Intraoperative floppy iris syndrome: report of a case and histopathologic analysis.
OBJECTIVE
To understand the role of the α(1A)-adrenoreceptors (ARs) in the pathophysiologic mechanism of intraoperative floppy iris syndrome (IFIS).


METHODS
Iris specimens from a patient with tamsulosin hydrochloride-induced IFIS were obtained during trabeculectomy. Specimens underwent histological analysis and immunohistochemical analysis with antibodies specific for actin, myoglobin, α(1A)-ARs, and myosin. Iris specimens from a patient without IFIS were used for comparison. Samples were processed for transmission electron microscopy.


RESULTS
Histological examination showed normal dilator muscle, arterioles, stroma, and pigment epithelium. Actin, myosin, and myoglobin distribution and intensities were similar between IFIS and non-IFIS tissue. The staining pattern and colocalization with myosin suggested that α(1A)-ARs are present in iris arteriolar muscularis in addition to the dilator muscle in both IFIS and control irides. Significantly less staining of IFIS tissue was found compared with the non-IFIS iris. Ultrastructures of melanocytes and stroma appeared to be normal. Iris arterioles possessed thick endothelial basement membranes, semilongitudinally oriented muscularis, and abundant perivascular collagen coats.


CONCLUSIONS
We confirm the presence of α(1A)-ARs in human iris by results of immunohistochemical analysis. The α(1A)-ARs localize to iris arteriolar muscularis in addition to the iris dilator muscle. This localization suggests that IFIS may develop because of iris vascular dysfunction and that iris vasculature may have structural in addition to nutritive functions.
Department of Ophthalmology, Mount Sinai School of Medicine, New York, NY 10029, USA. lpanagis@gmail.com
Lampros
L
Panagis
Maria
M
Basile
Alan H
AH
Friedman
John
J
Danias
D000199:Actins / Q000378:metabolism; D058668:Adrenergic alpha-1 Receptor Antagonists / Q000009:adverse effects*; D000369:Aged, 80 and over; D006801:Humans; D007431:Intraoperative Complications; D007498:Iris / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D007499:Iris Diseases / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology*; D008297:Male; D046529:Microscopy, Electron, Transmission; D009211:Myoglobin / Q000378:metabolism; D009218:Myosins / Q000378:metabolism; D018340:Receptors, Adrenergic, alpha-1 / Q000378:metabolism; D013449:Sulfonamides / Q000009:adverse effects*; D013577:Syndrome; D000077409:Tamsulosin; D014130:Trabeculectomy
C541116:ACTA2 protein, human; D000199:Actins; D058668:Adrenergic alpha-1 Receptor Antagonists; D009211:Myoglobin; D018340:Receptors, Adrenergic, alpha-1; D013449:Sulfonamides; D009218:Myosins; D000077409:Tamsulosin