Assessment of the correlation of the tear breakup time with quality of vision and dry eye symptoms after SMILE surgery

Purpose: It is well reported that dry eye symptoms can increase after many refractive surgery procedures. This study aims to provide a clinical understanding of the correlation of fluorescein tear film breakup time (FTBUT) with quality of vision (QoV) and dry eye symptoms following small incision lenticule extraction surgery (SMILE). Methods: Patients electing to have SMILE surgery were subdivided into 2 groups: Group 1 included short preoperative FTBUTs of 3 to 6 seconds (s); Group 2 included long FTBUTs of ≥ 8 s. Uncorrected distance visual acuity, corrected distance visual acuity, manifest refraction, FTBUT, QoV and Ocular Surface Disease Index (OSDI) questionnaires were recorded 1 and 6 months postoperatively. Results: Thirty-nine subjects were included in each group. There was no significant difference in visual outcomes between the 2 groups at both the 1- and 6-month postoperative assessments. FTBUT remained significantly lower in group 1. Oxford staining was initially higher for group 1 at 1 month (P = 0.007), but there was no significant difference at 6 months (P = 0.180). There was no significant difference in QoV or OSDI scores between the 2 groups at both postoperative visits. Conclusions: Low preoperative FTBUT (3–6 s) does not appear to negatively affect postoperative visual outcomes or results in a greater likelihood of dry eye symptoms and poor ocular surface compared to eyes with a longer preoperative FTBUT. These results suggest that a low preoperative FTBUT does not necessarily increase the likelihood of poor visual acuity, dry eyes symptoms, or poor ocular surface outcomes following SMILE surgery

Origin of the potassium and voltage dependence of the cardiac inwardly rectifying K-current (IK1).

Using various voltage clamp protocols, we have examined the activation and deactivation kinetics of IK1 recorded in dissociated myocytes obtained from canine purkinje fibers. Exponential current relaxations following step changes of the membrane potential were characterized at several different K levels (5, 12, 42, and 82 mM) and several voltages (K reversal potential +/- 40 mV). We have interpreted our data according to a K-activated, K-channel model of IK1 gating. Our data suggests that at least two binding sites for extracellular K must be occupied before the channel opens and occupancy of about three more higher affinity sites for K on the open channel will slow the closing of that channel. In our model, the voltage dependency of gating arises from a combination of three voltage dependent steps: (a) isomerization between open and closed states, (b) binding of K, and (c) occupancy of the channel by internal Mg. Lowering internal K to 40 mM causes major changes in the voltage and K dependence of IK1 gating. However, these changes could be accounted for in our model by relatively small (approximately 20 to 30 mV) shifts in the voltage dependence of several of the steps that govern gating. Our data further suggest that there is an interaction between both extracellular and intracellular K levels and the ability of intracellular Mg to block the IK1 channel

Internal and external K+ help gate the inward rectifier.

Recent investigations have demonstrated substantial reductions in internal [K+] in cardiac Purkinje fibers during myocardial ischemia (Dresdner, K.P., R.P. Kline, and A.L. Wit. 1987, Circ. Res. 60: 122-132). We investigated the possible role these changes in internal K+ might play in abnormal electrical activity by studying the effects of both internal and external [K+] on the gating of the inward rectifier iK1 in isolated Purkinje myocytes with the whole-cell patch-clamp technique. Increasing external [K+] had similar effects on the inward rectifier in the Purkinje myocyte as it does in other preparations: increasing peak conductance and shifting the activation curve in parallel with the potassium reversal potential. A reduction in pipette [K+] from 145 to 25 mM, however, had several dramatic previously unreported effects. It decreased the rate of activation of iK1 at a given voltage by several-fold, reversed the voltage dependence of recovery from deactivation, so that the deactivation rate decreased with depolarization, and caused a positive shift in the midpoint of the activation curve of iK1 that was severalfold smaller than the associated shift of reversal potential. These changes suggest an important role of internal K+ in gating iK1 and may contribute to changes in the electrical properties of the myocardium that occur during ischemia