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OBJECTIVE: To identify factors predictive of operative success or failure for vertical muscle surgery performed in patients with Graves' ophthalmopathy. DESIGN: Prospective noncomparative case series. PARTICIPANTS: Thirty-one consecutive patients with Graves' ophthalmopathy who demonstrated vertical ocular motor imbalance, with or without simultaneous horizontal muscle imbalance. INTERVENTION: Vertical extraocular muscle surgery performed either in isolation or in association with horizontal muscle surgery. MAIN OUTCOME MEASUREMENTS: Vertical limitations of extraocular muscles were correlated with preoperative hypertropia. Stepwise linear regression was used to determine the significant predictors of postoperative hypertropia in primary gaze. Logistic analysis was used to estimate the probability of surgical failure (>5 diopters) on the basis of preoperative parameters. RESULTS: The amount of preoperative hypertropia was negatively correlated with total restriction of vertical ductions (r = -0.52, P < 0.01). Preoperative hypertropia was positively correlated with asymmetry in muscle restriction between the two eyes (r = 0.67, P < 0.0001). The best predictor of preoperative hypertropia was the difference between restriction of the contralateral opposing recti, namely the right superior rectus, and the left inferior rectus, as well as the right inferior rectus and the left superior rectus (r = 0.74, P < 0.0001). Restriction of the contralateral opposing recti was also the most significant predictor of surgical success (postoperative hypertropia < 5 prism diopters). CONCLUSIONS: Surgery tailored to address restriction of ductions, specifically the difference between contralateral opposing recti, is likely to improve the success of initial surgery beyond that based primarily on the magnitude of the vertical deviation.

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In the hopes of reducing the unpredictability associated with refractive surgical procedures and ultimately improving surgical techniques, many investigators have attempted to determine the elastic moduli of the cornea. Techniques such as stress-strain tests of corneal strips and the measurement of mercury drop displacement in a whole eye under increasing pressure have resulted in a range of values for Young's modulus from 10(5) to 10(7) Nm-2. Both of these methods are limited because these mechanical tests cannot be performed in the physiological state and because of the large amount of force applied during testing. We used an ultrasonic technique to determine the elastic moduli of the human cornea. Two groups of six corneas prepared under different conditions (in saline and in dextran) were examined separately and the shear waves were generated and detected in these 12 human eye bank eyes. All the waveforms were digitized and saved in files of binary format. Fast Fourier transformation (FFT) was applied to calculate the speed and attenuation of the shear wave. Using the resulting wave speeds and attenuation coefficients, the Young's moduli of the corneal samples were calculated as (5.3 +/- 1.1) x 10(6) Nm-2 and (2.0 +/- 1.0) x 10(7) Nm-2 for cornea samples prepared in saline and in dextran at 2.25 MHz, respectively.

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To determine the potential rate of intraoperative parenteral exposure of physicians and patients caused by glove perforation during ophthalmic surgery, gloves were analyzed after 125 procedures. Gloves were collected from all surgical team members (surgeon, assistants, scrub nurse, and circulating nurse). The rate of glove perforation was significantly lower for the surgeon, 0.3% (one of 303 gloves) than for the assistants, 5% (ten of 202 gloves [P = .001]), scrub nurses, 16% (52 of 326 gloves [P = .0001]), and circulating nurses, 15% (43 of 293 gloves [P = .0001]); similarly, assistants had a significantly lower rate than did scrub nurses (P = .0001) and circulating nurses (P = .001). There was no statistically significant difference in number of perforations on the basis of surgery duration or type of ophthalmic procedure. These findings suggest that the risk of parenteral exposure during ophthalmic surgery is low for the surgeon, and higher for other surgical personnel. We also analyzed additional safety precautions. Further study is warranted to determine the effectiveness of precautions and to guide policy formulation.

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Activation of alpha 1-adrenergic receptors in BC3H-1 muscle cells has been shown previously to mobilize intracellular Ca2+, which can be monitored as enhanced 45Ca2+ unidirectional efflux. We report here that histamine also stimulates 45Ca2+ efflux in these cells (Kact = 5.50 microM, nH = 0.94 +/- 0.04), reflecting mobilization of intracellular Ca2+ from a source similar to that accessed by alpha 1-adrenergic receptor activation. In addition, histamine stimulates substantial transmembrane 45Ca2+ influx into BC3H-1 cells. The actions of histamine are inhibited by the H1-selective antagonist, diphenhydramine (IC50 = 1.01 microM), but are unaffected by the H2-selective antagonist, cimetidine (1 nM-10 microM) indicating that histamine regulates cellular Ca2+ via a functional H1 receptor. The presence of independent receptor types which mobilize Ca2+ originating from common intracellular stores has been exploited in order to evaluate the determinants of receptor responsiveness following prior agonist exposure. After exposure with 45Ca2+ to achieve radioisotopic equilibrium, 30 min incubation with increasing concentrations of norepinephrine reduces to similar extents (30-40%) the unidirectional 45Ca2+ efflux responses to subsequent challenges by maximally effective concentrations of norepinephrine or histamine. The decrement in response following norepinephrine exposure appears to reflect an altered disposition of agonist-sensitive intracellular Ca2+, whereas the concentration dependence for alpha 1-adrenergic receptor activation remains unchanged. Prior exposure of cells to increasing concentrations of histamine also reduces the efflux response to norepinephrine challenge (approximately 30% decrease), whereas the response to subsequent histamine challenge is specifically and completely abolished. The loss of histamine responsiveness is accompanied by a marked shift in the concentration dependence for histamine receptor activation toward higher histamine concentrations. These results indicate that substantial alpha 1-receptor responsiveness is maintained following agonist exposure and that the observed reduction in response occurs distally to the receptor itself at some point common to alpha 1- and H1-receptor-effector coupling. By contrast, the H1-histamine receptor exhibits refractoriness, indicative of agonist-induced receptor desensitization.

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