Real-time optical coherence tomography of the anterior segment at 1310 nm.

BACKGROUND: Recent advances in high-speed scanning technology have enabled a new generation of optical coherence tomographic (OCT) systems to perform imaging at video rate. Here, a handheld OCT probe capable of imaging the anterior segment of the eye at high frame rates is demonstrated for the first time. OBJECTIVE: To demonstrate real-time OCT imaging of anterior segment structures. DESIGN: Survey of anterior segment structures in normal human subjects. SETTING: Laboratory. MAIN OUTCOME MEASURES: Achieving real-time imaging of the anterior segment, satisfactory image quality, and convenience of a handheld probe. RESULTS: Optical coherence tomographic imaging of the anterior segment of the eyes of human subjects was performed using 1310-nm wavelength light with an image rate of 8 frames per second. Imaging trials demonstrated clear resolution of corneal epithelium and stroma, sclerocorneal junction, sclera, iris pigment epithelium and stroma, and anterior lens capsule. The anterior chamber angle was clearly visualized. Limited imaging of the ciliary body was performed. Real-time imaging of pupillary constriction in response to light stimulus was also performed. CONCLUSION: High-speed OCT at 1310-nm wavelength is a potentially useful technique for noninvasive assessment of anterior segment structures. CLINICAL RELEVANCE: Our results suggest that real-time OCT has potential applications in glaucoma evaluation and refractive surgery.

Simplified method for polarization-sensitive optical coherence tomography.

We report a method for extracting the birefringence properties of biological samples with micrometer-scale resolution in three dimensions, using a new form of polarization-sensitive optical coherence tomography. The method measures net retardance, net fast axis, and total reflectivity as a function of depth into the sample. Polarization sensing is accomplished by illumination of the sample with at least three separate polarization states during consecutive acquisitions of the same pixel, A scan, or B scan. The method can be implemented by use of non-polarization-maintaining fiber and a single detector. In a calibration test of the system, net retardance was measured with an average error of 7.5 degrees (standard deviation 2.2 degrees ) over the retardance range 0 degrees to 180 degrees , and a fast axis with average error of 4.8 degrees over the range 0 degrees to 180 degrees .

Regional distribution and characterization of [3H]dextrorphan binding sites in rat brain determined by quantitative autoradiography.

The pharmacologic specificity and anatomic distribution of [3H]dextrorphan recognition sites in the rat brain was characterized by quantitative autoradiography. Equilibrium saturation analysis indicated that [3H]dextrorphan labeled a single population of high affinity binding sites. These sites are heterogeneously distributed throughout rat forebrain with the following order of binding densities: hippocampal formation > cerebral cortex > thalamic nuclei > striatum. The association rate of [3H]dextrorphan with its binding site in area stratum radiatum of CA1 is accelerated by the addition of glycine and glutamate. [3H]Dextrorphan binding is, however, relatively insensitive to glycine and glutamate under equilibrium conditions, despite extensive prewashing procedures to deplete endogenous levels of these substances. The competitive N-methyl-D-aspartate (NMDA) antagonist D(-)-2-amino-5-phosphonopentanoic acid (D-AP5) and the glycine site antagonist 7-chlorokynurenic acid completely inhibit specific [3H]dextrorphan binding. D-AP5 suppresses [3H]dextrorphan binding in a regionally distinctive manner; a population of binding sites is weakly inhibited by D-AP5 in the lateral thalamic regions, whereas D-AP5 potently inhibits [3H]dextrorphan binding in the cerebral cortex. The rank order of potencies of an array of noncompetitive antagonists to inhibit [3H]dextrorphan binding unambiguously displays the pharmacologic profile of the noncompetitive antagonist domain of the NMDA receptor-channel complex. Furthermore, the distribution of [3H]dextrorphan binding sites in slide-mounted tissue appears qualitatively similar to the distribution of NMDA receptors previously reported using NMDA-displacement of [3H]glutamate, [3H](+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imi ne (MK-801) and [3H]1-[1-(2-thienyl)cyclohexyl]-piperidine (TCP) in most brain areas examined except the cerebellum. The molecular layer of the cerebellum displays a particularly high density of [3H]dextrorphan binding sites. The regional distribution of [3H]dextrorphan binding sites in rat brain does not correspond to the reported distributions of [3H]dextromethorphan or sigma binding sites.

The sigma receptor ligand 1,3-di(2-tolyl)guanidine is anticonvulsant in the rat prepiriform cortex.

Unilateral focal injection of 1,3-di(2-tolyl)guanidine (DTG) caused a dose-dependent and potent (ED50 = 5.25 nmol, 95% confidence limits 1.1 to 25.0 nmol) suppression of generalized motor seizures induced by (-)-bicuculline methiodide in the rat prepiriform cortex. These findings indicate that DTG is equipotent to the noncompetitive NMDA receptor antagonist MK-801 ((+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate) as an anticonvulsant. This potent pharmacological effect of DTG distinguishes it from two other prototypic sigma ligands, haloperidol and (+)-pentazocine, which are ineffective as anticonvulsants. Pretreatment of animals with haloperidol failed to block the anticonvulsant effects of DTG. These data therefore document a novel anticonvulsant action of DTG in vivo by a mechanism that does not involve sigma receptors.

Dextrorotatory opioids and phencyclidine exert anticonvulsant action in prepiriform cortex.

We have investigated the ability of an array of putative noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonists to suppress convulsions induced by a unilateral, focal injection of (-)-bicuculline methiodide (118 pmol) into the rat prepiriform cortex. The anticonvulsant potency of these compounds, (+)-5-methyl-10,11- dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate (MK-801) greater than dextrorphan greater than or equal to 1-(1-phenylcyclohexyl)piperidine hydrochloride (PCP) greater than dextromethorphan greater than (+)-pentazocine, upon microinjection into the prepiriform cortex, was highly correlated (r = 0.971; P less than 0.01) with their respective affinities for the [3H]dextrorphan-labelled NMDA receptors in rat forebrain membranes. These results suggest that noncompetitive antagonism of NMDA receptors underlies the anticonvulsant action of these compounds.

Pulsed carbon dioxide laser for cartilage vaporization and subchondral bone perforation in horses. Part II: Morphologic and histochemical reactions.

A pulsed carbon dioxide laser was used to vaporize articular cartilage in four horses, and perforate the cartilage and subchondral bone in four horses. Both intercarpal joints were examined arthroscopically and either a 1 cm cartilage crater or a series of holes was created in the third carpal bone of one joint. The contralateral carpus served as a control. After euthanasia at week 8, the treated and control joints were examined for gross changes, and samples of cartilage and subchondral bone, synovial membrane, and peripheral lymph nodes were examined histologically. Depletion of cartilage matrix glycosaminoglycan was assessed by safranin-O histochemical staining of the laser site and adjacent cartilage. Cartilage removal by laser vaporization resulted in rapid regrowth, with fibrous and fibrovascular tissue and occasional regions of fibrocartilage at week 8. The subchondral bone, synovial membrane, and draining lymph nodes appeared essentially unaffected by the laser cartilage vaporization procedure. Conversely, carbon dioxide laser drilling of subchondral bone resulted in poor penetration, extensive areas of thermal necrosis of bone, and significant secondary damage to the apposing articular surface of the radial carpal bone.

Pulsed carbon dioxide laser for cartilage vaporization and subchondral bone perforation in horses. Part I: Technique and clinical results.

A carbon dioxide laser, used in a rapidly pulsed mode, was evaluated for intra-articular use in horses. Under arthroscopic guidance, a lensed 5 mm laser probe attached directly to a hand-held carbon dioxide laser was inserted into one intercarpal joint of eight horses. In four horses, a cartilage crater 1 cm in diameter was created to the level of the subchondral bone of the articular surface of the third carpal bone. In four horses, the laser was directed perpendicular to the articular surface of the third carpal bone and activated to penetrate the cartilage and subchondral bone. The intercarpal joint of the opposite carpus in each horse was subjected to arthroscopic examination and insertion of the laser probe for an equivalent time. The laser was not activated and these joints served as sham operated controls. The horses were evaluated clinically for 8 weeks, then euthanatized, and the joints were examined radiographically, grossly, and histologically. Pulsed carbon dioxide laser vaporized cartilage readily but penetrated bone poorly. Cartilage vaporization resulted in no greater swelling, heat, pain on flexion, lameness, or synovial fluid reaction than the sham procedure. Laser drilling resulted in a shallow, charred hole with a tenacious carbon residue, and in combination with the thermal damage to deeper bone, resulted in increased swelling, mild lameness and a low-grade, but persistent synovitis. The carbon dioxide laser is a useful intra-articular instrument for removal of cartilage and has potential application in inaccessible regions of diarthrodial joints. It does not penetrate bone sufficiently to have application in subchondral drilling.