overall outflow across the trabecular meshwork.

Reported values for intraocular compliance in anesthetized rabbits ranged from 33 ± 14 to 36 ± 12 nL/mm Hg at IOP values similar to those of the present study (17) and from 183 ± 86 to 186 ± 113 nL/mm Hg at IOP values lower than those of the present study (14). In the present study, intraocular compliance during sevoflurane 1%, 2%, and 3% spanned the range of previously reported intraocular compliance values and was inversely related to sevoflurane concentration (17). Intraocular compliance is determined primarily by the intrinsic elastic elements of the eye. The present results suggest less relaxation of these elements at higher sevoflurane concentrations than at lower sevoflurane concentrations.

Reported values for rate of anterior chamber aqueous formation in unanesthetized rabbits range from 2.65 ± 0.22 to 4.0 µL/min (18–20). Values in anesthetized rabbits (ethyl urethane, pentobarbital, or halothane/N2O alone or combined with propofol, cocaine, or lidocaine) range from 2.13 ± 0.12 to 3.79 ± 1.25 µL/min (13,14,17,18). In the present study, the mean values for rate of anterior chamber aqueous formation with sevoflurane or sevoflurane + remifentanil were similar to the above range. Aqueous humor formation rate is determined, in part, by energy-dependent processes in nonpigmented ciliary epithelium that transport sodium into the posterior chamber and, in part, by the energy-independent processes ultrafiltration (and the related dialysis) and diffusion (17,20). The energy-dependent processes include the movement of water from the stromal pool into the posterior chamber in response to sodium transport. The energy-independent processes include ultrafiltration from ciliary capillaries into pigmented epithelium across the stroma basement membrane and diffusion from nonpigmented epithelium into the posterior chamber across the internal limiting membrane. The present results suggest either that sevoflurane or sevoflurane + remifentanil does not substantially inhibit these processes or that anesthetic concentration-related decrease in energy-dependent processes are counterbalanced by increases in the energy-independent processes.

Reported values for IOP in unanesthetized rabbits range from 12.0 ± 2.0 to 24.4 ± 1.3 mm Hg (average 19.0 mm Hg) (13,18,19,21,22). Values in anesthetized rabbits range from 10.0 ± 2.0 to 15.0 ± 6.3 mm Hg (average 12.5 mm Hg) (14,17,22). In the present study, sevoflurane 1%, 2%, or 3% or sevoflurane 1% + remifentanil did not significantly alter IOP compared with baseline values obtained during halothane anesthesia, and values during both sevoflurane and halothane anesthesia were similar to those previously reported in anesthetized rabbits. As previously mentioned, IOP is determined by ocular volume (IOF volume, choroidal blood volume, and vitreous volume) and ocular compliance (scleral rigidity and extraocular muscle tone) (4,5). IOF volume, in turn, is determined by aqueous humor formation rate and facility of outflow of aqueous humor (6,7). Although the decrease of intraocular compliance with increasing sevoflurane concentration was statistically significant in the present study, the magnitude was so small that IOP did not differ among groups and was similar to IOP during halothane anesthesia.

In summary, in this rabbit model, sevoflurane caused a dose-related decrease of intraocular compliance but no dose-related effect on IOP. The addition of remifentanil to sevoflurane anesthesia caused a significant increase in intraocular compliance. With both sevoflurane anesthesia and sevoflurane + remifentanil anesthesia, IOP was not significantly different from IOP during halothane anesthesia. Taken together, these results suggest that the statistically significant changes in intraocular compliance caused by sevoflurane and/or sevoflurane + remifentanil do not have a meaningful impact on IOP. With both sevoflurane and sevoflurane + remifentanil, IOP decreased compared with the average of previously reported IOP values in awake rabbits (13,18,19,21,22) and was similar to that previously reported in rabbits anesthetized with ethyl urethane, pentobarbital, or halothane alone or in combination with propofol, cocaine, or lidocaine (14,17,22).


   Appendix 1
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Appendix 1
References
 
Abbreviations for IOF dynamics are unfamiliar to most anesthesiologists. For that reason, those abbreviations were not used in the article. For the interested reader, the abbreviations for IOF dynamics traditionally used in the ophthalmological literature are presented below: C = intraocular compliance Ctr = trabecular outflow facility Fa = rate of aqueous humor formation Ftr = outflow across the trabecular meshwork Fu = uveoscleral outflow Pcs = hydrostatic pressure of the canal of Schlemm Rtr = resistance to trabecular outflow


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Appendix 1
 References
 

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  7. Hayashi M, Yablonski ME, Mindel JS. Methods of assessing the effects of pharmacologic agents on aqueous humor dynamics. In: Tasman W, Jaeger EA, eds. Foundations of clinical ophthalmology. vol 3. Philadelphia:JB Lippincott, 1992:1–9.
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  12. Jay JL. Functional organization of the human eye. Br J Anaesth 1980;52:649–54.[Free Full Text]
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  14. Artru AA. Trabecular outflow facility and formation rate of aqueous humor during propofol anesthesia in rabbits. Anesth Analg 1993;77:564–9.[Abstract/Free Full Text]
  15. Gelatt KN, Gum GG, Merideth RE, Bromberg N. Episcleral venous pressure in normotensive and glaucomatous beagles. Invest Ophthalmol Vis Sci 1982;23:131–5.[Abstract/Free Full Text]
  16. Barrie KP, Gum GG, Samuelson DA, Gelatt KN. Morphologic studies of uveoscleral outflow in normotensive and glaucomatous beagles with fluorescein-labeled dextran. Am J Vet Res 1985;46:89–97.[Web of Science][Medline]
  17. Artru AA. Trabecular outflow facility and formation rate of aqueous humor during intravenous cocaine or lidocaine in rabbits. Anesth Analg 1994;78:889–96.[Abstract/Free Full Text]
  18. Stone HH, Prijot EL. The effect of a barbiturate and paraldehyde on aqueous humor dynamics in rabbits. Arch Ophthalmol 1955;54:834–40.[Abstract/Free Full Text]
  19. Poyer JF, Gabelt B, Kaufman PL. The effect of topical PGF2 alpha on uveoscleral outflow and outflow facility in the rabbit eye. Exp Eye Res 1992;54:277–83.[Web of Science][Medline]
  20. Stamper RL. Aqueous humor: secretion and dynamics. In: Tasman W, Jaeger EA, eds. Foundations of clinical ophthalmology. vol 2. Philadelphia:JB Lippincott, 1992:1–25.
  21. Liu JH. Aqueous humor messengers in the transient decrease of intraocular pressure after ganglionectomy. Invest Ophthalmol Vis Sci 1992;33:3181–5.[Abstract/Free Full Text]
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Accepted for publication January 5, 1999.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 1999 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press