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Biomedical subjects

G A Heatley

Publications and source records attributed to G A Heatley.

5 recordsLinked to original sources
PubMed1998

The rarity of clinically significant rise in intraocular pressure after laser peripheral iridotomy with apraclonidine.

OBJECTIVE: To determine the incidence of intraocular pressure (IOP) rise of varying degrees after laser peripheral iridotomy (LPI) in patients with and without glaucoma treated perioperatively with pilocarpine and apraclonidine. DESIGN: A retrospective chart review. PARTICIPANTS: A total of 289 eyes in 179 patients with narrow occludable angles (NOA) (N = 148), open-angle glaucoma or ocular hypertension (OAG) (N = 115), or chronic-angle closure glaucoma (CACG) (N = 26) were reviewed. MAIN OUTCOME MEASURES: The difference between preoperative and postoperative IOP, absolute postoperative IOP, and the need for acute IOP-lowering treatment was noted. RESULTS: Only 1.1% (95% confidence interval [CI], 0.03%-5.8%; 1 of 94) of patients and 0.7% (95% CI, 0.02%-3.7%; 1 of 148) of eyes with NOA experienced a rise of more than 10 mmHg 1 to 2 hours after LPI. The incidence of postoperative IOP greater than 25 mmHg and acute postoperative IOP-lowering management was 0% (95% CI, 0%-3.8%). Intraocular pressure in 1 of 115 eyes (0.9%, 95% CI, 0.02%-4.7%) with OAG rose more than 10 mmHg, requiring acute treatment. None of the 26 CACG eyes experienced a rise of more than 10 mmHg (95% CI, 0%-13.2%). CONCLUSION: The IOP rise that requires further intervention after LPI with the perioperative use of pilocarpine and apraclonidine is very uncommon. In patients with NOA, routine postiridotomy IOP monitoring may not be required.

Adrenergic alpha-Agonists↗
PubMed1998

Trabeculectomy with mitomycin C: intermediate-term results.

PURPOSE: This study was performed to provide results 2 to 3 years after trabeculectomy with mitomycin C (MMC). METHODS: A consecutive series of all 68 patients who underwent trabeculectomy with MMC was analyzed using Kaplan-Meier life-table statistics and compared with other published retrospective analyses. RESULTS: At 2- and 3-year follow-up examinations, 59% (95% confidence interval [CI], 44-70%) and 47% (95% CI, 32-61%) of patients, respectively, avoided an intraocular pressure (IOP) of more than 21 mmHg or less than 20% below their preoperative level without glaucoma medication on two consecutive occasions more than 1 month apart after 3 months follow-up (75% [95% CI, 60-84%] and 70% [95% CI, 53-81%], respectively, with medication) and avoided additional glaucoma surgery. Loss of more than three lines of visual acuity on two occasions more than 1 month apart after 3 months follow-up occurred in 28% of patients (> 2 lines in 44%) at 3 years. Nonreversible causes of loss of three lines of acuity occurred in 13% of patients. Complications requiring reoperation occurred in 16% of patients and included hypotony maculopathy (4%) and late bleb leaks (4%). CONCLUSIONS: At the 3-year follow-up evaluation, trabeculectomy with MMC provided an approximately 50% chance of maintaining IOPs less than 21 mmHg and a more than 20% IOP reduction without concomitant use of glaucoma medication, which increased to 70% with the addition of medication. This procedure was associated with an approximately 30% risk of substantial visual loss (approximately 15% nonreversible) and a 15% chance of reoperation for complications.

Adult↗
PubMed1995

Adjunctive mitomycin C in Molteno implant surgery.

PURPOSE: The authors assessed the efficacy of adjunctive intraoperative mitomycin C to produce lower intraocular pressures (IOPs) in patients with complicated glaucoma who underwent double-plate Molteno implantation. METHODS: A pilot series of 21 consecutive patients who underwent double-plate Molteno implantation with adjunctive intraoperative mitomycin C (0.5 mg/ml) for 5 minutes was compared with a historical control group who received Molteno implants without mitomycin C (n = 18). With failure defined as an IOP greater than 21 or less than 6 mmHg at two observations 1 month apart, the addition of medication, re-operation for glaucoma, or tube removal, a life-table analysis of IOP was performed on patients with at least 3 months' follow-up. RESULTS: Success in the mitomycin C group was higher (68% at 1 year) than the control group (17% at 1 year; P = 0.006). Loss of more than one line of vision (33%) and re-operation for complications (including flat anterior chamber, choroidal detachment, and tube blockage) (38%) were slightly but not significantly more frequent in the mitomycin C group than in the control group. CONCLUSION: This study suggests that intraoperative mitomycin C in conjunction with Molteno implant may offer a better chance of achieving target IOPs in the low teens in patients with complicated glaucoma than Molteno implantation alone.

Adult↗
PubMed1982

Thyrotropin-releasing hormone mobilizes Ca2+ from endoplasmic reticulum and mitochondria of GH3 pituitary cells: characterization of cellular Ca2+ pools by a method based on digitonin permeabilization.

Treatment of 45Ca2+-loaded GH3 pituitary cells with various concentrations of digitonin revealed discrete pools (I and II) of cellular 45Ca2+ defined by differing detergent sensitivities. Markers for cytosol and intracellular organelles indicated that the two 45Ca2+ pools were correlated with the two major cellular Ca2+-sequestering organelles, endoplasmic reticulum (I) and mitochondria (II). Studies with various inhibitors were consistent with these assignments. Mitochondrial uncouplers preferentially depleted 45Ca2+ pool II while trifluoperazine selectively depleted 45Ca2+ pool I. Control experiments indicated that translocation of in situ organellar 45Ca2+ during and after permeabilization was negligible. We used the digitonin-permeabilization method to examine the effect of thyrotropin-releasing hormone (TRH) treatment on intracellular Ca2+ pools of GH3 pituitary cells. TRH was found to rapidly deplete both endoplasmic reticulum and mitochondrial exchangeable Ca2+ by 25-30%. The 45Ca2+ loss from both pools was maximal by 1 min after TRH addition and was followed by a recovery phase; mitochondrial 45Ca2+ content returned to control levels by 30 min. Previous treatment of cells with the mitochondrial uncoupler carbonyl cyanide p-trifluoromethoxy-phenylhydrazone blocked TRH-induced 45Ca2+ efflux from mitochondria, while previous treatment with valinomycin, an agent that depleted both 45Ca2+ pools, blocked any additional effect of TRH on these pools. We conclude that TRH rapidly promotes a net loss of exchangeable Ca2+ from GH3 cells as a result of hormone-induced mobilization of Ca2+ from endoplasmic reticulum and mitochondria.

Calcium↗