Rates of glaucomatous visual field change after trabeculectomy.

BACKGROUND: Trabeculectomy is frequently performed in patients with glaucoma who are deteriorating, although its effects on rates of visual field (VF) progression are not fully understood. We studied the rate of VF progression post trabeculectomy comparing with medically treated patients matched for VF loss. METHODS: Medical records of patients who underwent trabeculectomy alone or combined with cataract extraction were reviewed. Patients with 5 or more 24-2 VF examinations post trabeculectomy were selected. The rate of mean deviation (MD) change after surgery was calculated for each patient. These patients were pairwise matched based on baseline MD with patients with glaucoma who were treated medically and had at least 5 VF tests. RESULTS: 180 surgical patients were identified and matched with 180 medically treated patients (baseline MD of -8.72 (5.24) dB and -8.71 (5.22) dB, respectively). Surgically and medically treated patients were followed for 7.4 (2.9) and 6.8 (3.1) years respectively. The MD slopes were -0.22 (0.55) dB/year and -0.08 (1.10) dB/year in the surgically and medically treated patients, respectively, and not statistically different (p=0.13, 95% CI -0.31 to 0.04). More patients in the surgical group had fast progression (rates worse than -1 dB/year) than in the medical group (17 and 7 patients, respectively, p=0.05). CONCLUSIONS: Our findings suggest that most patients who undergo trabeculectomy demonstrate relatively slow rates of VF progression postoperatively, similar to patients treated medically, although some patients can continue to progress despite adequate surgical control of intraocular pressure.

Orthovanadate inhibits adrenaline-induced hyperpolarization in amphibian sympathetic ganglia.

The adrenaline-induced hyperpolarization of neurones in sympathetic ganglia of Rana pipiens was recorded by means of the sucrose gap technique. This hyperpolarization was inhibited in a concentration-dependent manner by sodium orthovanadate (0.1-1.0 mM). Although orthovanadate inhibited the hydrolysis of ATP by preparations of microsomal Na+/K+ ATPase from frog nerve (IC50 = 3.0 microM), extracellularly-applied orthovanadate did not inhibit electrogenic sodium pumping in intact sympathetic ganglia of Rana pipiens. This and other observations that extracellularly-applied orthovanadate did not enter sympathetic neurones and did not have access to intracellular enzyme systems. It is suggested that orthovanadate acts at an extracellular site to inhibit the adrenaline-induced hyperpolarization.

Examination of the role of calcium in the adrenaline-induced hyperpolarization of bullfrog sympathetic neurons.

The adrenaline-induced hyperpolarization, which was recorded in neurons of bullfrog paravertebral sympathetic ganglia by means of the sucrose gap technique, was antagonized by 1 mM 4-aminopyridine. The response was unaffected by drugs which influence intracellular Ca2+ movements or Ca2+-sensitive K+ conductances, i.e. 100 or 200 microM Cd2+, 60 microM dantrolene Na+, 10 mM tetraethylammonium bromide, 0.5-2.0 microM apamin or 70 microM (+)-tubocurarine chloride. The spontaneous, rhythmic hyperpolarizations which occur in ganglionic neurons in the presence of 5 mM caffeine and reflect activation of Ca2+-sensitive K+ conductances following mobilization of intracellular Ca2+, were examined by means of intracellular recording. These responses were often biphasic, comprising a transient rapid early phase and a slow late phase. Tetraethylammonium (10 mM) and 0.5-2.0 microM apamin antagonized the rapid early phase and 70 microM (+)-tubocurarine chloride antagonized both phases of the response. Neither phase of these spontaneous, rhythmic, caffeine-induced hyperpolarizations were affected by 1 mM 4-aminopyridine. Although the adrenaline-induced hyperpolarization was antagonized by 50 microM 8-(diethylamino)octyl-3,4,5-trimethoxybenzoate and by 50 microM quinidine, the majority of the results argue against the hypothesis that mobilization of intracellular Ca2+ is required for activation of the K+ conductance thought to underlie the adrenaline-induced hyperpolarization.

Alpha 2-adrenergic hyperpolarization is not involved in slow synaptic inhibition in amphibian sympathetic ganglia.

The adrenaline-induced hyperpolarization (AdH), slow inhibitory postsynaptic potential (slow i.p.s.p.) and hyperpolarizing phase of the response to methacholine (MChH) in Rana pipiens sympathetic ganglia were studied by means of the sucrose-gap technique. Desmethylimipramine (DMI, 0.5 microM) lowered the EC50 for adrenaline from 1.65 microM (1.23-2.21 microM, n = 10) to 0.30 microM (0.21-0.41 microM, n = 8). DMI did not potentiate the slow i.p.s.p. or the MChH. Propranolol, sotalol or prazosin (1 microM) did not antagonize the AdH. The response was antagonised by phentolamine (IC50 = 0.53 microM), yohimbine (IC50 = 6.2 nM) and idazoxan (IC50 = 0.59 microM). Yohimbine (0.1 microM) did not reduce the amplitude of the slow i.p.s.p. or the MChH. The slow i.p.s.p. was eliminated in Ringer solution containing Cd2+ (100 microM). This concentration of Cd2+ did not reduce the amplitude of the MChH. Alpha-Methylnoradrenaline produced a concentration-dependent hyperpolarization with an EC50 of 0.31 microM (0.13-0.73 microM, n = 5), in the presence of DMI (0.5 microM). These results are consistent with the hypothesis that the AdH may be generated by activation of a receptor similar to the mammalian alpha 2-adrenoceptor. No evidence was found in support of the hypothesis that an adrenergic interneurone is involved in the synaptic pathway for the slow i.p.s.p.

Effects of mammalian brain extracts and chlormadinone acetate on neuronal Na+,K+-ATPase and electrogenic Na+,K+-pump activity in vitro.

Acid-acetone extracts of brain (from beef and guinea pig) and chlormadinone acetate (CMA) were compared with ouabain for their ability to inhibit the electrogenic Na+,K+-pump and the Na+,K+-ATPase of neuronal tissues. The membrane potential of neurones in the paravertebral sympathetic ganglion of the bullfrog was recorded in K+-free Ringer's solution by means of the sucrose gap technique. The potassium activated hyperpolarization (K+H), induced by the re-introduction of potassium, was used as an index of electrogenic Na+, K+-pumping. The K+H was blocked by 1 microM ouabain. Na+,K+-ATPase activity was measured in microsomal membrane preparations of frog and beef brain using a continuous spectrophotometric assay. Although ouabain consistently inhibited beef brain Na+,K+-ATPase (IC50 = 2.2 microM), acid-acetone extracts prepared from guinea pig and beef brain produced only partial inhibition. Neither of the extracts significantly reduced the K+H of the frog ganglion. CMA inhibited Na+,K+-ATPase prepared from bullfrog brain and spinal cord with slightly greater potency (IC50 = 4.5 microM) than did ouabain (IC50 = 10 microM). In contrast, electrogenic Na+,K+-pumping (i.e. the K+H) in the frog ganglion was not affected by this steroid. It is concluded that although both the extracts and CMA inhibited Na+,K+-ATPase, neither can be considered ouabain-like due to their failure to affect the electrogenic Na+,K+-pump in situ.

Effects of Healon vs. Viscoat on endothelial cell count and morphology after phacoemulsification and posterior chamber lens implantation.

The endothelial cell count and several morphologic characteristics of the cells were examined before and after surgery in 56 consecutive patients (60 eyes) who underwent phacoemulsification and implantation of a posterior chamber intraocular lens with either Healon (30 eyes) or Viscoat (30 eyes) as the viscoelastic material. In all cases the technique was the same, including removal of the viscoelastic from the anterior chamber at the end of the operation. The mean cell loss was greater in the Viscoat group than in the Healon group (9.27% +/- 2.52% vs. 2.71% +/- 2.53%), but not significantly so. There was a significantly greater reduction in polymegathism in the Healon group than in the Viscoat group (p less than 0.05). Although the results suggest that Healon has a greater protective effect on the corneal endothelium than Viscoat, the greater effort needed to remove Viscoat from the anterior chamber may have adversely affected the endothelium. Further studies in which Viscoat is left in the eye are warranted.

Initial identification of antinuclear-antibody-negative systemic lupus erythematosus on ophthalmic examination: a case report, with a discussion of the ocular significance of anticardiolipin (antiphospholipid) antibodies.

A 21-year-old man presented with an acute life-threatening illness that was diagnosed and treated as thrombotic thrombocytopenic purpura. The patient survived and during his recovery noted that his central vision was markedly impaired in both eyes. An ophthalmologic examination showed inflammatory and ischemic changes in the retinal vasculature consistent with a diagnosis of systemic lupus erythematosus (SLE). Review of the patient's clinical and laboratory findings did in fact support a diagnosis of SLE that was negative for antinuclear antibody but positive for anticardiolipin antibody. The authors discuss the importance of an ophthalmic examination in patients with SLE-like syndromes and the significance of positivity for anticardiolipin antibody and other antiphospholipid antibodies in patients with thrombosis in the eye or elsewhere.

Effects of Valsalva's manoeuvre on intraocular pressure.

We examined the effects of breath holding against a closed glottis (Valsalva's manoeuvre) on intraocular pressure (IOP) in four groups of volunteer subjects: 37 healthy young control subjects, 10 patients with chronic open-angle glaucoma, 11 age-matched control subjects and 8 glaucoma suspects. IOP was recorded by one person using a Digilab 30R/T Pneuma-Tonometer. Chart recordings of the IOP were measured independently by a second investigator. Recordings were taken before, during and 5 minutes after the seated subject exhaled into an aneroid manometer to a pressure of 25 to 35 cm H2O. There was marked variability in the individual responses to Valsalva's manoeuvre in all four groups, with substantial increases (to +9.5 mm Hg) and decreases (to -4.0 mm Hg) in IOP seen. The mean change in IOP during Valsalva's manoeuvre was a small, statistically insignificant decrease in all four groups. The mean change in IOP following Valsalva's manoeuvre was a larger, but still clinically small, decrease. The clinician should be aware of the individual variability in IOP changes with Valsalva's manoeuvre.

Potassium currents in cultured rabbit retinal pigment epithelial cells.

Membrane potential and ionic currents were studied in cultured rabbit retinal pigment epithelial (RPE) cells using whole-cell patch clamp and perforated-patch recording techniques. RPE cells exhibited both outward and inward voltage-dependent currents and had a mean membrane capacitance of 26 +/- 12 pF (SD, n = 92). The resting membrane potential averaged -31 +/- 15 mV (n = 37), but it was as high as -60 mV in some cells. When K+ was the principal cation in the recording electrode, depolarization-activated outward currents were apparent in 91% of cells studied. Tail current analysis revealed that the outward currents were primarily K+ selective. The most frequently observed outward K+ current was a voltage- and time-dependent outward current (IK) which resembled the delayed rectifier K+ current described in other cells. IK was blocked by tetraethylammonium ions (TEA) and barium (Ba2+) and reduced by 4-aminopyridine (4-AP). In a few cells (3-4%), depolarization to -50 mV or more negative potentials evoked an outwardly rectifying K+ current (IKt) which showed more rapid inactivation at depolarized potentials. Inwardly rectifying K+ current (IKI) was also present in 41% of cells. IKI was blocked by extracellular Ba2+ or Cs+ and exhibited time-dependent decay, due to Na+ blockade, at negative potentials. We conclude that cultured rabbit RPE cells exhibit at least three voltage-dependent K+ currents. The K+ conductances reported here may provide conductive pathways important in maintaining ion and fluid homeostasis in the subretinal space.

Left atrial myxoma causing ophthalmic artery occlusion.

A 45-year-old Caucasian woman presented with sudden onset right-sided hemiparesis, aphasia and a painful left eye. Examination revealed a bone-white fundus with no perfusion of either the retinal or choroidal circulations. Magnetic resonance imaging showed increased signal density of the left optic nerve sheath, orbital fat and extraocular muscles consistent with infarction of the ophthalmic artery distribution. An echocardiogram disclosed a mobile, multilobulated mass attached to the septal wall of the left atrium. Pathological examination of the resected tumour confirmed the diagnosis of endocardial myxoma. A colour Doppler study performed 1 month after surgery demonstrated absence of flow in the left ophthalmic artery. At 2 months, the left eye had no light perception and an intraocular pressure of 2 mmHg. This clinicopathological report describes the rare presentation of an acute ophthalmic artery obstruction secondary to atrial myxoma.