Aqueous humor is secreted into the posterior chamber by the ciliary processes at a nearly constant rate ( 5) and enters the anterior chamber via the pupil. IOP is determined by the turnover of aqueous humor, a clear watery fluid that inflates the ocular globe and is the primary source of nourishment to the avascular lens, cornea, and trabecular meshwork. Understanding the factors regulating IOP is therefore important for understanding ocular physiology in health and disease. All current treatments for glaucoma lower IOP to prevent further glaucomatous damage to retinal ganglion cell axons, regardless of whether ocular hypertensive or normotensive ( 3, 4). Glaucoma is characterized by death of retinal ganglion cells that relay visual information from the retina to the brain. An IOP above 21 mmHg is classified as ocular hypertension, which is the primary risk factor for glaucoma, a blinding group of diseases afflicting 80 million people worldwide ( 2). IOP in healthy individuals typically lies between 10 and 21 mmHg ( 1). Intraocular pressure (IOP) is important for maintaining the refractive shape and dimensions of the eye necessary for vision. These studies reveal a dynamic component to outflow function that responds instantly to the ocular pulse and may be important for outflow regulation and IOP homeostasis. Thus, the ocular pulse causes an immediate increase in outflow facility in mice, with roughly one-half of the facility increase attributable to NO production. This effect was partly inhibited by L-NAME, where pressure pulsations increased outflow facility by 8% ( P < 0.001). During the pulsatile period in the vehicle-treated eye, outflow facility increased by 16 % ( P < 0.001) relative to the facility measured during the preceding and subsequent steady periods. One eye of each cadaver was perfused with 100 µM L-NAME to inhibit NO synthase, whereas the contralateral eye was perfused with vehicle. Eyes were retained in situ, with an applied mean pressure of 8 mmHg and 1.0 mmHg pk-pk pressure amplitude at 10 Hz to mimic the murine heart rate. Using iPerfusion, we measured outflow facility (flow/pressure) during alternating periods of steady or pulsatile IOP in both eyes of 16 cadaveric C57BL/6J mice (13-14 weeks). We confirmed that living mice exhibit an ocular pulse with a peak-to-peak (pk-pk) amplitude of 0.5 mmHg under anesthesia. We hypothesize that the ocular pulse modulates outflow facility by stimulating shear-induced nitric oxide (NO) production by SC cells.
The ocular pulse induces pulsatile shear stress in Schlemm’s canal (SC). Intraocular pressure (IOP) is not static, but rather oscillates by 2–3 mmHg because of cardiac pulsations in ocular blood volume known as the ocular pulse.
0 kommentar(er)
